PHARMACEUTICAL COMPOUNDS

Abstract: Compounds or their salts having general formulas (I) and (II): wherein s is and integer equal to 1 or 2, preferably s = 2; A is the radical of a drug and is such as to meet the pharmacological tests reported in the description, C and C1 are two bivalent radicals. The precursors of the radicals B and B1 are such as to meet the pharmacological test reported in the description.

Description: " PHARMACEUTICAL COMPOUNDS " • k -k -x T -k -k The present invention relates to novel drugs for systemic use and non systemic use, and the composition thereof, to be used in oxidative stress and/or endothelial dysfuntions cases. By oxidative stress it is meant the generation of free radicals or radicalic compounds, which causes injury both of the cell and that of the surrounding tissue (Pathophysiology: the biological basis for disease in adults and children, McCance & Huether 1998 pages 48-54). By endothelial dysfunctions it is meant those relating to the vasal endothelium. The damage of the vasal endothelium is known as one of those important events that can cause a series of pathological processes affecting various organs and body apparatuses, as described hereinafter (Pathophysiology: The biological basis for disease in adults and children, McCance & Huether 1998 page 1025). As known, the oxidative stress and/or the endothelial dysfunctions are associated to various pathologies as reported hereinafter. The oxidative stress can also be caused by toxicity of a great variety of drugs, which significantly affects their performances. Said pathological events are of a chronic, debilitating character and are very often typical of the elderly . As already said, in said pathological conditions the drugs used show a remarkably worsened performance. Examples of pathological situations caused by the oxidative stress and/or by the endothelial dysfunctions, or present in elderly, are the following: For the cardiovascular system: myocardial and vascular ischaemia in general, hypertension, stroke, arteriosclerosis, etc. For the connective tissue: rheumatoid arthritis and connected inflammatory diseases, etc. For the pulmonary system: asthma and connected inflammatory diseases, etc. For the gastrointestinal system: ulcerative and non ul- cerative dyspepsias, intestinal inflammatory diseases, etc. For the central nervous system: Alzheimer disease, etc. For the urogenital system: impotence, incontinence. For the cutaneous system: eczema, neurodermatitis , acne. The infective diseases in general (ref . : Schwarz-KB, Brady "Oxidative stress during viral infection: A review" Free radical Biol. Med. 21/5, 641-649 1996). Further the ageing process can be considered as a true pathologic condition (ref. Pathophysiology: the biological basis for disease in adults and children, pages 71-77). The known drugs when administered to patients having pathologies associated to oxidative stress and/or endothelial dysfunctions, show a lower activity and/or higher toxicity. This happens for example for drugs such as the antiinflammatory, cardiovascular drugs, respiratory apparatus drugs, central nervous system drugs, bone system drugs, antibiotics, urogenital , endocrine drugs, etc. Drug research is directed to find new molecules having an improved therapeutic index ( efficacy/toxicity ratio) or a lower risk/benefit ratio, also for pathological conditions as those above mentioned, wherein the therapeutic index of a great number of drugs results lowered. In fact in the above mentioned conditions of oxidative stress and/or endothelial dysfunctions, many drugs show a lower activity and/or higher toxicity. For instance antiinflammatory drugs, such as NSAIDs and anticolitic drugs, such as 5 -aminosalicylic acid and its derivatives, show the following drawbacks. NSAIDs result toxic particularly when the organism is debilitated or affected by morbid conditions associated to oxidative stress. Said conditions are for example the following: age, pre-existing ulcer, pre-existing gastric bleeding, debilitating chronic diseases such as in particular those affecting cardiovascular, renal apparatuses, the haematic crasis, etc. ( "Misoprostol reduces serious gastrointestinal complications in patients with rheumatoid arthritis receiving non- steroidal anti - inflammatory drugs. A randomized, double blind, placebo-controlled trial." F.E. Silverstein et Al . , Ann. Intern. Med. 123/4, 241-9, 1995; Martindale 31a eά . 1996, pag . 73, Current Medical Diagnosis and Treatment 1998, pages 431 and 794). The administration of anti - inflammatory drugs to patients in the above mentioned pathological conditions can be made only at doses lower than those used in therapy in order to avoid remarkable toxicity phenomena. Thus anti- inflammatory activity results poor. Beta-blockers , used for the angina, hypertension and cardiac arrhythmia treatment, show side effects towards the respiratory apparatus (dyspnoea, bronchoconstriction) , and therefore they can cause problems in patients affected by pathologies to said organs (asthma, bronchitis). Therefore beta-blockers further worsen respiratory diseases such as asthma. Therefore in asthmatic patients reduced doses of said drugs must be used in order not to jeopardize even more the respiratory functionality. Thus the efficacy of the beta-blockers results very reduced. Antithrombotics , such as for example dipyridamole , aspirin, etc., used for the prophylaxis of thrombotic phenomena, have the same drawbacks. In patients affected by pathologies connected to oxidative stress and/or endothelial dysfunc ions, the therapeutic action or the tolerability of these drugs, as in the case of aspirin, is greatly reduced. Bronchodilators for example salbutamol, etc., are used in the asthma and bronchitis treatment and drugs active on the cholinergic system are used in pathologies such as urinary cholinergic incontinence. Their administration can produce similar side effects affecting the cardiovascular apparatus, causing problems both to cardiopathic and to hypertensive patients. Cardiopathies and hypertension are pathologies associated, as above said, to the oxidative stress and/or endothelial dysfunctions. Also these drugs show the same drawbacks as those above mentioned. Expectorant and ucolytic drugs, which are used in the therapy of inflammatory states of the respiratory organs, show drawbacks in patients affected by the above described conditions. Their administration can give rise to heartburn and gastric irritability, particularly in the elderly. Bone resorption inhibitors, such as diphosphonates (for example alendronate, etc.) are drugs showing high gastrointestinal toxicity. Therefore also these drugs can show the same drawbacks as those above mentioned. Phosphodiesterase inhibitors, such as for example sildenafil, zaprinast , used in the cardiovascular and respiratory system diseases, are charaterized by similar problems as to tolerability and/or efficacy in the mentioned pathological conditions of oxidative stress and/or endothelial dyεfuntions . Antiallergic drugs, for example cetirizine, montelukast, etc. show similar problems in the mentioned pathological conditions, particularly for that it concerns their efficacy. Anti-angiotensin drugs, f.i. ACE- inhibitors , for example enalapril, captopril, etc., and receptor inhibitors, for example losartan, etc., are used in the cardiovascular disease treatment. Their drawback is to give side effects to the respiratory apparatus (i.e. cough, etc.) in the above mentioned pathological conditions. Antidiabetic drugs, both of the insulin- sensitizing and of hypoglycaemizing type, such as for example sulphonylureas , tolbutamide , glypiride, glyclazide, glyburide, nicotinamide etc., are ineffective in the prophylaxis of diabetic complications. Their administration can give side effects, such as for example gastric lesions. These phenomena become more intense in the pathological conditions above mentioned. Antibiotics, for example ampicillin, clarihtromycin, etc., and antiviral drugs, acyclovir, etc., show problems as regards their tolerability, for example they cause gastro- intestinal irritability. Antitumoral drugs, for example doxorubicine, daunorubicin, cisplatinum, etc., have high toxicity, towards different organs, among which are stomach and intestine. Said toxicity is further worsened in the above mentioned pathologies of oxidative stress and/or endothelial dys unctions. Antidementia drugs for example nicotine and colino- mimetics, are characterized by a poor tolerability especially in the above mentioned pathologies. The need was felt to have available drugs showing an improved therapeutic performance, i.e. endowed both of a lower toxicity and/or higher efficacy, so that they could be administered to patients in morbid conditions of oxidative stress and/or endothelial dysfunctions, without showing the drawbacks of the drugs of the prior art. It has now surprisingly and unexpectedly found that the aforementioned problems evidenced the administration of drugs, to patients affected by oxidative stress and/or endothelial dysfunctions, or to the elderly in general, are solved by a novel class of drugs as described hereinafter. An object of the invention are compounds or their salts having the following general formulas (I) and (II): A—B—C-N(0) B (I) wherein: s = is an integer equal to 1 or 2, preferably s = 2; A = R— 1 - , wherein R is the drug radical and 2 = (CO) t or (X) t ., wherein X = O, S, NR 1C , R lc is H or a linear or branched alkyl, having from 1 to 5 carbon atoms, or a free valence, t and t' are integers and equal to zero or 1, with the proviso that t = 1 when t' = 0; t = 0 when t' = 1; B = -T B —X 2 —T BI - wherein T B and T BI are equal or different; T B = (CO) when t = 0, T B = X when t ' = 0 , X being as above defined ; T BI = (CO) tx or (X) txx wherein tx and txx have the 0 or 1 value; with the proviso that tx = 1 when txx = 0, and tx = 0 when txx = 1; X is as above defined; X is a bivalent bridging bond as defined below; C is the bivalent -T c -Y- radical, wherein T c = (CO) when tx = 0 , T c = X when txx = 0 , X being as above defined; Y is an alkylenoxy group R'O wherein R' is linear or branched when possible C--C 20 . preferably having from 1 to 6 carbon atoms, most preferably 2-4, or a cycloalkylene having from 5 to 7 carbon atoms, in the cycloalkylene ring one or more carbon atoms can be substituted by heteroatoms, the ring may have side chains of R' type, R' being as above defined; or IX IIX I 3 I - [ C ] n ιχ— Y 3 — [ C ] n ιιχ " 0- ( HI ) I I RΓI ' RTI IX ' wherein : nIX is an integer between 0 and 3, preferably 1; nllX is an integer between 1 and 3, preferably 1; Rpjxf R τιx ' ' ∑^ TIIX ' ^Γ IIX ' ' eα - u l to or different from each other are H or a linear or branched C-^-^ alkyl; prefe¬ rably -rx . ϊ^rix ' . ^ TIIX - ^ IIX' are H. Y 3 is a saturated, unsaturated or aromatic heterocyclic ring containing at least one nitrogen atom, preferably one or two nitrogen atoms, said ring having 5 or 6 atoms. wherein n3 is an integer from 0 to 3 and n3 ' is an integer from 1 to 3 ; wherein n3 and n3 ' have the above mentioned meaning (CH 2 -CH-CH 2 -0) nf , ONO- (CH 2 -CH-CH 2 -0) nf , - ONO- wherein nf ' is an integer from 1 to 6 preferably from 1 to 4 ; - (CH-CH 2 -0) nf - I R lf - (CH 2 -CH-0) nf - I R lf wherein R lf = H, CH 3 and nf is an integer from 1 to 6; preferably from 1 to 4; preferably Y = -R'O- wherein R' is as above defined; preferably R' is a C j -Cg alkylene; wherein: c ι ~ ~τ cι γ ' τ cn wherein T CI and T CII are equal or different, T CI = (CO) when t = 0, T CI = X when t' = 0, X being as above defined; τ cn~ (CO) tI or (X) t ιι/ wherein tl and til have the 0 or 1 value; with the proviso that tl = 1 when til = 0, and tl = 0 when til = 1; X is as above defined; Y' is as Y above defined, but with three free valences instead of two, preferably: a -R'O- group wherein R' is as above defined, I preferably from 1 to 6 carbon atoms, most preferably 2 - 4 , or wherein n3 is an integer from 0 to 3 and n3 ' is an integer from 1 to 3; wherein n3 and n3 ' have the above mentioned meaning; I (CH 2 -CH-CH 2 -0) nf , - I 0N0 2 wherein one hydrogen atom on one of the carbon atoms is substituted by a free valence; - (CH 2 -CH-CH 2 -0) nf ,- I wherein nf ' is an integer from 1 to 6 preferably from 1 to 4 ; wherein one hydrogen atom on one of the carbon atoms is substituted by a free valence; - ( CH - CH 2 - 0 ) nf - I wherein one hydrogen atom on one of the carbon atoms is substituted by a free valence; - (CH 2 -CH-0) n --- I Rif wherein R lf = H, CH 3 and nf is an integer from 1 to 6; preferably from 1 to 4; wherein one hydrogen atom on one of the carbon atoms is substituted by a free valence; preferably Y' = - R'O- wherein R' is a linear or I branched C 2 -C 4 , the oxygen which in Y' is covalently linked to the -N(0) s group is at the end of the free bond indicated in C formula; B l = " BII x 2a wherein X a is a monovalent radical as defined below, T B II = ( c °) when tl = 0 , T BII = X when til = 0, X being as above defined; X 2 , bivalent radical, is such that the corresponding precursor of B: -T B —X 2 —T BI - meets the test 4, precursor in which the T B and T BI free valence are each saturated with -OZ, -Z, or with -Z I -N-Z 11 , Z 1 and Z 11 being equal I or different and have the Z values as defined below, depending on the fact that T B and/or T BI = CO or X, in connection with the values of t, t', tx and txx; X 2a monovalent radical, such that the corresponding precursor of ± - -T BII —X 2a meets the test 4, precursor wherein the free valence of T BII is saturated with -OZ, -Z or with -Z I -N-Z 11 , Z 1 and Z 1 - being equal or different and I having the Z values as defined below, depending on the fact that T BII = CO or X, in connection with the values of tl and til; the drug A = R—T ] _-, wherein the free valence is saturated as indicated hereinafter: when t ' = 0 with: O-Z wherein Z = H or R la , R la being a linear or when possible branched C 1 -C 10 alkyl, preferably C 1 -C 5 , or with Z I -N-Z 11 , Z 1 and Z 11 being as above defined, I when t = 0 with -Z, wherein Z is as above defined, with the proviso that the drug is not a steroid, is such to meet at least one of the tests 1-3; wherein test 1 (NEM) is a test in vivo carried out on four groups of rats (each formed by 10 rats), the controls (two groups) and the treated (two groups) of which one group of the controls and one group of the treated respectively are administered with one dose of 25 mg/kg s.c. of N-ethylmaleimide (NEM), the controls being treated with the carrier and the treated groups with the carrier + the drug of formula A = R- T 1 - wherein the free valence is saturated as above indicated, administering the drug at a dose equivalent to the maximum one tolerated by the rats that did not receive NEM, i.e. the highest dose administrable to the animal at which there is no manifest toxicity, i.e. such as to be symptomatologically observable; the drug complies with test 1, i.e. the drug can be used to prepare the compounds of general formula (I) and (II), when the group of rats treated with NEM + carrier + drug shows gastrointestinal damages, or in the group treated with NEM + carrier + drug are observed gastrointestinal damages greater than those of the group treated with the carrier, or of the group treated with the carrier + drug, or of the group treated with the carrier + NEM; wherein test 2 (CIP) is a test in vitro wherein human endothelial cells from the umbilical vein are harvested under standard conditions, then divided into two groups (each group replicated five times), of which one is treated with a mixture of the drug 10 "4 M concentration in the culture medium, the other group with the carrier; then cumene hydroperoxide (CIP) having a 5 mM concentration in the culture medium is added to each of the two groups; the drug meets test 2, i.e. the drug can be used to prepare the compounds of general formula ( I ) and (II), if a statistically significant inhibition of the apoptosis (cellular damage) induced by CIP is not obtained with p < 0.01 with respect to the group treated with the carrier and CIP ; wherein test 3 (L-MAME) is a test in vivo carried out on four groups of rats (each group formed by 10 rats) for 4 weeks and receiving drinking water, the controls (two groups) and the treated (two groups), of which one group of the controls and of the treated respectively receives in the above 4 weeks drinking water added of N-ω -nitro- L- arginine methyl ester (L-NAME) at a concentration of 400 mg/litre, the controls in the 4 weeks being administered with the carrier and the treated in the 4 weeks with the carrier + the drug, administering the carrier or the drug + carrier once a day, the drug being administered at the maximum dose tolerated by the group of rats not pretreated with L-NAME, i.e. , the highest dose administrable to animals at which no manifest toxicity appears, i.e. such as to be symptomatologically observable; after the said 4 weeks, the water supply is stopped for 24 hours and then sacrified, determining the blood pressure 1 hour before sacrifice, and after sacrifice of the rats determining the plasma glutamic pyruvic transaminase (GPT) after sacrifice, and examining the gastric tissue; the drug meets test 3, i.e. the drug can be used to prepare the compounds of general formula (I) and (II), when in the group of rats treated with L-NAME + carrier + drug, greater hepatic damages (determined as higher values of GPT) and/or gastric and/or cardiovascular damages (determined as higher values of blood-pressure) are found in comparison in comparison respectively with the group treated with the carrier alone, or with the group treated with the carrier + drug, or with the group treated with the carrier + L-NAME; the precursors of B or B-_ with the free valences saturated as above defined must meet test 4: it is an analytical determination carried out by adding portions of methanol solutions of the precursor of E cr B at a 10 "4 M concentration, to a methanol solution of DPPH ( 2 , 2 -diphenyl- 1-picryl hydrazyl - free radical); after having maintained the solution at room temperature away from light for 30 minutes, it is read the absorbance at the wave length of 517 nm of the test solution and of a solution containing only DPPH in the same amount as in the test solution; and then the inhibition induced by the precursor towards the radical production by DPPH is calculated as a percentage by means of the following formula: (1 - A S /A C )X100 wherein A s and A c are respectively the absorbance values of the solution containing the test compound + DPPH and that of the solution containing only DPPH; the precursor complies with test 4 when the percentage of inhibition as above defined is equal to or higher than 50%. Preferably the precursor compound of B or B 1 (precursor of the X 2 or X 2a radical in the formulas (I) and (II) respectively), is selected from the following classes of compounds: Aminoacids, selected from the following: L-carnosine (formula Cl ) , anserine (CII), selenocysteine (CIII), selenomethionine (CIV), penicilia-mine (CV), N-acetyl- penicillamine (CVI), cysteine (CVII), N-acetyl- cysteine (CVIII), glutathione (CIX) or its esters, preferably ethyl or isopropyl ester: (Cl] (CII) (CIII) (CIV) (CV) , (CVI) (CVII) (CVIII) (CIX) hydroxyacids, selected from the following: gallic acid (formula DI ) , ferulic acid (DH), gentisic acid (Dili), citric acid (DIV), caffeic acid (DV), hydro caffeic acid (DVI), p-coumaric acid (DVII), vanillic acid (DVIII), chlorogenic acid (DIX), kynurenic acid (DX) , syringic acid (DXI): (DI) (DH) (Dili) (DIV) (DV) (DIX) (DX) (DXI) Aromatic and heterocyclic mono- and polyalcohols, selected from the following: nordihydroguaiaretic acid (El), quercetin (EH), catechin (EIII), ka- empferol (EIV), sulphurethyne (EV), ascorbic acid (E- VI), isoascorbic acid (EVII), hydroquinone (EVIII), gossypol (EIX) , reductic acid (EX), methoxy- hydroquinone (EXI), hydroxyhydroquinone (EXII), propyl gallate (EXIII), saccharose (EXIV), vitamin E (EXV), vitamin A ( EXVI ) , 8-quinolol (EXVII), 3- ter-butyl-4-hydroxyanisole (EXVIII), 3 -hydroxyflavone (EXIX), 3,5-ter-butyl-p-hydroxytoluene (EXX), p-ter- butyl phenol (EXXI), timolol (EXXII), xibornol (EXXIII) , 3,5-di-ter-butyl-4-hydroxybenzyl-thio- glycolate (EXXIV), 4 ' -hydroxybutyranilide (EXXV), guaiacol (EXXVI), tocol (EXXVH), isoeugenol (EX- XVIII), eugenol (EXXIX), piperonyl alcohol (EXXX), allopurinol (EXXXI), conyferyl alcohol (EXXXII), 4- hydroxyphenetyl alcohol (EXXXIII), p-coumaric alcohol (EXXXIV), curcumin (EXXXV): :EI) (EH) (EIII) (EIV) (EV) (EVI) (EVII) (EVIII) (EIX) (EX) (EXI) (EXII) (EXIII) (EXIV) (EXV) ( EXVI ) (EXVII) (EXVIII) (EXIX) (EXXI) (EXX) (EXXII) (EXXIII) ( EXXIV ) (EXXV) (EXXVI) EXXVI I) ( EXXXI ) (EXXVIII) ( EXXIX ) (EXXX) (EXXXI i ; (EXXXIII) (EXXEV) ( EXXXV ) aromatic and heterocyclic amines, selected from the following: N, N' -diphenyl -p-phenylenediamine (Ml), ethoxyquin (Mil), thionine (Mill), hydroxyurea (M- IV) (MI) (Mil) (MIII; (MIV) Compounds containing at least a free acid function, selected from the following: 3 , 3 ' - thiodipropionic acid (NI), fumaric acid (Nil), dihydroxymaleic acid (NIH), thioctic acid (NIV), edetic acid (NV), bilirubin (NVI), 3 , -methylendioxycinna ic acid (NVI- I), piperonylic acid (NVIII): HOOC HOOC COOH HOOC ' COOH \ CCOH HO OH (NI) ;NII ) (NIH (NIV) ;NV) (NVI (NVII) (NVIII) The above mentioned precursors are prepared according to the known methods in the prior art , for example described in "The Merck Index, 12a Ed. (1996), herein incorporated by reference. When available, the corresponding isomerε and optical isomers can be used. Tests 1-3 that are carried out for selecting the precursor drug (hereafter indicated in the tests also as "drug") to be used for the synthesis of the products of the invention are in details the following: Test 1 (NEM) : evaluation of the gastrointestinal damage from oxidative stress induced by free radicals formed following administration of N-ethylmaleimide (NEM) (H.G. Utley, F. Bernheim, P. Hochstein "Effects of sulphydril reagents on pe- roxidation in microsomes" Archiv. Biochem. Biophys. 118, 29-32 1967). The animals (rats) are distributed in the following groups (no. 10 animals for group) : A) Control groups : 1° group: treatment: only carrier (aqueous suspension 1% w/v of carboxymethylcellulose , dose: 5 ml/Kg when the drug is administered by os, or a physiologic solution when parenterally administered, i.e. by subcutaneous , intraperitoneal, intravenous or intermuscular route) , 2° group: treatment: carrier as above defined + NEM, B) Groups treated with the drug: group I : treatment : carrier + drug , gruppo II: treatment: carrier + drug + NEM. The administration routes are those known for the drug, and can be the oral or subcutaneous , intraperitoneal , intravenous or intramuscular route . The NEM dose is of 25 mg/kg in physiologic solution (sub cutaneous route) and the drug is administered one hour later, in suspension in the carrier, as a single dose which corresponds to the maximum one, or the highest still tolerated by the animals of the group of rats not pretreated with NEM, i.e. the highest administrable dose to said group at which there is no manifest toxicity in the animals, defined as a toxicity that is clearly recognizable for its symptoms. The animals are sacrificed after 24 hours and then one proceeds to the evaluation of the damage to the gastrointestinal mucosa. The drug meets test 1, i.e. it can be used to prepare the compounds of general formula (I) and (II), when the group of rats treated with NEM + carrier + drug shows gastrointestinal damages, or in said group the gastrointestinal damages noticed are greater than those shown by the group treated with the carrier alone, or the group treated with carrier + drug, or the group treated with carrier + NEM, even though the drug pharmacotherapeutic efficacy, assayed by using specific tests, is not significantly reduced. Test 2 (CIP): Protection parameter of endothelial cell against the oxidative stress induced by cumene hydroperoxide (CIP). Human endothelial cells of the umbilical vein are prepared according to an usual standard procedure. Fresh umbilical veins are filled with a 0.1% by weight collagenase solution and incubated at 37°C for 5 minutes. Afterwards the veins are perfused with medium M 199 (GIBCO, Grand Island, NY) pH 7.4 further added of other substances, as described in the examples. The cells are collected from the perfusate by centrifugation and harvested in culture flasks T-75, pretreated with human fibronectin. The cells are then harvested in the same medium, further added with 10 ng/ml of bovine hypothalamic growth factor. When the cells of the primary cell culture (i.e. that directly obtained from ex-vivo) form a single layer of confluent cells (about 8,000,000 cells/flask), the culture is stopped and the layers washed and trypsinized. The cellular suspensions are transferred into the wells of a cell culture plate having 24 wells , half of which is then additioned with the same culture medium containing the drug at a 10 "4 M concentration, and harvested in a thermostat at 37°C at a constant moisture. Only the cells coming from said first sub-cultures are used for the experiments with cumene hydroperoxide (CIP). The cells are identified as endothelial cells by morphological examination and by their specific immunological reaction towards factor VIII; said cultures did not show any contaminations from myocytes or fibroblasts. Before starting the test, the cellular culture medium is removed and the cellular layers are carefully washed with a physiologic solution at a temperature of 37°C. The wells of the culture plate are then incubated for one hour with CIP at a 5 mM concentration in the culture medium. The evaluation of cellular damage (apoptosis) is carried out by determining the per cent variation of the DNA fragmentation with respect to the control group (treated with CIP alone), evaluating the fluorescence variation at the wave length of 405-450 nm. 5 replicates for each sample are carried out . The drug meets the test, i.e. it can be used for preparing the compounds of general formula (I) and (II), when a statistically significant inhibition of apoptosis (cellular damage) induced by CIP with respect to the group treated with CIP alone is not obtained at p < 0.01. Test 3 (L-NAME) : evaluation of the endothelial dysfunction induced by administration of L-NAME (N -nitro-L- arginine -methyl ester) J. Clin. Investigation 90, 278-281,1992. The endothelial dysfunction is evaluated by determining the damage to the gastrointestinal mucosa, the hepatic damage and blood hypertension induced by administration of L-NAME. The animals (rats) are divided in groups as herein below shown. The group receiving L-NAME is treated for 4 weeks with said compound dissolved at a concentration of 400 mg/litre in drinking water. The following groups are constituted (No. 10 animals for group) : A) Control groups: 1° group: only carrier (aqueous suspension 1% w/v of carboxy- methylcellulose, dose: 5 ml/Kg when the drug is administered by os , phisiologic solution when administered parenterally) , 2° group: carrier + L-NAME, B) Groups administered with the drug: 3° group: carrier + drug, 4° group: carrier + drug + L-NAME. The administration routes are those known for the drug, and can be the oral or subcutaneous , intraperiteneal , intravenous or intramuscular route . The drug is administered at that dose which results the highest still tolerated by the animals of the group of rats not pretreated with L-NAME, i.e. the highest administrable dose at which there is no evident toxicity in the animals, i.e a toxicity recognizable for its symptoms. The drug is administered once a day for 4 weeks . At the end of the four weeks treatment access to water is prevented and after 24 hours the animals are sacrificed. One hour before the sacrifice blood-pressure is determined, and a blood pressure increase is taken as an evaluation of the damage to vascular endothelium. The damage to the gastric mucosa is evaluated as illustrated in test 1 (see example Fl ) . The hepatic damage is determined by evaluation of the glutamic -pyruvic transaminase (GPT increase) after sacrifice. The drug meets test 3, i.e. it can be used for preparing the compounds of general formula (I) and (II), when in the group of rats treated with L-NAME + drug + carrier it is found an higher hepatic damage (GPT) and/or an higher gastric damage and/or an higher cardiovascular (blood-pressure ) damage in comparison to that of the group treated with the carrier alone, or of the group treated with carrier + drug, or of the group treated with carrier + L-NAME; even if the drug pharmaco- therapeutic efficacy, assayed by specific tests, is not significantly reduced. Under the conditions indicated in the above described in vivo tests 1 and 3 the therapeutic index of the drug is reduced since the usual doses at which the drug can be effective are no longer tolerated. Test 4 is a colorimetric test which affords to establish whether the precursor of B or B 1 (precursor of the X 2 or X 2a of the formulas (I) and (II) respectively), inhibits the production of radicals from DPPH ( 2 , 2 -diphenyl- 1 - icryl-hydrazyl ) (M.S. Nenseter et Al . , Atheroscler. Throm . 15, 1338- 1344, 1995). 100 μM solutions in methanol of the tested substances are prepared, and an aliquot of each of said solutions is added to a DPPH solution in methanol 0.1 M. After having stored the solutions at room temperature away from light for 30 minutes, their absorbances are read at the wave length of 517 nm, together with that of the corresponding DPPH solution at the same concentration. The absorbance decrease with respect to that of the solution of DPPH at the same concentration of the test solutions is determined. The effectiveness of the tested compound in inhibiting formation of radicals by DPPH is expressed by the following formula: (1 - A S /A C )X100 wherein A s and A c are respectively the absorbance values of the solution containing the test compound together with DPPH and of the solution containing only DPPH. The B or B-L precursor satisfies test 4 if their effectiveness in inhibiting radical production as above defined, is equal to or higher than 50% at the indicated concentration (10 "4 M) . Unexpectedly the products of the invention of the formulas (I) and (II) in oxidative stress conditions have an improved therapeutic index compared with the precursor drugs. For illustrative purposes the above mentioned tests are referred to the following compounds (see the Examples): Test 1: precursor drug: indomethacin Maximum administrable dose to rats: 7.5 mg/Kg p.o. By administering a higher dose a toxicity is manifested, characterized by enteropathy, tremor, sedation until death (within 24 hours). The group of rats treated with NEM + indomethacin at the above mentioned dose shows gastrointestinal damages. Since indomethacin in the groups treated with NEM causes gastrointestinal damages, it meets test 1. Indomethacin can therefore be used as a drug for preparing the compounds (I) and (II) of the present invention. Test 2: precursor drugs: indomethacin, paracetamol and mesala- mine Indomethacin and paracetamol meet test 2 since the cellular damage (apoptosis) inhibition induced by CIP is not significantly different with respect to that of the controls. Therefore the above drugs can be used as drugs for preparing the compounds (I) and (II) of the present invention. On the contrary mesalamine does not meet test 2, since it inhibits the apoptosis induced by CIP. Therefore mesalamine according to test 2 could not be used as a precursor to prepare the compounds (I) and (II) cf the present invention. It has been however found that mesalairiine submitted to test 1 causes gastrointestinal damages . Thus also mesalamine can be used as a precursor for preparing the compounds (I) and (II) of the present invention. Test 3 (L-NAME) precursor drugs: paracetamol, simvastatin, omeprazole Paracetamol and simvastatin meet test 3 since they cause gastric and hepatic damages greater than those induced both by L-NAME + carrier and by the drug + carrier. Therefore they can be used as precursors to prepare the compounds (I) and (II) of the present invention. On the contrary it has been found that omeprazole neither causes gastric nor hepatic damages, nor influences blood- pressure. According to test 3 omeprazole could not be used as a precursor for preparing the compounds (I) and (II) of the present invention. Test 4 (test for the precursor of B and B 1 used as bivalent linking bridge): precursor N-acetylcysteine N-acetylcysteine inhibits of 100% the production of radicals induced by DPPH, therefore it meets test 4. Therefore it can be used as precursor of B or B 1 . In formula (III) Y 3 is preferably selected from the following: (Y9 ) (Y1C ) (ni) (r 2) (Y13) (Yi4) ( yl5 ) The most preferred of Y is Y12 (pyridyl) substituted in positions 2 and 6. The bonds car- also be in asymmetric position, for example Y12 (pyridyl) car- be substituted also in position 2 and 3; Yl (pyrazcl) may be 3 , 5 -diεubεtituted. The compounds according to the present invention of formula (I) and (II) can be transformed into the corresponding salts. For example one route tc fcm the salts is the following: when in the molecule one nitrogen atom sufficiently basic to be saiified, in organic solvent such as for example acetonitrile, tetrahydrofuran, is present, it is reacted with an equimolecular amount of the corresponding organic or inorganic acid. To form the salt, preferably in the formula of the invention compounds Y or Y' of formula (III) is present. Examples of organic acids are: oxalic, tartaric, maleic, succinic, citric acids. Examples of inorganic acids are: nitric, hydrochloric, sulphuric, phosphoric acids. The derivatives according to the invention can be used in the therapeutic indications cf the precursor drug, allowing to obtain the advantages exemplified hereinafter for some groups ese drugs : Anti- inflammatory drugs NSAIDs: the invention compounds result very well tolerated and effective, even when the organism is debilitated and is under conditions of oxidative stress. Said drugs can be used also in those pathologies wherein inflammation plays a significant pathogenetic role, such as for instance, but not limited to, in cancer, asthma, miocardic infarction. Adrenergic blockers, of cc- or 3-blocker type: the action spectrum of the compounds of formula (I) and (II) results wider than that of the starting drugs; to a direct action on the smooth musculature the inhibition of the nervous beta-adrenergic signals governing the contraction of the hematic vessels is associated. The side effects (dyspnoea, bronchoconstriction) affecting the respiratory apparatus are lower . Antithrombotic drugs: the antiplatelet activity is potentiated and in the case of the aspirin derivatives the gastric tolerability is improved. Bronchodilators and drugs active on the cholinergic system: the side effects affecting the cardio-vascular apparatus (tachycardia, hypertension) result lowered. Expectorants and mucolytic drugs: the gastrointestinal tolerability results improved. Diphosphonates : the toxicity relating to the gaεtrointe- stinal tract is drastically lowered. Phosphodieεteraεe (PDE) (bronchodilatorε ) inhibitors: the therapeutic efficacy is improved, the dosage being equal; it is therefore possible, using the compounds of the invention to administer a lower dose of the drug and reduce the side effects. Anti leukotrienic drugs: better efficacy. ACE inhibitorε: better therapeutic efficacy and lower side effects (dyspnoea, cough) affecting the respiratory apparatus . Antidiabetic drugs ( insulin- sensitizing and hypoglycaemizing) antibiotic, antiviral, antitumoral, anticolitic drugs, drugs for the dementia therapy: better efficacy and/or tolerability. The drugs which can be used as precursors in formulas (I) and (II) of the compounds of the invention are all those meeting at least one of the above mentioned tests 1, 2, 3. Examples of precursor drugs which can be used are the following: For anti -inflammatory/analgesic drugs, the following can for example be mentioned: anti -inflammatory drugs: aceclofenac, acemetacin, acetylsali- cylic acid, 5-amino-acetylsalicylic acid, alclofenac, al i- noprofen, amfenac, bendazac, bermoprofen, α-bisabolol, bromfe- nac, bromosaligenin, bucloxic acid, butibufen, carprofen, cinmetacin, clidanac, clopirac, diclofenac sodium, diflunisal, ditazol , enfenamic acid, etodolac, etofenamate, felbinac, fenbufen, fenclozic acid, fendosal, fenoprofen, fentiazac, fepradinol, flufenamic acid, flunixin, flunoxaprofen, flur- biprofen, glucametacin, glycol salicylate, ibuprofen, ibupro - xam, indomethacin, indoprofen, isofezolac, isoxepac, isoxicam, ketoprofen, ketorolac , lornoxicam, loxoprofen, meclofenamic acid, mefenamic acid, meloxicam, mesalamine, metiazinic acid, mofezolac, naproxen, niflumic acid, oxaceprol , oxaprozin, oxyphenbutazone , parsalmide, perisoxal, phenyl ace- tylsalicylate, olsalazine, pyrazolac, piroxicam, pirprofen, pranoprofen, protizinic acid, salacetamide , εalicilamide O- acetic acid, salicylsulphuric acid, salsalate, sulindac, supro- fen, suxibuzone, tenoxicam, tiaprofenic acid, tiaramide, tinoridine, tolfenamic acid, tolmetin, tropesin, xenbucin, ximoprofen, zaltoprofen, zomepirac , tomoxiprol ; analgesic drugs: acetaminophen, acetaminosalol, aminochlor- thenoxazin, acetylsalicylic 2 -amino-4 -picoline acid, acetyl- salicylsalicylic acid, anileridine, benoxaprofen benzylmorphi - ne, 5-bromosalicylic acetate acid, bucetin, buprenorphine , butorphanol , capsaicine, cinchophen, ciramadol, clometacin, clonixin, codeine, desomorphine , dezocine, dihydrocodeine, dihydromorphine , dimepheptanol , dipyrocetyl, eptazocine, ethoxazene, ethylmorphine , eugenol , floctafenine, fosfosal , glafenine, hydrocodone, hydromorphone , hydroxypethidine , ibu- fenac, p- lactophenetide , levcrphanol , meptazinol, metazocine, metopon, morphine, nalbuphine , nicomorphine , norlevorphanol , normorphine, oxycodone, oxymorphone, pentazocine, phenazocine, phenocoll, phenoperidine , phenylbutazone, phenylsalicylate, phenylramidol , salicin, salicylamide , tiorphan, tramadol , dia- cerein, actarit; for respiratory and urogenital apparatus drugs (bronchodilators and drugs active on the cholinergic system, expectorants/mucolytics , antiasthmatic/antiallergic antihi- staminic drugs), the following can be mentioned: broncodilators and drugs active on the cholinergic system : acefylline, albuterol, bambuterol, bamifylline, bevonium methyl sulphate, bitolterol, carbuterol, clenbuterol, chlorprenaline, dioxethedrine , difylline, ephedrine, epinephrine, eprozinol, etafredine, ethylnorepinephrine , etofylline, fenoterol, flutoprium bromide, hexoprenaline , ipratropium bromide, isoetharine, isoprotenerol , mabuterol, metaproterenol , oxybutynin, oxitropium bromide, pirbuterol, procaterol, protokylol , proxyphylline, reproterol , rimiterol, salmeterol, soterenol, terbutaline, 1-teobromineacetic acid, tiotropium bromide, tretoquinol, tulobuterol, zaprinast , cyclodrine, NS- 21, 2 -hydroxy-2 , 2 -diphenyl -N- ( 1, 2 , 3 , 6-tetra hydro-pyridin-4 - ylmethyl )acetamide ; expectorant/ ucolytic drugs: ambroxol, bromhexine, domiodol, erdosteine, guaiacol, guaifenesin, iodinated glycerol, leto- steine, mesna, sobrerol , stepronin, terpin, tiopronin; antiaεthmatic/antiallergic antihiεtaminic drugε: acrivastine, alloclamide, amlexanox, cetirizine, clobenzepam, chromoglycate, chromolyn, epinastine, fexofenadine, formoterol, histamine, hydroxyzine, levocabaεtine , lodoxamide, mabuterol, metron ε, montelukast , nedocromil, repirinast, seratrodaεt , suplatast tosylate, terfenadine, tiaramide, urushiol , bromhexine; for cardiovascular drugs (ACE- inhibitors , beta-blockerε , antithrombotic and vasodilator drugs, antidiabetic and hypo- glycemic drugs), the following can be mentioned: ACE- inhibitors : alacepril, benazepril, captopril, ceronapril, cilazapril, delapril, enalapril, enalaprilat, fosinopril, imidapril, lisinopril, losartan, moveltipril, naphthopidil , perindopril, quinapril, ramipril, spirapril, temocapril, trandolapril , urapidil; beta-blockers: acebutolol, alprenolol , amosulalol , arotinolol, atenolol, betaxolol, bevantolol , bucumolol , bufetolol, bufuralol, bunitrolol , bupranolol, butofilol, carazolol , car- teolol, carvedilol, celiprolol, cetamolol, dilevalol, epanolol , esmolol, indenolol, labetalol, mepindolol, etipranolol , metoprolol, oprolol, nadolol , nadoxolol , nebivolol, nifenalol, nipridalol , oxprenolol , penbutolol , pindolol , practolol , pronethalol, propranolol , sotalol , sulfinalol, talinolol, ter- tatolol, tilisolol, timolol, toliprolol, xibenolol ; antithrombotic and vasoactive drugs: acetorphan, acetylsa- licylic acid, argatroban, bamethan, benfurodil hemisuccinate, benziodarone, betahistine, brovincamine , bufeniode, citicoline, clobenfurol, clopidogrel, cyclandelate , dalteparin, dipyrida- mole, droprenilamine , enoxaparin, fendiline, ifenprodil, iloprost, indobufen, isbogrel , isoxsuprine, heparin, lamifiban, midrodine, nadroparin, nicotinyl alcohol, nylidrin, ozagrel , perhexiline, phenylpropanolamine , prenylamine, papaveroline, reviparin sodium salt, ridogrel, suloctidil, tinofedrine, tinzaparin, triflusal, xanthinol niacinate; antidiabetic drugs: acarbose, carbutamide, glibornuride glybuthiazol(e) , miglitol, repaglinide, troglitazone, 1 -butyl - 3 -metanyl-urea, tolrestat , nicotinamide; for antitumor drugs, the following can be mentioned: ancitabine, anthramycin, azacitidine, azaserine, 6 -azauridine, bicalutamide , carubicin, carzinophilin, chlorambucil , chlorozotocin, cytarabine, daunorubicin, defosfamide, deme- colcine, denopterin, 6 -diazo-5 -oxo-L-norleucine, docetaxel, doxifluridine, doxorubicin, droloxifene, edatrexate, eflorni- thine, enocitabine, epirubicin, epitiostanol , etanidazole, etoposide, fenretinide, fludarabine, fluorouracil , gemcitabi- ne, hexestrol , idarubicin, lonidamine, mannomustine, melphalan, enogaril, 6-mercaptopurine , methotrexate, mitobronitol , mitolactol, mitomycins, mitoxantrone, mopidamol, mycophenolic acid, ninopterin, nogalamycin, paclitaxel, pentostatin, pira- rubicin, piritrexim, plicamycin, podophyllic acid, porfimer sodium, porfiromycin, propagermanium, puromycin, ranimustine, retinoic acid, roquinimex, streptonigrin, streptozocin, te- nipoεide, tenuazonic acid, thiamiprine, thioguanine, tomudex, topotecan, trimetrexate , tubercidin, ubeni ex, vinblaεtine, vincriεtine, vindeεine, vinorelbine, zorubicin; for antiulcer drugε the following can be mentioned: ε - acetamidocaproic acid, arbaprostil, cetraxate, cimetidine, eca- bet , enprostil, eεaprazole, irsogladine, misoprostol, omeprazole, ornoprostil, pantoprazole , plaunotol, rioprostil, roεaprostol , rotraxate, sofalcone, trimoproεtil ; among anti -hyperlipidemic drugs (statines) the following can be mentioned: atorvastatin, cilaεtatin, dermostatin, fluvastatin, lovastatin, mevastatin, nyεtatin, pentostatin, pepstatin, privaεtatin sodium, simvastatin; among antibiotic/antiviral drugs the following can be mentioned: antibiotics: amdinocillin, amoxicillin, ampicillin, apal- cillin, apicycline, aεpoxicillin, azidamfenicol , azidocillin, azlocillin, aztreonam, benzoylpas , benzyl penicillinic acid, biapenem, bicozamycin, capreomycin, carbenicillin, carindacillin, carumonam, cefaclor, cefadroxil, cefamandole, cefatrizine, cefazedone, cefazolin, cefbuperazone , cefclidin, cefdinir, cefditoren, cefepime, cefeta et , cefixime, cefmeno- xime, cefmetazole, cefminox, cefodizime, cefonicid, cefopera- zone, ceforanide, cefotaxime, cefotetan, cefotiam, cefoxitin, cefozopran, cefpimizole, ce iramide, cefpirome, cefprozil, cefroxadine, cefsulodin, ceftazidime, cefteram, ceftezole, ceftibutεn, ceftiofur, ceftizoxime, ce riaxone, cefuroxime , cefuzonam, cephacetrile sodium., cephalexin, cephaloglycin, cephaloridine , cephaloεporin C , cephalothiπ, cep apirin sodium, cephradine , chloramphenicol, chlortetracycline , cinoxacin, clavulanic acid, clometocillin, cloxacillin, cyclacillin, cycloserine, demeclocycline , dicloxacillin, epicillin, fenbe- cillin, flomoxef, floxacillin, hetacillin, imipenem, ienampi- cillin, loracarbef , lymecycline, afenide, meclocycline, mero- penem, metampicillin, methacycline , methicillin sodium, mezlo- cillin, minocycline, moxalactam , mupirocin, myxin, negamycin, novobiocin, oxacillin, panipene , penicillin G potassium εalt, penicillin N, penicillin O, penicillin V, phenethicillin potassium salt, pipacycline, piperacillin, pirlimycin, porfi- romycin, propcillin, quinacillin, ritipenem, rolitetracycline, sancycline, sedecamycin, spectinomycin, εulbactam, sulbe- nicillin, temocillin, tetracycline, ticarcillin, tigemonam, tubercidin, azithromycin, clarithromycin, dirithromycin, enviomycin, erythromycin, josamycin, midecamycin, miokamycin, oleandomycin, rifabutin, rifamide, rifamycin, rifaximin, rokitamycin, spiramycin, troleandromycin, viomycin, virginiamycin; amikacin, apramycin, arbekacin, dibekacin, dihydrostreptomycin, fortimicins, gentamicin, micronomicin, neomycin, netilmicin, paromo ycin, riboεtarrycin, sisomicin, spectinomycin, streptomici , tobrarrycin, troεpectomycin; baca piciliir-, cefcapeπe pivoxil, cefpodoxime proxetil, paniper.e , pivampiciilin, pivcefaiexin, sultamicillin, talampicillir. ; carbomycin, clir-aamycin, linccmycin, mikarr-ycin, rosaramicin, ciprof loxacir- , clinaf lcxacir- , difloxacin, enoxacin, enroflcxacin, fleroxacin, flumequine, grepafloxacin, lomefloxacir-, nadifloxacin, r-alidixic acid, norfloxacin, ofloxacin, pazufloxacin, peflcxacin, pipemidic acid, piromidic acid, ruflcxacin, s arfloxacin, toεufloxacin, trovafloxacin, clomocycline , g arr.ecycline , oxytetracycline , nifurpirinol , nifurprazine ; p-arrιinosalicylic acid, p-aminosalicylic acid hydrazide, ciofazimine, deoxydihydrostreptomycin, etha butol , glyconiazide , iεcniazid, opiniazide, phenyl aminosalicylate, rifampin, rifapentinε, salinazid, 4-4 ' - εulfynyldianiline, Acediasulfone, dapsone, succiεulfone , p- sulfanilylbenzylamine , thiazolsulfone, acetyl sulfamethoxypyrazine, mafenide, 4'- (methylεulfamoyl ) sulfanilanilide , salazosulfadimidine , sulfabenzamide, sulfacetamide , sulfachlorpyridazine , sulfachrysoidine, sulfacytine, sulfadiazine, sulfadicramide, sulfadimethoxine , εulfadoxine, sulfaethidole, sulfaguanidine, sulfaguanole , sulfalene, sulfamerazine , sulfameter, sulfa ethazine , sulfamethizole , sulfamethomidine , sulfamethoxazole, sulfamethoxypyridazine, sulfamethylthiazole, sulfametrole , sulfamidochrysoidine, sulf mcxole , sulf nilamide , 2 -p- sulf nilylanilinoethanol , N ~ - sulfanilylsuifanilamide , sulfanilylurea, N- sulfanilyl - 3 , 4 -xyia ide , εulfaperine, sulf aphenazole, su 1 f apr oxy 1 ine , sul f apyr az ine , sulfapyridine , sulfaεcmizole , sulfasyrr-aziπe, sulfathiazole , sulfathiourea , sulfisomidine , sulfiεoxazole , 4 - sulf niiamido salicylic acid; negar-iyci , caru onan, cloxyquin, nitroxoline , arginine, metronidazole ; antiviral drugs: aciclovir, a antadine, cidofovir, cytarabi- ne, didanosine, dideoxyadεnoεine , edoxudine, famciclovir, flo- xuridine, ganciclovir, idoxuridine, indanavir, kεthoxai , lami- vudinε, MADU , penciclovir, podophyllotoxin, ribavirin, rimanta- dinε, saquinavir, scrivudine, stavudine, trifluridine, valacy- clovir, vidarabine, xenazoic acid, zalcitabine, zidovudine; among inhibitors of the bone resorption (diphoεphonatεε ) the following can be mentionεd: alεndronic acid, butedronic acid, etidronic acid, oxidronic acid, pamidronic acid, riεedronic acid; among antidemence drugε the following can be mentioned: amiridine, lazabemide, mofegilinε, εalbeluzol, oxiracεta , ipidacrine , nebracetam, tacrine, velnacrine. The preferred substances are the following: among anti-inflammatories : acetylsalicylic acid, 5- aminoacetylεalicylic acid, carprofen, diclofenac sodium, diflu- nisal, etodolac, flufenamic acid, flunixin, flurbiprofen, ibuprofen, indomethacin, indoprofen, ketoprofen, ketorolac , lornoxicam, loxoprofεn, meclofenamic acid, mεfεnamic acid, mεloxicam, mesalamine, naproxen, niflumic acid, olsalazine, piroxicam, salεalate, εulindac, εuprofen, tenoxicam, tiaprofenic acid, tolfena ic acid, tolmetin, zomεpirac, to oxi- prol ; among analgesic drugs: acetaminophen, acetylεalicylεalicylic acid, bεnoxapro en, buprenorphine , butorphanol , capεaicin, diacereine, dihydrocodeine , ethyimorphinε , eugεnol, phenylbuta - zone, eptazinol, morphine, nalbuphine, pentazocine, thiorphan, tramadol , actarit ; among reεpiratory and urogεnital apparatuε drugs: (bronchodilators, drugs active on the cholinergic system, expectorants / mucolytics, antiaεthmaticε/antiallergic antihiεtaminic drugε) : bronchodilators and drugε active on thε cholinergic system: albuterol, carbuterol, clenbuterol, difhylline, etofylline, fenoterol, ipratropium bromide, metaproterenol , oxybutynin, pirbutεrol , salmεterol, terbutaline, tiotropium bromidε, zaprinast , cyclodrinε, NS-21, 2 -hydroxy- 2 , 2 -diphenyl -N- (1,2,3, 6-tetrahydro-pyridin-4 -ylmethyl )acetamide; expectorant/mucolytic drugε : ambroxol , bromexine, guaiacol , so- brerol ; antiasthmatic/antiallergic antihistaminic drugε: cetirizine, chromoglycate, hiεtamine, levocabaεtine, lodoxamide, montelu- kast, ter enadine, bromexine; among cardiovascular drugs : ACE- inhibitors : captoprii, enalapril, liεinopril, loεartan, ramipril ; Beta blockers: aiprenoiol, atenoiol, bupranolol , labεtalol, metipranolcl , metoprolol, pindolol, prcpranolol, timolol; an ithrombotic and vasoactive drugs: acetylsalicylic acid, acεtorphan, argatroban, clopidogrei, aiteparin, dipyridamole , enoxaparin, heparin, iioproεt, midodrine, ozagrel, phenyipropanolar.ine , trifusal ; antidiabetic drugs: tclrestat , nicotinamide ; among antitumor drugs: anthrarr.ycin, da norubicin, doxorubicin, epirubicin, fluorouracyl , methotrexate, vinblaεtine; among antiuicer drugε: ci etidinε, omeprazole, pantoprazole; among antihyperlipide ic drugs: lovastatin, pravastatin εodium, simvastatin; among antibiotic/antiviral drugs: antibiotic drugs : amoxicillin, ampicillin, aztreonam, biapenεm, carbenecillin, cefaclor, cefadroxil, cefamandole, cefatrizine, cefoxitin, clavulanic acid, dicloxacillin, imipenεm, mεclocy- clinε, methacyclinε, moxalactam, panipεnεm, εulbactam, azithro- mycin, erythromycin, joεa ycin, miokamycin, rifabutine, rifamide, rifamycin, gentamicin, paromomycin, εisomicin, baca picillin, carbomycin, clinda ycin, ciprofloxacin, clinafloxacin, difloxacin, enrofloxacin, lomεfloxacin, nadifloxacin, norfloxacin, ofloxacin, pipemidic acid, apicycline, clomocycline , oxytetracycline , nifurpirinol , nifurprazine , iεoniazid, rifampin, rifapεntinε, dapεonε , thiazolεulfone , sulfamethoxazole , εulfamoxole , metronidazole , arginine; antiviral drugε: aciclovir, famciclovir, ganciclovir, pεnci- clovir, ribavirin, vidarabine, zidovudine; among inhibitors of the bone reabsorption: alendronic acid, εtidronic acid, pamidronic acid; among antidεmεncε drugs: oxiracetam, tacrine, vεlnacrinε. Thε above mentioned substances, precursor drugε, are prepared according to the methods known in the prior art. Sεε for example in "The Merck Index, 12a Ed. (1996), herein incorporated by refεrεnce. When available, the corresponding isomers, compriεing optical iεomεrε, can bε usεd. Tomoxiprol is obtainεd according to thε mεthod dεscribεid in EP 12,866. The compounds of formula (I) or (II) are prepared with synthesis methods mentionεd bεlow. Thε choicε of the reactions for εach method depends on the reactive groups preεεnt in thε precurεor drug molecule, in the precursor compound of B or B 1 , which can be, as above mentioned, bivalent or monovalent, and in thε precursor compound of C. The reactions are carried out with methods well known in the prior art, which allow to obtain bonds among the precursor drug, thε prεcurεor drug of B cr B- and the precursor compound of C aε above definεd. When the reactive function of thε precurεor drug (for example -COOH, -OH) is involved in a covalent bond, for example of eεtεr, amide, ether type, said function can be restorεd with thε mεthods well known i the prior art. Some synthesis schem.es for obtaining the compounds of the invention are reported hereinafter: A) Synthesis of thε compounds of formula (I). 1. Synthesis of thε compound obtainεd by rεaction between the prεcursor drug and the compound prεcursor of B. la. When the drug haε general formula -COOH and the functional group cf the precurεor compound of B which bindε itself to the drug carboxylic function has the formula XZ , X being as above defined and Z = H, the reactions which take place depεnd on thε nature of the second reactivε group present in the prεcursor compound of B. la.l When the sεcond rεactive group presεnt in thε prεcursor compound of B is a carboxylic group, the synthesis general scheme expects the initial formation of the halide of the R-COHal acid (Hal = Cl , Br) and the subsequent reaction with the HX group of the precursor compound of B: RCOOH • RCOHal + H-X-X 2 -COOH ► R-T 1 -T 3 -X 2 -COOH (IA.l) X 2 , i , T 3 being aε above defined. When in thε two reaction compounds other functional groups COOH and/or HX are preεent , they must be protectεd bεforε thε reaction according to the methods known in the art; for example as described -in the volume by Th. W. Greene : "Protective groups in organic syntheεiε", Harward University Press, 1980. Thε RCOHal acylhalide is preparεd according to the methods known in thε prior art, for example by thionyl or oxalyl chloride, p 111 or P v halideε in inert solvent under the reaction conditionε, εuch as for example toluene, chloroform, DMF, etc. Specifically, if the HX group of the precurεor compound of B is NH 2 , or OH or SH, the prεcursor drug of formula R- COOH is first converted into the corresponding acyl halidε RCOHal, as above mentioned, and then reacted with thε HX group of the precursor compound of B in the presence of an organic baεe, εuch as triethylamine, pyridine, etc. using an inεrt solvεnt in thε rεaction conditions such as toluenε, tεtrahydrofuran, etc. at a temperature in the range 0°C-25°C. Alternatively to the previous synthesiε, the precursor drug of formula R-COOH can be treated with an agent activating the carboxyl group selected from N,N' -carbonyldii- midazol (CDl), N-hydroxybenzotriazol and dicyclohεxylcar- bodiimide in solvent such as for example DMF, THF, chlo- roform εtc. at a temperature in the range -5°C-50°C and the obtained commpound reactεd in εitu with thε reactive function of the precurεor compound of B for obtaining thε compound of formula (IA.l). la.2 Whεn the precurεor compound of B containε two functional groupε XZ , equal to or different from each other, X bεing as abovε dεfinεd and Z = K, thε precursor drug having formula R-COOH is first treated with an agent activating the carboxyl group, as above described in la.l, and then with the precursor compound of 3, after having protected one of the two reactivε HX groupε , for example with acetyl or ter-butyloxycarbonyl , restoring the initial function at the syntheεiε εnd . Thε εcheme iε the following: CDl, HX-X 2 -X-G RCOOH - R-T : -T 3 -X 2 -X- R-T, -T -X P -XH (IA.2 wherein X, T x , T B , X 2 are as above dεfined and G is a protective group of the HX function. 2. Nitroxyderivative synthεsis. 2a.1 When the compound obtained at the end of the previous step la. has formula (IA.l), the acid can be converted into the corresponding sodic salt and then one can follow the known prior art methods for preparing the final compound, for example according to one of the following εyntheεiε schemes : A.) R-T 1 -T B -X 2 -COONa + R 4 -X 1 -R 3 ► AgNO-. R-T i -T 3 -X 2 -T BI -T c -X 1 -R 3 (lA.lb) - - - - ~ R-T 1 -T B -X 2 -T 3I -T c -Y-NO 2 wherein ^ , T 3 , X 2 , T BI , T c are as above defined, R 4 is selected from Cl, Br, Y is as above defined, X 1 is the Y radical frεε from thε oxygεn atom, R 3 is Cl , Br, Iodinε, OH. If R 3 = OH thε compound of formula (lA.lb) is subje- ctεd to halogεnation, for example with PBr 3 , PC1 5 , S0C1 2 , PPh 3 + I 2 , and then reacted with AgN0 3 in organic solvent such as acetonitril , tetrahydrofuran. If R 3 is Cl, Br, Iodine, the compound of formula (lA.lb) is directly reacted with AgN0 3 as above mεntioned. 3.) R-T 1 -T 3 -X 2 -COONa + Hal-Y-N0 2 R - τ l " T B " x 2 " BI - τ c " γ " N0 2 C.) R-T 1 -T B -X 2 -C0C1 + R 5 -X 1 -R 3 -→R-T 1 -T B -X 2 -T BI -T C -X 1 -R 3 (lA.lc) AgN0 3 R~T l ~T 3 ~X 2 ~T BI ~T C ~X l 'R 3 >R"T 1 "T B "X 2 "T BI "T C "Y"N0 2 wherein R 5 = OH or NHR 1C , R lc , R 3 and the other symbols being as above defined. The above shown reactions are well known in the prior art. See for example the patent applications in the name of the Applicant WO 94/12463, WO 95/09831 and WO 95/30641. When X χ is a linear C 4 alkyl, the corresponding acid R-T 1 - T B -X 2 -COOH is rεacted with triphenylphosphine in the prεsεnce of an halogenating agεnt such as CBr 4 or N-bro- moεuccinimidε in tetrahydrofuran obtaining the compound (lA.lc) wherεin R 3 = Br . 2a.2 Whεn the compound obtained at the end of th previouε εtep la haε formula (IA.2) , the correεponding nitroxyderivative iε obtainεd by trεating an halogen- carboxylic acid of formula Hal - X 1 -COOH, X λ being aε above definεd, firεt with an agεnt activating the carboxyl group as describεd in IA.l, and thεn with thε compound of formula (IA.2), obtaining an halogεn dεrivativε, which iε iεolated and then diεεolvεd in organic εolvεnt , (ref. paragraph 2a.1), and trεatεd with εilvεr nitratε. Thε global reaction scheme is the following : 1) CDl, 2) R-T-L-T B -X^ J -XH Hal -X χ - COOH AgN0 3 R-T 1 -T B -X 2 -T 3I -T c -X 1 -Hal → R-T 1 -T B -X 2 -T BI -T C -Y-NO 2 wherein T 1 , T 3 , X 2 , T BI , T c , Y are as above defined. Alternativεly, the halide Hal-X j^ -COCl can be used, whεrεin Hal is preferably bromine, which is lεt react with the compound of formula (IA.2). lb. When the drug precursor has the reactivε function HX, wherein X is as above definεd, instεad of a carboxylic group, the two functional groups presεnt on the precursor compound of B can be the following: lb.l A carboxylic group, which reacts with the HX function of the drug precursor, and a HX group, the latter reactive group of the prεcursor compound of B bεing εqual to or diffεrεnt from thε functional group of thε drug precursor. Thε formula of the precursor compound of B iε of the H-X-X 2 -COOH type, wherein X and X 2 are aε above defined. The H-X- function of the precursor compound of B is protected according to the known prior art methods and the carboxyl group is reacted, as above mentioned, according to the following εcheme: H-X-X 2 -COOH ► G-X-X 2 -COOH + R-XH ► R-T 1 -T B -X 2 -X-G ► R-T 1 -T B -X 2 -X-H ( IB .1 ) At the end of the reaction the HX function of the precursor compound of B is restored. lb.2 When thε prεcursor compound of B contains two carboxylic groups, it is trεated with an equimolar amount of an agent activating thε carboxyl group undεr the conditions previously deεcribed in la.l, and then reacted with the reactive HX function of the drug precurεor molecule. Possible other reactivε functions of HX typε prεsεnt in the two compounds muεt be protectεd aε previously mentioned. Lastly a compound of formula R-T 1 -T B -X 2 -COOH (IB.2) is obtained. 2b. Nitroxyderivative synthesis. 2b.1 To obtain the final nitroxyderivativε starting from thε compound of formula R-T -T B -X 2 -X-H (1B.1), obtained at the end of the εyntheεiε dεscribεd in lb.l, thε (1B.1) compound is rεacted with an halogenacid of formula Hal-X 1 - COOH which has bεεn trεatεd as prεviously dεscribεd in paragraph la.l, or with the corresponding halogenacid chloride. The reεulting compound iε diεεolved in organic εolvent , for example acetonitrile or tetrahydrofuran and reacted with εilver nitratε. b.2 To obtain the final nitroxyderivativε εtarting from thε compound of formula R-T L -T B -X 2 -COOH ( IB .2 ) , obtainεd at the end of the synthesis described in lb.2, the acid is transformed into the corrεsponding sodic salt, it is rεactεd with a R 4 -X 1 -R 3 compound, prεviously dεfinεd in thε rεaction A. εcheme of paragraph 2a.1, obtaining according to thε same proceεs thεrεin mεntionεd thε final nitroxydεrivativε . Alternatively, when X- | _ is a linear C 4 alkyl, the acid (IB.2) is reacted with triphenyl -phosphine in the presence of an halogenating agent such as CBr 4 or N-bromosuccinimide in tetrahydrofuran and the resulting compound disεolvεd in organic εolvent for example acetonitrile, tetrahydrofuran, iε reactεd with silver nitrate. b.3 Alternatively to the synthesiε process according to lb.l and 2b.1, it is possible to react in a first εtep the HX- function of the precursor compound of B HX-X 2 -COOH with thε acyl chloridε of an halogεnacid of formula Hal-X 1 -C0- Cl , whεrein Hal is preferably Br , and subsequently the carboxylic function of the εo obtained compound, with thε drug precurεor R-HX. In the third and laεt step the -Hal group is substituted with -ON0 2 according to the process dεscribed in 2b.1. The reaction εcheme iε thε following: HX-X 2 -COOH + Hal-X- L -COCl ► Hal -X χ -T C -T BI -X 2 -COOH R-XH Hal -X 1 -T C -T BI -X 2 -COOH (2B.3) ► Hal-X 1 -T c -T BI -X 2 -T B -T 1 -R AgN0 3 H a l - X 1 - T c - T B1 - X 2 - T B - T 1 - R ► 0 2 N- Y - T c - ? B1 -X 2 - T B - T 1 - R whεrεin T c , T BI , T B , T x , X 2 , X 1 , Y arε aε abovε defined. In the previous scheme the nitration can alternativεly bε carriεd out on thε acid compound of formula (2B.3). B) Synthesiε of compoundε of formula (II). la. Whεn thε drug prεcurεor iε of formula R-COOH and thε prεcurεor compound of B ] _ containε only onε functional rεactivε group of formula XH, X bεing aε above defined, R- COOH is initially convertεd into thε corresponding acylhalide, or treatεd with an agεnt activating thε carboxyl group as dεscribεd in la.l, and thεn rεacted with the HX function of an halogen-acid compound, said function being equal to or different from that preεent on the precursor compound of B-^, said halogen-acid having the formula: HX-X χ ' -COOH I (IIA.l) Hal wherein X-_' is Y' as above defined without the oxygen atom through which the -N0 2 group is linked, X and Hal are as abovε dεfined. The compound (IIA.l) can be obtained with the known method of thε prior art. For example when X = NH , it can be obtained from thε corresponding hydroxy-aminoacid , protecting the a inic group by the corresponding ter-bu- tyloxycarbonyl derivative and transforming the hydroxyl function into halogen group as described for the halogenation of the compound (lA.lb) in 2a.1. The free carboxylic function of the compound resulting from the rεaction with the molecule cf the drug precurεor iε reacted with the function present in the molecule of the precurεor compound of B j _ , aε previously illustrated in la.l for the reaction between the R-CCOH acid and the precursor compound of B. In the final εtep the halogen atom (Hal) preεεnt on thε radical X' j is substituted with an ON0 2 group by adding Ag 0 3 to an organic solution of the compound. Thε rεaction scheme is the following, exemplified starting from the RCOCl acid halide: R-COCl + HX-X- -COOH-- R-T 1 -T CI -X 1 ' -COOH (HA.2) +HX-X 2a -→ Hal Hal R - T l - T CI lb. When the drug precursor and the precurεor compound of B 1 contain each a reactivε group of gεnεral formula XH, the two groups in each of the two molecules being equal to or differεnt from εach other, wherεin X is aε abovε dεfinεd, thε εyntheεiε iε carried out starting from an halogenacid compound of formula HOOC-X ' -COOH f Hal X- ' being as above dεfinεd, said compound being prepared from the corresponding hydroxy-diacid as describεd for thε halogεnation of the compound (lA.lb) in 2a.1. The halogεndiacid compound is trεatεd with an εquimolar amount of an agεnt activating the carboxyl group, under the conditions prεviously described in la.l., and then it is reacted with the reactivε function of the drug precursor molεculε. In thε subεεquεnt step the second carboxylic function is treated with an activating agent, as previously made for the first, and reactεd with thε prεcursor compound of B 1 according to thε following scheme : CDl, HX-R HOOC-X^-COOH ► HOOC-X 1 '-T CI -T 1 -R ► I I Hal Hal CDl, HX-X 2a HOOC-X-j -T CI -T 1 -R ► X2a "T Bli " cn "x l' "τ cι" τ l" R I I Hal Hal The halogen atom is then εubεtituted with thε ON0 2 group as abovε mεntioned. 3. Synthesis of the nitroso (s=l) derivatives of formula (I). a.1 The compound of formula (lA.lb) wherεin R 3 = OH iε rεactεd with sodium nitritε in a solvent formed of a mixture of watεr with tεtrahydrofuran in thε presence of hydrochloric acid. The rεaction is widely illuεtrated in the prior art. The general εchemε is the following: R-T 1 -T B -X 2 -T BI -T c -X 1 -OH + NaN0 2 ► A-B-C-NO a.2 If the compound obtained at the end of step A in la .2 has formula (IA.2) thε corrεεponding nitroεo derivative iε obtained treating an hydroxyacid of formula HO-X-^COOH, X χ being as above defined, first with an agent activating the carboxyl group, aε deεcribεd in la.l, then reacting it with 1A.2 and the resulting product with sodium nitrite as dεscribεd in 3a.1. b.1 To obtain thε nitroso dεrivative starting from the compound of formula R-T 1 -T B -X 2 -XH ( IB .1 ) obtained at the end of the εynthesis deεcribed in lb.l, thε compound (1B.1) is reacted with an hydroxyacid as dεscribεd in 3a.2. 3b.2 To obtain the nitroso derivativε from thε compound of formula R-T 1 -T β -X 2 -COOH (IB.2) obtainεd at thε end of the synthesis described in lb.2, the acid is tranεformed into the sodic salt and reacted with a compound Hal-X 1 -OH, as previously describεd, and thε obtained alcohol is treated as described in 3a.1. 4) Synthesis of the nitroso derivativεs of formula (II) hen the drug is of formula R-COOH and the precursor compound of B* λ contains only one function reactive group of formula XH, X being as above definεd, R-COOH is initially convεrted into the corrεponding acyl-halidε or trεatεd with an agεnt activating the carboxyl group aε describied in la.l, and then reactεd with thε HX function of an hydroxy- acid compound, said function bεing εqual to or diffεrεnt from that prεsent on thε prεcursor compound of B- L , said hydroxy-acid having thε formula: HX-X^ -COOH f (4A.1) OH wherein X 1 ' is Y' as above defined without the oxygen atom through which the -NO group is linkεd, X is as above defined. The free carboxylic function of the compound resulting from the reaction with the drug molecule iε reacted with the function presεnt in the molecule of the prεcursor compound of B l t aε prεviouεly illuεtrated in la.l for the reaction betwεεn thε R-COOH acid and the precursor compound of B. In the final step the alcohol is transformed into the nitroso-derivative as dεscribεd in 3a.1. The reaction sche ε iε thε following, εxεmplified starting from the RCOC1 acid halide: R-COC1 + HX-X- -COOH-→ R-^ -T CI -X ' -COOH (4A.2) + HX-X 2a -→ I I OH OH R-T^TC - ^ -T cττ -T Bττ -X 2a + NaN0 2 -→ R-T^T^-X, -T Bττ -X 2a I I OH ONO When thε drug and thε prεcurεor compound of λ contain each a reactive group of general formula XH, the two groupε in each of the two moleculεε bεing equal to or different from each other, wherein X iε aε above definεd, thε synthεsiε iε carriεd out starting from an hydroxy- diacid compound of formula HOOC-X 1 ' -COOH f OH X-L ' bεing as abovε defined, εaid hydroxydiacid compound iε treated with an equimolar amount of an agent activating the carboxyl group, under the conditionε prεviously dεscribed in la.l., and then it is reactεd with thε rεactive function of the drug molecule. In the εubεequεnt stεp thε sεcond carboxylic function is treated with an activating agent, as previously made for thε first onε, and reacted with the precursor compound of B x according to the following scheme: CDl, HX-R HOOC-X -COOH «• HOOC-Xi' -T CI -T 1 -R ► I I OH OH CDl, HX-X 2a HOOC-Xi'-Tc j -Ti-R → X 2 a-TBiι-T C ιι- ι'-T CI -T 1 -R I I OH OH The obtained compound is reactεd as dεscribed in 3a.1. Thε compounds objεct of thε prεsεnt invεntion arε formulated in the corrεsponding pharmaceutical compoεitionε for parεntεral , oral and topic usε according to thε well known methods in the art, togεthεr with the uεual excipiεnts; sεε for example the volume "Remington's Pharmaceutical Sciεncεε 15a Ed. " Thε amount on molar baεiε of the active principle in theεe for ulationε iε thε same, or lower, in comparison with that used of the corrεsponding precurεor drug. The daily adminiεtrable doεεε are thoεe of the precurεor drugs, or in the case lower. The daily doseε can be found in the publicationε of the field, εuch aε for example in "Phyεi- cian's Desk reference" . The following examplεs havε the purpoεe to illustrate the invention and are not to be considerεd aε limitativε of thε same. EXAMPLE 1 Synthesis of (S,S) -N-acetyl-S- ( 6-methoxy-α-methyl- 2 -naphthalen acetyl)cistεinε 4 - (nitroxy)butyl εstεr (NCX 2101) having formula The precursor is naproxene (Formula VI), the precurεor of B iε N-acεtylcisteine (formula CVIII) (VI) (CVIII) a) Synthesiε of ( S , S) -N-acetyl- S- ( 6 -methoxy- o -mεthy1- 2 -naphtha- len acetyl )ciεteine To a solution of 6 -methoxy-α-mεthyl - 2 -naphthalεnacetic acid (10 g, 43.4 mmoles) in chloroform (100 ml) and N,N-dime- thylformamide (6 ml), 1 , 1 ' -carbonyldiimidazolε (CDl) (7.04 g, 43.4 mmoles) is added. Aftεr 15 minutεs thε obtained solution is treatεd with ( S ) -N-acεtylcisteine (7.08 g, 43.4 mmoles) and left at room temperature for 12 hours. The reaction mixture is washed with HCl 5%, then with water and lastly with brine. The organic phase is anhydrified with sodium sulphate and then evaporated at reduced pressurε. Thε obtainεd residue is purified by chromatography on silica gel eluting with ethyl acetate. 11.66 g of the expected product in the form of a white solid .p. 122°-126°C, is obtained. X H-NMR (CDC1 3 ): 7.71-7.65 (3H, m) , 7.34 (IH, dd ) , 7.16-7.09 (2H, m), 6.36 (IH, d), 4.67 (IH, m) , 4.00 (IH, q) , 3.90 (3H, s) 3.32 (2H, t), 1.84 (3H, s), 1.59 (3H, d) . b) Synthesis of ( S , S ) -N-acetyl -S- ( 6 -methoxy-α. -methyl- 2-napht- halen acεtyl ) cistεine 4 - (bromobutyl ) ester To a solution of ( S , S ) -N-acetyl - S- ( 6 -methoxy-o -methyl- 2 - naphthalenacεtyl )cisteine (11.3 g, 30.1 mmoles) in tetrahydrofuran (200 ml), triphenylphosphine (23.7 g, 90.3 mmoles) and carbon tetrabromide (28.85 g, 90.3 mmoles) are added. The reaction mixturε is left under stirring for 24 hours at room temperature. The εolvent iε removεd by evaporation at reduced preεεure. The obtained crudε product iε purifiεd by chromatography on εilica gεl eluting with n-hexanε/εthyl acεtatε 7/3. 4 g of the estεr in thε form of a white solid with m.p. 67°- 71°C, are obtained. c) Synthεsiε of ( S , S ) -N-acetyl - S- ( 6 -methoxy-or-methyl- 2 -napht- halen acεtyl ) ciεtεine 4 - (nitroxy) butyl εεtεr To a solution of thε εster obtained at the end of the previouε εtep (1 g, 1.96 mmoles) in acεtonitrilε (20 ml), silver nitrate (0.66 g, 3.92 mmoles) is added. The reaction mixture is heated for 7 hours under reflux away from light. Thε formεd salt is rεmovεd by filtration and thε solution is evaporated at reducεd prεεsurε. Thε obtainεd rεsiduε is purifiεd by chromatography on silica gel eluting with n-hexanε- /ethyl acetate 7/3. 0.47 g of (S, S) -N-acetyl -S- ( 6 -methoxy-α- ethyl - 2 -naphthalenacetyl )cisteinε 4 - (nitroxy)butyl ester in the form of a white solid m.p. 56-59°C, arε obtained. 1 H-NMR (CDC1 3 ): 7.80-7.68 (3H, m) , 7.37(1H, d), 7.20-7.13 (2H, ), 6.12 (IH, d) 4.40 (2H, dd), 4.26 (IH, m) , 4.15-3.87 (3H, m), 3.92 (3H, ε) , 3.33 (2H, ά. , 1.86 (3H, d) , 1.74-1.67 (4H, m) , 1.61 (3H, d) . Elementary analyεiε: Calculated C: 56.08% H: .73% N: 71% S: 6.51 ! Found C: 99% H: Ξ.68% N: 5.60% S: 6.35s EXAMPLE 2 Synthεεiε of ( S ) -N-acetyl - S- { r-methyl [ 4 - ( 2 -methylpropyl ) ben- zεnε] acεtyl } cistεine 4 - (nitroxy ) butyl εstεr (NCX 2111) having formula (NCX 2111) Thε prεcursor is ibuprofen (Formula VII) , the precurεor of B is N-acetylcisteinε (formula CVIII) , (VII) (CVIII) a) Synthesis of ( S) -N-acetyl-S- {cr-methyl [ 4 - ( 2-mεthylpropyl ) benzene ]acetyl } cisteinε To a solution of cr-methyl [ 4- ( 2 -methylpropyl )benzene] acetic acid (10 g, 48.48 mmolεε) in chloroform (100 ml) and N,N- dimethylformamide (6 ml) 1 , 1 ' -carbonyldiimidazole (7.86 g, 48.48 mmolεs) is addεd . Aftεr 1 hour thε obtainεd solution iε trεated with ( S ) -N-acetylciεteine (7.91 g, 48.47 mmolεs) and lεft at room tεmperature for 24 hours. The reaction mixturε is washed with HCl 5%, then with water and lastly with brine. The organic phasε is anhydrifiεd with sodium sulphatε and then evaporatεd at rεduced pressure. The obtained rεsiduε iε purifiεd by chromatography on εilica gel eluting with ethyl acetatε. 13.3 g of the expεctεd product in the form of an oil arε obtainεd. ^- MR (CDC1 3 ): 10.17 (IH, ε) 7.13 (2H, d) 6.54 (IH, d), 4.76 (IH, m) , 3.93 (IH, q), 3.42-3.30 (2H, m) , 2.49 (2H, d), 1.85-1.83 (4H, m) , 1.55 (3H, d), 0.93 (6H, d). b) Synthεis of (S) -N-acεtyl-S- {α-mεthyl[ 4- ( 2 -methylpropyl ) -benzene ]acetyl) cisteine 4 - (bromobutyl ) ester To a solution of ( S) -N-acetyl-S- {α-methyl [ 4 - ( 2 -mεthylpro- pyl)benzene ]acetyl}ci teine (12.8 g, 36.4 mmoles) in tetrahydrofuran (100 ml), triphenylphosphinε (28.65 g, 109.23 mmoles) and carbon tetrabromide (36.23 g, 109.23 mmoles) are added. The reaction mixture is let under stirring for 48 hours at room temperature. The solvent is removεd by evaporation at reduced pressure. The crude product is purified by chromatography on silica gel eluting with cyclohexane/ethyl acetate 1/1. 5.79 g of the ester in the form of an oil are obtained. c) Synthesis of (S) -N-acetyl-S- {α-mεthyl[ 4- ( 2 -methylpropyl) bεnzεne]acetyl)cisteinε 4 - (nitroxy)butyl εεtεr To a εolution of the ester obtained at thε εnd of the previous step (5.5 g, 11.3 mmoles) in acεtonitrilε (100 ml) silver nitrate (2.69 g, 15.8 mmoles) is added. The reaction - mixture is heated for 24 hours under rεflux away from light. The formed salt is removed by filtration and the εolution iε evaporated at reduced preεεure. The obtained reεidue iε purified by chomatography on εilica gel eluting with cyclohexa- ne/ethyl acetate 7/3. 1.18 g of ( S ) -N-acetyl-S- {cr-methyl [ 4 -( 2 - methylpropyl )benzene ] acεtyl} cistεinε 4- (nitroxy)butyl ester in the form of an oil are obtained. ^-H-NMR (CDC1 3 ): 7.27-7.09 (4H, m) , 6.19 (IH, d), 4.75 (IH, m) , 4.47 (2H, t), 4.15-4.02 (2H, m) , 3.86 (IH, q), 3.31 (2H, d), 2.44 (2H, d), 1.89 (3H, d), 1.86-1.76 (5H, m) , 1.51 (3H, d) , 0.89 (6H, d). Elementary analysis: Calculated C: 56.39% H: 6.88% N: 6.00% S: 6.84% Found C: 56.22% H: 6.79% N: 5.88% S: 6.92% EXAMPLE 3 Synthesis of ( S) -N-acetyl-S- [ 1- ( 4 -chlorobenzoyl) -5 -mεthoxy- 2 - methyl-lH-indol-3-acetyl]ciεteinε 4 - (nitroxy)butyl ester (NCX 2121) having formula Thε precurεor iε indomethacin (Formula VIII), the precurεor of B is N-acetylcistεine (formula CVIII) , (VIII) (CVIII) a) Synthesis of (S) -N-acetyl-S- [ 1- ( 4 -chlorobenzoyl )- 5 -mεthoxy- 2 -methyl-IH- indol- 3 -acetyl Jcistεine To a solution of 1- ( 4 -chlorobenzoyl ) -5 -methoxy- 2 -methyl - IH- indol- 3 -acetic acid (10 g, 28.00 mmoles) in chloroform (100 ml) and N,N-dimethylformamide (2 ml) 1 , 1 ' -carbonyldiimidazole (4.53 g, 28.00 mmoles ) is added. After 1 hour the obtained solution is treated with ( S) -N-acetylcisteinε (4.56 g, 28.00 mmoles) and left at room temperature for 24 hours. The rεaction mixture is washed with HCl 5%, then with watεr and lastly with brine. The organic phase is anhydrified with sodium sulphate and then evaporatεd at rεducεd pressure. The obtained residuε is purified by chromatography on silica gel eluting with ethyl acetatε. 7.79 g of thε expected product in the form of a yellow solid m.p. 129°C, are obtained. 1 H-NMR (DMSO-d 5 ): 12.90 ( IH , s), 8.21 (IH, d), 7.69-7.64 (4H, m) , 7.06 (IH, d), 6.96 (IH, d), 6.73 (IH, dd), 4.33 (IH, m) , 4.02 (2H, ε), 3.77 (3H, ε), 3.33-2.96 (2H, m) , 2.22 (3H, s), 1.78 (3H, s). b) Synthesis of ( S ) -N-acetyl -S- [ 1 -( 4 -chlorobεnzoyl ) -5 -methoxy- 2 -mεthyl-lH- indol- 3 -acεtyl ]ciεtεinε 4 - ( bromobutyl ) eεter To a εolution of ( S ) -N-acetyl-S- [ 1- ( 4 -chlorobεnzoyl ) -5 - methoxy- 2-mεthyl-lH- indol- 3 -acetyl ] ciεteine (3.09 g, 6.14 mmoles) in N,N dimethylformamidε (50 ml), εodium εthylatε (0.42 g, 6.14 mmolεs) and, aftεr 30 minutεs , 1 , 4 -dibromobutanε (2.18 ml, 18,00 mmolεs) disεolvεd in 25 ml of N, N dimεthylformamid , arε added. The reaction mixture is left under stirring for 20 hours at room temperature, then it is diluted with ethyl ether and washed with water. After the organic phase has been anhydrified with sodium sulphatε, thε solvεnt is removed by evaporation at reduced pressure. The obtained crude product is purified by chromatography on silica gel, eluting with cyclohεxane/εthyl acetate 1/1. 1.7 g of the ester in the form of a yellow solid with m.p. 130°-134°C are obtained. c) Synthesis of (S) -N-acetyl-S- [ 1- (4 -chlorobenzoyl) -5-mεthoxy- 2-methyl-IH- indol -3 -acetyl ]cisteine 4- (nitroxy)butyl ester To a solution of the ester obtained at the end of the previous εtep (1.6 g, 2.5 mmoles) in acetonitrile (30 ml) silver nitrate (0.6 g, 3.51 mmoles) is added. The reaction mixture iε heated for 8 hourε under reflux away from light. The formed salt is removed by filtration and the solution is evaporated at reducεd prεεεure. The obtained reεidue iε purified by chromatography on silica gεl εluting with cyclohexane/εthyl acetate 4/6. 1.2 g of ( S) -N-acetyl-S- [ 1- ( 4 - chlorobenzoyl ) -5 -methoxy-2 -methyl- IH- indol- 3 -acetyl ]cistεinε 4- (nitroxy)butyl ester in the form of an oil arε obtainεd. 1 H-NMR (CDC1 3 ): 7.66 (2H, d), 7.48 (2H, d), 6.90 (2H, m) , 6.68 (IH, m) , 6.14 (IH, d), 4.77 (IH, m) , 4.43 (2H, t), 4.08 (2H, m) , 3.87 (2H, s), 3.83 (3H, s), 3.34 (2H, d) , 2.38 (3H, s), 1.90 (3H, s), 1.78-1,70 (4H, m) . Elementary analysis: Calculated C: 54.24% H: 4.88% N: 6.80% S: 5.17% Cl: 5.72% Found C: 54.32% H: 4.93% N: 6.91% S: 5.13% Cl : 5.84? EXAMPLE 4 Synthesis of (S) -N-acetyl- [ 2-fluoro-α-mεthyl- ( 1 , 1 ' -biphεnyl) -4 ■ acetyl] cisteine 4- (nitroxy)butyl eεtεr (NCX 2131) having for¬ mula Thε precursor is flurbiprofen (Formula IX), the precursor of B is N-acetylcistεine (formula CVIII) (IX) (CVIII) The NCX 2131 compound is synthεtizεd according to the proceεs describεd in Examplε 1. The substance appearε aε an oil. Yiεld: 26% ^-NMR (CDC1 3 ): 7.41-7.38 (6H, m) , 7.10 (2H, m) , 6.22 (IH, d), 4.78 (IH, m) , 4.46 (2H, t), 4.13 (2H, t), 3.92 (IH, q), 3.36 (2H, d), 1.93 (3H, d), 1.76 (4H, d) , 1.55 (3H, d) . Elementary analyεiε Calculated C: 56.91% H: 5.37% N: 5.55% S: 6.33% F: 3.75% Found C: 56.99% H: 5.41% N:5.66% 6.41% F: 3.83% EXAMPLE 5 Preparation of tranε-3- [ 4- [α-methyl- [ 4- ( -2 -methylpropyl )bεnze- ne] acetyloxy]- 3-mεthoxyphenyl ]- 2 -propenoyl 4- (nitroxy) butyl ester (NCX 2210) having formula: The precursor is ibuprofen (Formula VII), the precursor of B iε fεrulic acid (formula DH) (VII) (DH) a) Synthεεiε of trans - 3 -[ 4 -[ or-methyl- [ 4 -(- 2 -methylpropyl ) benzene ] acetyloxy ] - 3 -methoxyphenyl ] - 2 -propenoic acid To a εolution of α-methyl -[ 4 -( 2 -methylpropyl (benzene]acetic acid (5.03 g, 24.4 mmoles) in tetrahydrofuran (100 ml) and N,N-dimethylformamide ( 5 ml ) 1,1-carbonyldiimidazole (4.25 g, 24.8 mmolεs) is addεd. After 1 hour the obtained εolution iε treated with ferulic acid (4.90 g, 25 mmoles), sodium ethylatε (89 mg) is added and lεft at room temperaturε under stirring for 12 hours. The reaction mixture is washed with HCl 5%, then with water and lastly with brine. The organic phase is anhydrified with sodium sulphate and evaporatεd at reducεd pressure. The obtained residuε is purified by chromatography on silica gel, eluting with ethyl acetate/n-hexane 7/3. 5.1 g of trans - 3 - [ 4 - [ or-methyl - [ 4 - ( - 2 -methylpropyl ) benzene ] acetyl ] - 3 - methoxyphenyl] -2-propenoic acid as white εolid, with m.p. 131°- 137 0 C, are obtained. ^-NMR (CDC1 3 ): 7.72 (IH, d), 7.32 (2H, dd ) , 7.26 (IH, m) , 7.16-7.07 (4H, m) , 6.98 (IH, d) , 6.37 (IH, d) , 3.99 (IH, q) , 3.73 (3H, ε) , 2.47 (2H, d) , 1.88 (IH, m) , 1.63 (3H, d), 0.92 (6H, d) . b) εyntheεis of tranε - 3 - [ 4 - [ -methyl- [ 4 - ( - 2 -mεthylpropyl - )benzene ] acetyloxy] - 3 -methoxyphenyl ] -2 -propenoyl 4-bromobutyl εster To a solution of trans- 3 - [ 4 - [ α-methyl- [ 4 - ( 2 -methylpropyl ) - benzεne]acetyloxy]- 3 -methoxyphenyl ]- 2 -propenoic acid (5.33 g, 14 mmoles) in N,N-dimethylformamide (130 ml), sodium ethylatε (1.2 g, 16 mmoles) is added under εtirring. After 1 hour to the obtained mixturε 1 , 4 -dibromobutanε (10 g, 46 mmolεε) iε addεd and let react at room temperature for 12 hourε. The reaction mixture iε waεhed with HCl 5%, then with water and laεtly with brine, the organic phaεe iε anhydrifiεd with sodium sulphate and evaporatεd at rεducεd pressure. The obtained residuε is purified by chromatography on εilica gel eluting with n- hexane/ethyl acetate 8/2. 4.46 g of trans -3 -[ 4 -hydroxy- [σ- ethyl- [ 4 - ( - 2 -methylpropyl )benz nε ] acetyl ] - 3 -methoxyphenyl ] - 2 - propenoyl 4-bromobutyl ester are obtained. c) Synthesis of trans- 3- [ 4- [α. -methyl- [ 4- ( - 2 -methylpropyl )benzεne ]acetyloxy] - 3 -methoxyphenyl ] - 2 -propenoyl 4 - (nitroxy) butyl ester To a solution of trans- 3 -[ 4 - [α. -methyl- [ 4 -(- 2 -mεthylpropyl)benzene]acetyloxy] - 3 -methoxyphεnyl ] -2-propεnoyl 4-bromobutyl ester (4 g, 7.72 mmoles) in acetonitrile (70 ml) silver nitrate (2.58 g, 15 mmoles) iε added. The reaction mixture is hεated under reflux for 2 hours away from light. At the εnd the formed salt is removed by filtration and the solution is evaporatεd at rεducεd prεεsure. Thε recovered residue iε purified by chromatography on silica gel, eluting with n- hexane/ethyl acεtatε 8/2. 2.4 g of trans - 3 - [ 4 - [ or-methyl - [ 4 - ( - 2 - methylpropyl )benzene]acetyloxy ] - 3 -methoxyphenyl ] -2 -propenoyl 4- (nitroxy) butyl estεr as an oil, are obtained. " H-NMR (CDC1 3 ): 7.62 (IH, d), 7.32 (2H, d), 7.15 (2K, d), 7.16- 7.05 (2H, m) , 6.96 (IH, d), 6.35 (IH, d), 4.51 (2H, t), 4.24 (2H, t), 3.99 (IH, q), 3.74 (3H, s), 2.48 (2H, d), 1.89-1.83 (5H, m) , 1.62 (3H, d), 0.92(6H, d). Elemεntary analysis: Calculatεd C: 64.91% H: 6.66% N: 2.82% Found 64.83% H: 6.52 N: 2.69 5 EXAMPLE 6 Synthεsis of trans- 3 - [ 4 - [ 2-fluoro-α-mεthyl- ( 1 , 1 ' -biphεnyl ) -4- acetyloxy ] - 3 -methoxyphεnyl ] - 2 -propεnoyl 4 - ( nitroxy) butyl εεter (NCX 2216) having formula: (NCX2216) The precurεor iε flurbiprofen (formula IX), the precursor of B is ferulic acid (formula DH) (IX) (DH) The NCX 2216 compound is synthetized according to the proceεs described in Example 5. The total procesε yield is 32%. The subεtance appεarε aε an amorphous solid. 1 H- NMR (CDC1 3 ): 7.40-7.25 (9H, m) , 7.07-7.01 (2H, d), 6.98 (IH, ) , 6.38 (IH, d), 4.44 (2H, t), 4.46 (2H, t), 4.21 (2H, t), 4.04 (IH, q), 3.73 (3H, s), 1.72 (4H, m) , 1.65 (3H, d). Elementary analysis : Calculated C: 64.79 ζ , H: 5.255 N: 2.62% 3.53 ! Found C: 64.85% H: 5.31% N: 2.74% F: 3.48% EXAMPLE 7 Preparation of N- (4-nitroxybutyryl) -3-alanyl (L) -histidine 4- acetamido phenyl ester (NCX 2160) having formula: NHCO(CH 2 ) 2 NHCO(CH 2 ) 3 ONO 2 (NCX 2160) wherein the precursor is acetaminofεn (paracεtamol) having formula (X) and the precurεor of B iε (L) -carnoεine (NCX 2053) having formula ( Cl ) : NHCO(CH 2 ) 2 NH ; (X) (Cl) a) Synthεεiε of N- ( 4 -bromobutyryl ) -β -alanyl (L) -hiεtidinε To a εolution of carnoεine (5 g, 22.1 mmoles) in N,N-di- methylformamide (80 ml), triεthylaminε (4.62 ml, 33.1 mmoles) and 4 -bromobutyrylchloride (chloridε of 4 -bromobutyric acid - 83.85 ml, 33.1 mmolεs) arε addεd. Thε solution is left under stirring for 24 hours at room tempεrature, then it is dilutεd with ethyl acetate and the organic phasε is waεhed with water. The organic phase is then anhydrified with εodium εulphate and evaporated at reduced pressure. The obtained crude product iε purified by chromatography on εilica gel eluting with εthyl acetate, obtaining the final product. b) synthesis of N- ( 4 -bromobutyryl ) -β -alanyl (L) -histidine 4- acetamidophenyl ester To a solution of N- ( 4 -bromobutyryl ) -3-alanyl (L) -histidine (3 g, 8 mmoles) in chloroform (50 ml) and N,N-dimεthylformamidε (4 ml), paracεtamol (1.21 g, 8 mmoles), N,N-dicyclohexyl carbodiimide (1.65 g, 8 mmoles) and dimethylaminopyridine (0.04 g, 0.36 mmoles) are added under stirring. The mixture iε let react at room temperature for 6 hourε. Laεtiy it iε filterεd, dilutεd with chloroform and waεhed with water. The organic phase iε anhydrified with sodium sulphate and evaporatεd at rεduced presεurε. The obtainεd crude product iε purifiεd by chromatography on εiiica gεl, eluting with εthyl acεtate/n- hεxanε 7/3. N- ( 4 -bromobutyryl ) -β -alanyl (L) -histidine 4- acetamido phenyl ester is obtained. c) Syntheεiε of N- ( 4 -nitroxybutyryl ) - β -alanyl (L) -histidine 4- acetamidophenyl ester To a solution of N- ( 4 -bromobutyryl ) - β -alanyl (L) -histidine 4-acetamido phenyl εster (4 g, 7.87 mmoles) in acetonitrilε (70 ml), silvεr nitratε (1.87 g, 11 mmoles) iε added under stirring. The rεaction mixture is hεated for 5 hours under reflux, away from light. At the end the for εd salt iε rεmovεd by filtration and thε εolution iε evaporated at reduced pressure. The obtained residue is purified by chromatography on silica gel, eluting with n-hexane/ethyl acetate 3/7. The expected product iε obtained with an yield of 17%. Elementary analyεiε: Calculated C: 51.39% H: 5.34% N:17.19% Found C: 51.28% H: 5.28% N:17.06% EXAMPLE 8 Preparation of N-acetyl-S- [ (S) -or- ( 2 -chloropnenyl ) -6 , 7-dihydro- thieno[3,2-c]pyridin-5(4H)acetyl] (S)-ciεtεine 4- (nitroxy) butyl εstεr ( NCX 2136 ) whεrein the precursor is clopidogrel having formula (XI) and the precursor of B is N-aceticistεine having formula (CVIII): O^ / OH -CO H HS ' NHCOCH- (CVIII) The compound iε synthetizεd following thε procεdurε reported in Example 1. The yield is of 23%. Elementary analysis: Calculated C: 50.55% H: 4.95% N: 7.40% S: 11.24% Cl: 6.22% Found C: 50.70% H: 4.99% N: 7.60% S: 11.20% Cl : 6.15% EXAMPLE 9 Preparation of [ 3-methoxy-4- ( 4 -nitroxybutyryloxy) phenyl ] -2- trans -propεnoy1 - 4 - [ ( 2 - amino -3,5-dibromopheny1 )methylamino ; cyclohex wherein the prεcursor is ambroxol having formula (XII) and the prεcursor of B is rεpresented by ferulic acid having formula (DH): (XII) (DH) a) Synthesis of 4 - [ ( 2 - ter-butoxycarbonylamino- 3 , 5 -dibromophe- nyl )methylamino] trans cyclohexanol To a mixture of 4 - [ ( 2 -amino- 3 , 5 -dibromophenyl )methylamino- ]cyclohεxanol (5 g, 13.22 mmoles) in dioxanε (35 ml) and watεr (50 ml), triethylamine (3.31 ml, 23.7 mmoles) and di-ter- butyldicarbonate (3.46 g, 15.86 mmoles) are added undεr stirring. After 24 hours the solution is concentrated under vacuum, a HCl 1% solution until neutral pH (pH=7) is added and the organic phase is εxtracted with ethyl acetate. The organic phase is anhydrified with εodium εulphatε and evaporated under vacuum. 4- [ ( 2 -ter-butoxycarbonylamino-3,5-dibromophenyl ) methyl amino]cyclohexanol iε obtained which is used without further purification. b) Synthesis of (3 -methoxy- 4-hydroxyphenyl) -2-trans-propenoyl - 4 - [ ( 2- ter-butoxycarbonylamino- 3 , 5 -dibromo phenyl )methylamino] cyclohexanol ester To a solution of ferulic acid (4 g, 20.5 mmoles) in tetrahydrofuran (40 ml) cooled at 0°C, 1 , 1 ' -carbonyldiimidazol (3.34 g, 20.5 mmoles) is added. After 10 minutes thε solution is trεatεd with 4 -[( 2 -ter-butoxycarbonylamino- 3 , 5 - dibromophenyl) methyl amino] cyclohexanol (9.8 g, 20.5 mmoles) and let rεact at room tempεrature for 4 hours. The reaction mixture is concentrated under vacuum, trεatεd with methylen chloride, washed with a HCl 1% solution and then with water. The organic phasε iε anhydrifiεd with sodium sulphatε and then evaporatεd under vacuum. The obtained residuε is purified by chromatography on silica gεl, εluting with n-hεxanε/ethyl acetate 1/1. ( 3 -methoxy- 4 -hydroxyphenyl ) -2-tranε propenoyl 4- [( 2 -ter-butoxycarbonylamino- 3 , 5 -dibromo phenyl) methylamino] cyclohεxanol ester, is obtained. c) Synthesis of [ 3 -methoxy- 4 -( 4 -bromobutyryl-oxy)phenyl ] -2- trans propenoyl-4- [ ( 2 - ter-butoxycarbonylamino- 3 , 5 -dibromo- phenyl) methylamino] cyclohεxanol ester To a solution of ( 3 -methoxy-4 -hydroxyphenyl ) -2 -trans propenoyl - 4 - [ ( 2 - ter - butoxycarbonylamino -3,5 - dibromo - phenyl ) methylamino] cyclohexanol ester (4 g, 6.11 mmoles) in tetrahydrofuran (80 ml), triethylaminε (0.85 ml, 6.11 mmoles) and 4- bromobutyrylchloridε (0.7 ml, 6.11 mmolεs) arε added under stirring. It is let react at room temperature for 8 hours and then the organic solvent is evaporated at rεduced pressurε. The obtained crude product is treatεd with εthyl acεtatε and thε organic phasε washed with water. The organic phase iε anhydrified with sodium sulphate and evaporated under vacuum. The reεiduε iε purifiεd by chromatography on εilica gεl εluting with n-hεxanε/εthyl acetatε 7/3. [ 3 -methoxy- 4 - ( 4 -bromobu- tyryloxy) -phenyl ]- 2 -trans propenoyl 4 -[( 2 -ter-butoxycarbonylamino- 3 , 5 -dibromo phenyl) mεthylamino] cyclohexanol eεtεr is obtainεd. d) Synthesiε of [ 3 -methoxy- 4 - ( 4 -nitroxybutyryloxy)phεnyl ] - 2 - trans - propεnoyl 4 - [ ( 2 - ter - butoxycarbonylamino -3,5 - dibromo phenyl) methylamino] cyclohexanol ester To a solution of [ 3 -mεthoxy-4 - ( 4 -bromobutyryloxy)phεnyl ] - 2 -trans -propεnoyl - 4 - [ ( 2 - ter-butoxycarbonylamino- 3 , 5 -dibromophenyl )methylamino ] cyclohexanol ester (4 g, 4,98 mmoles) in acetonitrile (70 ml), silver nitrate (0.87 g, 4.98 mmoles) is added under εtirring. It iε heated under rεflux for 7 hours away from light and lastly thε formed salt is removed by filtration. The organic solution is evaporatεd at rεducεd pressure. The obtained residue is purified by chromatography on εilica gel eluting with n-hexane/ethyl acetate 7/3. [3 -methoxy- 4- ( 4 -nitroxybutyryloxy) phenyl ] - 2 - transpropenoyl 4- [ (2-ter- butoxycarbonylamino -3,5- dibromo - phεnyl ) m thylamino ] cyclohexanol eεter iε obtainεd. e) Synthesis of [ 3 -mεthoxy-4 - ( 4 -nitroxybutyryloxy)phεnyl ] -2- transpropenoyl 4 - [ ( 2 -amino-3,5-dibromo phεnyl ) mεthylamino ] cyclohεxanol εstεr To a solution of [ 3 -mεthoxy-4 -( 4 -nitroxybutyryloxy)phε- nyl ] - 2 -tranεpropεnoyl 4 - [ ( 2 -tεr-butoxycarbonylamino- 3 , 5 -dibromo phenil) -methylamino] cyclohexanol eεter (2 g, 2.54 mmolεs) in εthyl acetate (50 ml), cooled at 0°C and maintained under stirring, a HCl 5N solution in ethyl acetatε (3.17 ml) is addεd. Thε εolution iε lεft under εtirring at 0°C for 4 hourε. Laεtly the prεcipitate is filtered. The obtained crudε product is trεated with ethyl acetate, to which a 5% sodium bicarbonate solution is added. It is shaken and the bicarbonate εolution is substitutεd with an equal part of water. It iε εhaken again, the organic phase is recovered, anhydrified with sodium sulphate and evaproated at reducεd prεsεurε. [ 3 -mεthoxy-4 - ( 4 - nitroxybutyryloxy ) phεnyl ] - 2 - tranεpropεnoyl - 4 - [ ( 2 - amino -3,5- dibromophenyl ) methylamino] cyclohexanol eεter iε obtained. Yield: 36% Elementary analysis: Calculated C: 47.30% H: 4.56% N: 6.15% Br: 23.31% Found C: 47.26% H: 4.53% N: 6.00% Br : 23.42% EXAMPLE 10 Preparation of [ 4-amino- [ [ 3-methoxy-4- ( 4 -nitroxybutyrylo- xyjphenyl] -2-trans propenoyl] -1 -hydroxy-butyliden] -bispho- sphonic acid (NCX 2211), (NCX 2211) wherein the precursor is alεndronic acid of formula (XIII) and thε prεcursor of B iε thε fεrulic acid (formula DH ) : (XIII) (DH) a) Synthεεiε of [ 3 -methoxy- 4 - ( 4 -bromobutyryloxy)phenyl ] - 2- trans-propenoic acid To a solution of ferulic acid (1.2 g, 6.11 mmoles) in tetrahydrofuran (80 ml), triethylamine (0.85 ml, 6.11 mmoles) and 4-bromobutyrylchloride (0.7 ml, 6.11 mmoles) are added under stirring. It is let react at room tempεraturε for 3 hours and then evaporated at reduced pressure. The obtained crude product is treated with ethyl acetate and the organic phase washed with water. The organic phase is then anhydrified with sodium sulphate and evaporated under vacuum. The obtained residue is purified by chromatography on εilica gel eluting with chloroform/mεthanol 8/2. Thε [ 3 -methoxy- - ( 4 -bromobuty- ryloxy) -phenyl ] - 2- trans propenoic acid is lastly isolated. b) Synthesiε of the [ 3 -methoxy- 4 -( 4 -nitroxybutyryloxy) phenyl ] - 2-tranε propenoic acid To a εolution of [ 3 -methoxy- 4 - ( 4 -bromobutyryloxy ) phεnyl ] - 2 - tranε-propεnoic acid (1.5 g, 4.5 mmoleε) in acetonitrile (70 ml) εilver nitratε (0.87 g, 4.98 mmolεε) iε addεd undεr stirring. The mixture is heatεd undεr reflux and, under stirring, it is reacted for 3 hours εheltεrεd from thε light. The formed εalt iε removed by filtration and the organic phaεe is evaporated at reducεd pressure. The obtainεd rεsidue iε purified by chromatography on silica gel column, eluting with chloroform/methanol 8/2. The [ 3 -mεthoxy- 4 - ( 4 -nitroxybu- tyroyloxy) phenyl ]- 2 -tranε propenoic acid is recovεrεd. c) Synthesis of [ 4 -amino- [[ 3 -mεthoxy- 4 -( 4 -nitroxy buty- ryloxy)phenyl ]- 2 -trans propenoyl ]- 1 -hydroxy-butylidεn] bi- sphoεphonic acid To a solution of [ 3 -methoxy- 4 - ( 4 -nitroxybutyroyloxy) - phenyl ]- 2-tranε propenoic acid (2g, 6.4 mmoles) in N,N-dime- thylformamide (30 ml), cooled at 0°C, N,N'dicyclohexylcarbodi- i ide (1.3 g, 6.4 mmoles) and 1 -hydroxybenzotriazol (1.04 g, 7.68 mmoles) are added under stirring. Aftεr 30 minutes alendronic acid (1.6 g, 6.4 mmoles) is addεd. Thε reaction mixture is left under stirring at room tempεrature for 7 hours. At the end it is acidified with a HCl 5% solution and the organic phaεe iε extractεd with ethyl acetatε. The organic phaεε iε washεd with brinε, anhydrifiεd with sodium sulphatε and εvaporatεd at rεducεd presεure. The crude product is purified by chromatography on silica gεl column eluting with methylεnε chloridε/methanol 8/2, obtaining the [ 4 -amino- [ [ 3 - methoxy- 4 - ( 4 -nitroxybutyroyloxy) phenyl ] - 2 - trans propenoyl ] - 1 - hydroxy butyliden] bisphoεphonic acid. Yiεld: 11%. Elεmentary analysis: Calculated C: 19.71% H: 4.36% N: 5.07% P: 11.17% Found C: 19.56% H: 4.28% N: 5.04% P: 11.25% EXAMPLE 11 Preparation of S- [ [ 2- [ 4 - ( 4-chlorophenyl)phεnylmεthyl ) -1-pipεra- zinyl ]εthoxy] acεtyl ] pεnicillaminε 4 - (nitroxy)butyl εster (NCX 2060) having formula wherein the precurεor iε cetirizinε of formula (XIV) and thε precursor of B is penicillaminε (formula CV) : ( XIV ) ( CV ) a) Synthεεiε of S- [ [ 2 - [ 4 - [ ( 4 -chloropnenyl ) phenylm thyi ] - 1-pipe - razinyl ] ethoxy ]acεtyl ] N- tεr-butoxycarbonylpεnicillaminε-4 - (nitroxy)butyl eεtεr Thε compound iε prεparεd according to thε procedure reported in Example 1, by using N- ter -butoxycarbonyl -pεnicillaminε instεad of N-acetyl ciεteine. b) Syntheεiε ofS-[[2-[4-[(4 -chlorophenyl ) phenylmεthyl ] - 1-pipe- razinyl ] ethoxy ] acetyl ] -peniciila inε- 4 - (nitroxy )butyl eεter . Thε compound iε obtainεd from the previous one by following the procεdurε dεscribεd in stεp e) of Example 9 to remove the protectivε group N- tεr-butoxycarbonyl and rεcovεr thε aminic function. Yiεld: 26%. Elεmεntary analysis: Calculated C: 55.78% H: 6.49% N: 8.43% S: 4.80% Cl : 5.31% Found C: 55.61% H: 6.31% N: 8.29% S: 4.93% Cl : 5.43% EXAMPLE 12 Preparation of N-acetyl-S- [( S )- 1- [N- [ 1 -( εthoxycarbonyl )- 3 - phenylpropyl ] -L-alanyl ] -L-prolin]cistεinε 4 - (nitroxy) butyl ester of formula (NCX 2134) (NCX 2134) wherein the precursor is enalapril of formula (XV) and thε pre- cursor of a iε -acetylciεteine (formula CV±H ( V . (CVIII) Tne corr is syr.th- .oilowing the procedure repor ec n ---xamo--.. Yiεld: 27 --- J- t-l 1 εntarv ar- lvsis Calculatεd C: 5: 6.79% 8.62% 4.91. ΪOUΠG C: .30% H: 6.85% N: 8.71% S: 4.85 ! EXAMPLE 13 Prεparation cf 3- [4- D- or- aminobenzylpenicillaminoyloxy ] - 3 - methoxyphenyl - 2 - trans propenoyl 4 - (nitroxy)butyl ester (NCX 2080) having formula 0) wherein the precursor is represεntεd by ampicilline (formula XVI) and the precursor of B iε ferulic acid (formula DH): Thε compound iε εynthεtized following the method reported in Example 5. Yields: 11%. Elεmεntarv analavεiε Calculated C: 56.04% H: 8.75 : 4.99% Found C: 56.15% H: 5.48% 8.65% S: 4.83% EXAMPLE 14 Preparation of 9 - [ [ 2 - [ -N-acetyl - S- ( 4 -nitroxybutyroyl ) ci • εtεinyl ] ethoxy] -methyl ] guanine cf formula (NCX 2135), wherein the precurεor iε aciclovir of formula (XVII) and the precursor of B iε N-acetylciεtεinε (formula CVIII): (XVII) (CVIII) a) Syntheεiε of N-acetyl -S- ( 4 -bromobutyroyl ) ciεteine A εolution containing 4 -bromobutyric acid (5.1 g, 30.6 mmoleε) and 1 , 1 ' -carbonyldiimidazole (5.61 g, 34.6 mmoleε) in chloroform (50 ml) iε prεparεd and it iε left under εtirring at room temperature for 1 hour. To the reaction mixture a εolution of N-acetylciεtεine (5 g, 30.6 mmoles) in N,N-dimethylformamide (5 ml) containing εodium εthylatε (50 mg ) iε added. It iε lεt rεact under εtirring and after 24 hours the solution is waεhed with HCl 1% and then with brine. Thε organic phaεe iε anhydrified with εodium εulphatε and εvaporatεd at reduced pressure. The obtained crude product iε purified by chromatography on εilica gel column, eluεnt εthyl acεtatε/chlo- rofor 7/3, laεtly obtaining N-acetyl-S- ( 4 -bromobutyroyl ) cisteinε. b) Syntheεis of N-acetyl -S- ( 4 -nitroxybutyroyl )cistεinε To a solution of N-acetyl-S- ( 4 -bromobutyroyl )cistεine (3 g, 9.6 mmoles) in acetonitrile (70 ml) silver nitrate (1.7 g, 10 mmoles) is added. The reaction mixture is heatεd undεr stirring under reflux for 2 hours away from light. The formed salt is removed by filtration and the solution is evaporated at reduced pressure. The obtained residue is purified by chromatography on silica gel column eluting with ethyl acetate/chloroform 7/3, lastly obtaining N-acetyl-S- ( 4 -nitroxybutyroyl ) cisteinε . c) Synthesis of 9- [ [ 2- [N-Acetyl-S- ( 4 -nitroxybutyroyl )cistei- nyl ] ethoxy ]methyl ] guanine A εolution of N-acetyl -S- ( 4 -nitroxybutyroyl ) ciεtεinε (2.8 g, 9.6 mmolεε) and 1 , 1- carbonyldiimidazol (1.55 g, 9.6 mmolεs) in tetrahydrofuran (50 ml) is prepared and left under stirring at room temperture for 1 hour. Thε reaction mixture is treated with aciclovir (2.16 g, 9.6 mmoles). After 6 hours of reaction at room tempεraturε, the solution is evaporated at reducεd prεssurε, the obtained reεidue treatεd with ethyl acetatε and washed with brine. The organic phase is anhydrified with sodium sulphate and then dried undεr vacuum. The obtained residue is purified by chromatography on silica gel column eluting with ethyl acetate. 9- [ [ 2- [N-acetyl-S- ( 4 -nitroxybutyroyl ) ciεteinyl - ] ethoxy]methyl Jguanine iε obtained. Yiεlds: 9%. Elεmentary analysis Calculated C: 35.25% H: 3.95% N: 13.76% S: 47.05% Found 35.3. H: 3.99% N: 13.84% S: 47.20% EXAMPLE 15 Preparation of trans- 3 -[ 4 -( 5-amino- 2-hydroxybenzoyl )- 3 -methoxyphenyl ] 2 -propenoyl 4- (nitroxy) butyl estεr (NCX 2212), (NCX2212) wherein the prεcursor iε mesalamine of formula (XVIII) and the precursor of B is the ferulic acid (formula DH ) : (XVIII) (DH) a) syntheεiε of tranε - 3 - [ 4 - ( 5 - tεr-butyloxycarbonylamino- 2 - hydroxybenzoyl ) - 3 -methoxyphenyl ] 2 -propεnoic acid 4 - (nitroxy)butyl eεter The compound iε εynthetized according to the procedurε reported in Example 5, firεt protecting the primary aminic group of the mesalamine as deεcribεd in Examplε 9, εtep a). b) Obtaining of tranε- 3 -[ 4 -( 5 -amino- 2 -hydroxybεnzoyl )- 3 -methoxyphenyl] 2 -propenoyl 4 - (nitroxy) butyl estεr Thε final compound is obtained by hydrolizing the bond between the aminic function and thε N- ter-butoxycarbonyl protective group as describεd in Examplε 9, εtεp e). Yieldε : 28%. Elementary analyεiε: Calculated C: 56.49% H: 4.96% N: 6.30% Found C: 56.55% H: 4.82% N: 6.45% EXAMPLE 16 Preparation of 6-methylεn- 5 -hydroxy- 10 [ 2 -hydroxy- 5 -( 4-nitro- xybutyryloxy)benzoyl ] tetracyclinε of formula (NCX 2163) wherεin thε prεcursor is mεthacycline of formula (XIX) and the precursor of B is the gentisic acid (formula Dili): (XIX) (Dili) a) Synthesis of the 5 -( 4 -bromobutyryloxy) - 2-hydroxy-benzoic acid In a solution of 4 -bromobutyrylchloride (3 g, 16.17 mmoles) in tetrahydrofuran (50 ml), cooled at 0°C, triethylamine (4.5 ml, 32.34 mmoleε) and then gentisic acid (2.4 g, 16.16 mmoli) are dropped under stirring. It is let react at 0°C for 4 hourε, under εtirring, then it iε evaporated at reduced preεsure. Thε obtainεd crude product is trεated with ethyl acetatε, the organic phase is washed with HCl 1% and then brine. Thε organic phaεε iε anhydrifiεd with sodium sulphate and dried. The obtained residue is purified by chromatography on silica gel column, eluting with methylenε chloridε/mεthanol 95/5, obtaining the 5 -( -bromobutyryloxy )- 2-hydroxy-benzoic acid. b) Synthesiε of 5 -( 4 -nitroxybutyroyloxy)- 2 -hydroxybεnzoic acid To a εolution of 5 -( 4 -bromobutyryloxy )- 2 -hydroxy-benzoic acid (3 g, 9.6 mmolεs) in acεtonitrilε (150 ml) silver nitrate (1.7 g, 10 mmoles) is added under stirring. The mixture is heated under reflux for 7 hourε away from light. Lastly thε formed salt is removεd by filtration and thε εolution is evaporated at reduced pressure. The obtainεd residue is purified by chromatography on εilica gel column, eluting with methylene chloride/methanol 95/5. In thiε way the 5- (4- nitroxybutyryloxy) - 2 -hydroxy-benzoic acid iε iεolated at the pure state. c ) Synthεsis of 6 -mεthylεn- 5 -hydroxy- 10 [ 2 -hydroxy- 5 - ( 4 -nitroxybutyryloxy)bεnzoyl ] tetracycline A solution of 5 -( 4 -nitroxybutyryloxy)- 2 -hydroxy-bεnzoic acid (5 g, 16.4 mmoles) and 1 , 1 ' -carbonyldiimidazol (2.67 g, 16.4 mmoleε) in tetrahydrofuran (70 ml) iε maintained under stirring at room temperature for 1 hour. Adriamycin (7.2 g, 16.4 rπmoleε) iε added. It iε rεactεd undεr εtirring for 12 hourε at room temperature. The organic εoluticr- iε then evaporated at reduced presεurε, the obtained reεidue is trεated with εthyl acεtatε and -washed with brine. The organic phase, anhydrified with sodium, sulphate, is dried under vacuum.. The obtainεd reεiduε iε purifiεd by chromatography on εilica gel column εluting with εthyl acetatε. 6 -methylen- 5 -hydroxy- IC [ 2 - hydroxy- 5 - ( 4 -nitroxybutyryloxy ) benzoyl ] te racycline is obtained. Yield: 19%. Elementary analysis: Calculated C: 84% H: 4.40% 5.95% Found C: 55.95% H: 4.555 N: 5.98% EXAMPLE 17 Preparation of 5- [ [ 3 - [ 3 -methoxy- 4 - ( 4-nitroxy)butyry!oxy]phenyl • 2 -trans -propenoyl ] amino] -1,2,3,4 -tetrahydroacridine (NCX 221 wherein the precurεor is tacrinε of formula (XX) and thε prεcursor of B is thε fεrulic acid (formula DH): : χχ ) ( DH r. c r. iε εynthetized according to the procedure re- sor ed - r- " • T) ' & 10. Yield: 7%. Ξierr.en v ar.alvsij 64.13% H: 5.38% N: 8.34 ! r OUT-C .4.28% 5.46% N: 8.475 EXAMPLE Preparation of [ IS- [ la , 3a , 7/ , 8/3 , ( 2S* , 4S" ) ] ] - 2 , 2 - dimεthylbuta - noic acid 1 , 2 , 3 , 7 , 8 , 8 -hexahydro- 3 , 7 -dimethyl- 8 - [ tεtrahydro- 4 - [ 2 -hydroxy-5 - ( -nitroxybutyryloxy ) benzoyl -oxy[ - 6-oxo- 2H-piran- 2-yljethyi; -1-naphthalenyl ester (NCX 2164) wherein thε precurεor iε εimvaεtatine of formula (XXI) and the precursor of B is the gentisic acid (formula Dili): The compound is εynthetizεd following thε εthod deεcribed in Examplε 16. Yield: 13%. Ele εntary analysis: Calculated 63.50% H: 7.06% N: 2.01% Found C: 63.68% H: 7.21% N: 2.19% EXAMPLE 19 Preparation of 5-methoxy- 2- [ [ [ 4 - [N- [ 4- (nitroxy)butyl-/3-alanyl] (L) -histidinyloxy] - 3 , 5-dimethyl- 2-pyridinyl ]methyl ] sulphi ■ nyl]-lH-benzimidazol (NCX 2062) whεrein the precursor is 4 -hydroxyomeprazol of formula (XXII), obtained by treating omeprazol as described in Acta Chem. Scand. 43, 6 1989 pages 549-568 and the precursor of B is car- noεinε (formula Cl ) : Thε compound iε εynthetized according to the proceεε dεεcribεd in Examplε 7. Yield: 25% Elementary analyεiε: Calculatεd C: 51.97. H: 4.96% N: 16.79 5 4.7- Found C: 51.81% H: 4.8Q5 N: 16.6! S: 4.92? EXAMPLE 20 Prεparation of N-nicotinoyl - β -alanyl (L) -histidinε 4- (nitroxy)butyl εstεr (NCX 2073) (NCX2073) wherein the precursor iε nicotinamide of formula (XXIII) and the precursor of B is carnoεine (formula Cl ) : ( XXIII ) ( Cl ) a) Synthesis of N-nicotinoyl - β -alanyl (L) -histidine To a solution of nicotinic acid (2.5 g, 20.5 mmoles) in tetrahydrofuran (40 ml) coolεd at 0°C, 1 , 1 ' -carbonyldiimidazol (3.34 g, 20.5 mmolεs) is added under stirring. After 10 minutεs to thε εolution (L) - carnoεinε (4.6 g, 20.5 mmolεε) iε addεd and it iε lεft undεr εtirring at room temperature for 4 hourε. The reaction mixture iε concentrated under vacuum, trεatεd with mεthylεnε chloridε, waεhεd with HCl 1% and thεn with water. The organic phase iε anhydrified with εodium εulphate and evaporated under vacuum. The obtained reεiduε is chromatographed on silica gel column, eluting with ethyl acetate. N-nicotinoyl -β -alanyl (L) -histidine is recovered. b) Synthesiε of N-nicotinoyl - β -alanyl (L) -hiεtidine 4-bromobutyl ester To a εolution of N-nicotinoyl -/3 -alanyl- (L) -hiεtidinε (9.9 g, 30.1 mmoles) in tetrahydrofuran (200 ml) triphenylphoεphinε (23.7 g, 90.3 mmolεs) and carbon tetrabromide (28.85 g, 90.3 mmoles) are added under stirring. Thε rεaction mixture iε left under stirring at room temperature for 24 hours. Lastly the solvent is removed by evaporation at rεducεd prεssurε. The obtained crude product is purified by chromatography on silica gel column eluting with n-hexanε/εthyle acetatε 1/1. N-nicotinoyl-3-alanyl - (L) -hiεtidinε 4-bromobutyl εεtεr iε obtained. c) Synthesis of N-nicotinoyl - β -alanyl (L) -histidine 4 -nitroxy- butyl ester To a solution of N-nicotinoyl -β -alanyl (L) -histidinε 4- bromobutyl estεr (0.91 g, 1.96 mmolεs) in acεtonitrilε (20 ml) silver nitrate (0.66 g, 3.92 mmoles) is added under εtirring. Thε reaction mixture iε heatεd to reflux under εtirring for 4 hourε away from light. Laεtly thε formεd εalt is removed by filtration and the solution is evaporatεd at reduced presεure. The obtained residue is purified by chromatography on silica gel column eluting with n-hexanε/εthyl acεtatε 1/1. N- nicotinoyl-3 -alanyl - (L) -histidinε 4 -nitroxybutyl ester iε obtained. Yieldε: 32%. Elementary analyεiε: Calculated C: 49.50 5 H: 5.54% N: 19.32% Found C: 49.355 H: 5.28% N: 19.17% EXAMPLE 21 Preparation of N-acetyl-S- ( 4 -nitroxybutyroyl ) ciεteinε 1-[(1- methylethyl ) amino] - 3- ( 1-naphthalεn oxy) - 2-propanol ester (NCX 2132) wherein the precursor is propranolol of formula (XXIV) and the precurεor of B is N-acetylcisteinε (formula CVIII): (CVIII) The compound is synthetizεd with thε proceεε deεcribed in Example 14. Yieldε: 7%. Elεmεntary analyεiε: Calculatεd 56.04% H: 6.21% N: 7. 5.9. Found C: 56.135, H: 6.35^ N: 7.91. S: 6.045, EXAMPLE 22 Preparation of 2 - ( ter-butylamino) - 1- [ 4 -hydroxy- 3- [N-acetyl-S- ( 4 -nitroxybutyryl ) -penicillaminoyl ] oxyphenyl ]εthanol ( NCX 2133) wherein the precursor is salbutamol (albuterol) of formula (XX- V) and the precursor of B is N-acetylpenicillamine (formula CV) : (XXV) (CV) The compound iε εynthetized by following the procedure reported in Example 14, uεing N-acεtyl pεnicillaminε inεtead of N-acεtylcistεine . Yields: 43% Elementary analysiε: Calculated C: 53.01% H: 6.86% N: 7.76% S: 5.89% Found C: 53.19% H: 6.80% N: 7.66% 5.725 EXAMPLE 23 Preparation of 7- [ 2 -hydroxy- 3 -[ 3 -methoxy- 5 -( 4 -nitrooxybuty- ryloxy)benzoyl ] tranε- 2 -propenoyl ]theophy11ine (NCX 2213) (NCX2213) wherein the precursor iε the diphylline of formula (XXVI) and the precursor of B iε the ferulic acid (formula DH ) : ( XXVI ) ( DH ) Thε drug iε εynthεtizεd according to thε proceεε deεcribεd in Examplε 9. Yiεld: 22% Elementary analyεiε: Calculated C: 51.31% H: 4.84% N: 12.52% Found C: 51.50% H: 4.91% N: 12.68% EXAMPLE 24 Preparation of N-acetyl -S- ( 2 -acetylbenzoyl )ciεtεinε 4- (nitroxy)butyl eεter (NCX2138) of formula (NCX2138) wherein the precursor iε acetylεalicylic acid of formula (XX- VII) and the precursor of B is N-acetylcisteine (formula CVII - I): 3 (XXVII) (CVIII) The compound is synthetized according to the procεεs dεscribed in Example 1. Yield 36%. Elementary analaysis Calculated C: 48.85% H: 5.01% N: 6.36% S: 7.24% Found C: 48.75% H: 5.02% N: 6.28% S: 7.12% EXAMPLE 25 Preparation of 4 - [ 3 - [ 3 -methoxy- 5 - ( 4 -nitroxybutyryloxy) phεnyl ] • 2-propenoyloxy] - 2 -methyl -N- 2 -pyridinyl- 2H- 1 , 2 -benzothiazin- 3- carboxamidε- 1 , 1 -dioxidε (NCX2215) (NCX2215) wherein the precurεor iε piroxicam of formula (XXVIII) and the precurεor of B iε ferulic acid (formula DH ) : (XXVIII) (DH) The compound iε synthetizεd according to thε procesε reported in Example 9. Yield 18%. Elementary analysis Calculated 55.11% H: 4.47% N: 8.60% 4.90% Found C: 55. IS H: 4.52% N: 8.71% 4.98% EXAMPLE 26 Preparation of S- [ 2- [ ( 2 , 6 -dichlorophenyl )amino)bεnzeneaceti- loxy ] penicillamine 4 - ( nitroxy ) butyl ester ( NCX 2061 ) of formula wherein the precursor is diclofenac of formula (XXIX) and the precursor of B is penicillaminε (formula CV) : (XXIX) (CV) The compound is εynthetized according to the procesε deεcribεd in Examplε 11. Yiεld 21%. Elementary analyεis Calculated C: 50.72% H: 5.00% N: 7.75% S: 5.89% Cl : 13.02% Found C: 50.61% H: 4.89 ! N: 7.81% S: 6.01% Cl : 13.21% PHARMACOLOGICAL TESTS EXAMPLE Acute Toxicity Acute toxicity haε been evaluated by adminiεtering to a group of 10 rats wεighing 20 g a singlε dosε of εach of the tested compounds, by cannula, by os in an aqueous suspension of carboxymethylcellulose 2% w/v. The animals are kept undεr obsεrvation for 14 days. In no animal of thε group toxic symptoms appεared, evεn after administration of a 100 mg/Kg dose. EXAMPLE FI Test 1 - expεrimεntal model in vivo with N-ethylmalεimide (NEM) : study of the gastric tolεrability of εomε drugε εcrεεnεd as precursors of the compounds of the invεntion. The animalε (ratε, weight about 200 g) are diεtributed in the following groupε (No. 10 animalε for group): A) Control groupε: 1° group: trεatmεnt : only carriεr (aqueous suspension 1% w/v of carboxymethylcεllulosε, doεε: 5 ml/Kg whεn thε drug iε adminiεtεrεd by os, physiologic solution whεn by parenteral route), 2° group: treatment: carrier + NEM, B) Groups administerεd with each drug: group I: treatment: carrier + drug, group II: treatment: carrier + drug + NEM. The drugs assayed in this experimεnt are the following (Table I): indomethacin, ambroxol, mesalamine, sodic alendro- nate, tacrine, omeprazol, misoprostol. Indomethacin, ambroxol and alendronatε arε administered by os, mesalamine by intracolonic (rectal) route and tacrine, omeprazol, misoprostol by subcutaneous route. The maximum tolerated dose, determined by administering each substance by the above said routes to thε animals not treated with NEM, is reportεd in Table I. With higher doεes than, those reported in the Table, entεropathy, diarrhoεa, dεprεεεion, trεmor and sεdation havε appεarεd in thε animals. In thiε εxpεrimεntal modεl thε animalε arε at firεt treated with NEM by εubcutaneouε injection at a doεe of 25 mg/kg in phyεiologic solution. The drug is administεrεd one hour later, in suεpεnεion in thε carriεr. Animalε arε sacrificed after 24 hours and evaluation of the damage to thε gastrointεstinal mucoεa iε madε by counting the number of ratε, inside each group, with lesions to the stomach at a visual inspection. The total number of said rats is then divided by the total number of rats of the group and multiplied by 100. The thus obtained percentagεε are reported in Table I . The Table shows that in the groups of rats treatεd with said drugs without NEM, no gastric lesionε were detεctable. All the ratε of group II (treated with NEM) showed gastric lesions after administration with the following drugs: indomethacin, ambroxol, mesalamine, sodic alendronatε, tacrine. Said drugs therεfore can be used in the εynthesis of the products of the invention. Omeprazol and misoprostol cannot instead be used, on the basis of the results provided in test 1, for preparing the products of the invention. EXAMPLE F2 Test 2 (in vitro): inhibition of apoptosiε (DNA fragmentation) induced in thε εndothεlial cells by CIP in the presεnce of some drugs scrεened aε precurεorε of thε compounds of the invention. The following precurεor drugs (Table II): indomethacin, paracetamol, clopidogrel, salbutamol, ambroxol, sodic alεn- dronatε, diphyllinε, cεtirizine, enalapril, nicotinamide, ampicilline, aciclovir, mesalamine, tacrine, simvastine, omeprazol have beεn tεεtεd . Human εndothεlial cells of the umbilical vein arε prepared according to a standard method. Frεsh umbilical veins are filled with a collagenasε solution 0.1% by wεight and incubatεd at 37°C for 5 minutεs . Subsequently the veinε are perfuεεd with the medium M 199 (GIBCO, Grand Island, NY) pH 7.4 with 0.1% (weight/volume) of collagenase, added with 10% of bovinε fetus serum (10 mcg/ml), sodium heparin (50 mcg/ml), thimidine (2.4 mcg/ml), glutaminε (230 mcg/ml), pεnicillin (100 Ul/ml), streptomycin (100 mcg/ml) and streptomycin B (0.125 mcg/ml). The cells are collectεd from thε perfusate by centrifugation at 800 rpm and harvested in culture flaεkε T-75, pretreated with human fibronectin. Cεlls are then harvested in the same medium, added with bovine hypothalamic growth factor (100 ng/ml). When the cells of the primary cell culture (the cells directly removed from ex-vivo umbilical vein) form a single layer of confluεnt cellε (about 8,000,000 cellε/flaεk) , harvεsting is stoppεd and thε layεrs arε waεhed and trypεinized. The cellular suspensions are transferred into wells of a culture plate having 24 wells, half of εaid wells being added with the same culture medium containing the drug at a 10 M concentration, and harvestεd in a thεrmostat at 37°C at a constant moisture (90%), C0 2 = 5%. When the drug is not soluble in thε culturε mεdium, it iε formεrly dissolvεd in a εmall amount of di- methylsulphoxide. Thε maximum amount of dimεthylsulphoxidε which can be added to thε culture medium iε 0.5%. Only thε cells coming from thesε firεt εubculturεs arε used for the tests with cumene hydropεroxide (CIP) . The cells are identified as endothelial cells by morphological examination and by the specific immunological reaction towards factor VIII; these cultures did never show contaminations from myocytes or fibroblasts. Before starting the test, the cellular culture medium is removed and the cellular layers arε carefully washed with a standard physiologic solution buffered with phosphate 0.1 M pH 7.0, at thε temperature of 37°C. The content of each well is then incubated for one hour with a CIP suspension in the culture medium at a 5 mM concentration. Evaluation of the cellular damage (apoptosis) is carried out by determining the per cent variation of the DNA fragmentation in the cultures containing the drug + CIP with respect to the controls treated with CIP only. Said % variation of DNA fragmentation iε dεtermined by evaluating the fluoreεcence variation by a BX60 Olympus microscope (Olympus Co., Roma) set at the wave lεngth of 405-450 nm, of thε teεt samples with respect to the optical density of the controls. The fluoreεcencε of each sample was determined on 5 replicateε. Statiεtic evaluation haε bεεn made with t Student test (p < 0.01). Results are given in Table II and show that indomethacin, paracetamol, clopidogrel, εalbutamol , εodic alendronate, diphyllinε, cεtirizinε, enalapril, nicotinamide, ampicilline, aciclovir, tacrine, omeprazol do not εignificantly inhibit apoptosis; these drugs can therεfore be used for preparing the products of the invention. On the contrary ambroxol, mesalamine and εimvastatine inhibit apoptosis. Therefore on the basis of the rεsults of test 2 these compoundε could not be used for preparing the products of the invention. EXAMPLE F3 Test 3 - experimental in vivo model with N w -nitro-L-arginine- methyl ester (L-NAME): gastric tolerability (gastrointestinal damage incidence), hepatic (GPT dosage, glutamic -pyruvic transaminase) and cardiovascular (blood pressure) tolerability of some drugs screened as precursors of the compounds of the invention. The experimental model adopted is according to J. Clin. Invεstigation 90, 278-281,1992. Thε εndothεlial dyεfunction iε evaluated by determining the damage induced by L-NAME adminiεtration to the gaεtrointeεtinal mucosa, the hepatic damage (GPT increase), and the vascular endothεlium or cardiovaεcular damagε as blood hypεrtεnsion . Thε animalε (ratε, average weight 200 g) are divided in groups as hεrεin below deεcribed. The group recεiving L-NAME is trεated for 4 weεks with εaid compound diεsolvεd at thε concεntration of 400 mg/litrε in drinking watεr. Thε following groups (No. 10 animals for group) arε conεtitutεd: A) Control groups: 1° group: trεatmεnt: only carrier ( aqueous suspension 1% w/v of carboxymethylcellulose, doεe: 5 ml/Kg whεn thε drug iε adminiεtεrεd by oε , physiologic solution whεn by parenteral route), 2° group: treatment: carrier + L-NAME, B) Groups treated with the drug: 3° group: treatment: carrier + drug, 4° group: treatment: carrier + drug + L-NAME. The drugs used in the test are paracetamol, doxorubicine, simvastatine, omeprazol and misoprostol. Each drug is administered once a day for 4 weeks. The maximum tolerated dose of the drug being administered to the animals is determined by evaluating, in a separate dose scaling up εxpεrimεnt on untrεated animals, thε appearance in the animalε of symptoms such aε enteropathy, diarrhoea, depreεεion, trεmor, sεdation. At thε end of the four wεεks accεss to watεr is prevented and after 24 hours the animalε are εacrificed. One hour beforε thε εacrifice blood preεεure is detεrminεd and a blood prεsεure increaεe iε taken as an indication of a damage being occurred to vascular εndothεlium. The damage to the gastric mucosa is evaluatεd as prεviously mεntionεd in tεst 1 (εx. FI ) . Thε hepatic damage is determined by evaluation after the sacrificε of thε glutamic - pyruvic transaminase (GPT increasε). Thε drug mεεtε tεst 3 and it can thεrεforε bε uεεd for preparing the compounds of the invention, when in thε group of rats treated with L-NAME + drug + carrier, an higher hepatic damage (higher GPT values) and/or highεr gastric damagε and/or higher cardiovascular damage (highεr blood pεssure) are found in comparison with the group treated with the carriεr only, or the group treated with carrier + drug, or the group treated with carrier + L-NAME. The test resultε are reported in Table IV. The % gastric lesions have been determined as in Test 1. The % GPT and % blood pressure values are refεrred to the corresponding valuε found in thε animals of thε 1st group of thε control groups . The average value of the blood pressure in this group was of n: 105 + 8 m Hg . Thε rεεultε obtainεd show that paracεtamol, doxorubicin and simvaεtatinε cauεε hεpatic damagε and gaεtroεnteropathy (GPT values and thε gastric lesions are % highεr comparεd both with the corresponding groups treated with the drug, in thε abεεnce of L-NAME, and with the controlε treatεd with L-NAME) . Thεεe drugε can therεforε bε usεd for prεparing thε products of thε invεntion. Omeprazol and misoproεtol should not instead be usεd, on thε baεiε of this tεst, for prεparing the products of the invention. EXAMPLE F4 Test 4: inhibition of the radical production from DPPH of some substances to be usεd aε prεcurεorε of B or BI (rεf. Formulaε I and II of thε invention) The method iε basεd on a colorimetric test in which DPPH ( 2 , 2-diphεnyl- 1-picryl -hydrazyl ) is usεd as thε compound - forming radicals (M.S. Nensetεr et Al . , Atheroεclεr. Thromb. 15, 1338-1344, 1995). Solutions in methanol of the tested subεtances at a final concentration 100 μM are initially preparεd. 0.1 ml of εach of these solutions are added to aliquots of 1 ml of a methanol solution 0.1 M of DPPH and thεn thε final volume is brought to 1.5 ml. After having stored the solutions at room temperature away from light for 30 minuteε , the abεorbance at the wave length of 517 nm is read. It is determined the absorbance decreasε with rεspεct to thε absorbancε of a solution containing the same concentration of DPPH. The efficacy of the teεt compound to inhibit the production of radicalε, or antiradical activity, iε εxprεεεεd by thε following formula: (1 - A S /A C )X100 wherein A s and A c arε, rεεpεctivεly, thε abεorbancε valuεs of thε solution containing thε tεεt compound togεthεr + DPPH and of thε εolution containing only DPPH. Thε compound mεεtε teεt 4 if radical production inhibition, aε above dεfinεd, is εqual to or highεr than 50%. In Tablε V the resultε obtained with the following substances are reportεd: N-acetylcistein , ciεtεine, ferulic acid, (L) -carnosinε , gentisic acid. Table V shows that N-acetylcisteine, cisteine, ferulic acid, (L) -carnosinε, gεntisic acid mεεt test 4 since they inhibit the production of radicals formed from DPPH by more than 50%. EXAMPLE F5 Antiinflammatory activity and gastric tolerability of the compounds according to the invention in comparison with the corresponding precursor drugs in conditions of endothelial dysfunction induced by L-NAME (N w -nitro-L-arginine-methyl ester) The experimental model of Edwards εt Al . , J. Pathol . 134, 147-156, 1981 was followed. Groups formεd by 10 ratε, having an avεrage weigh of 200 g, have been conεtituted. Thε groups have been treated with L- NAME diεεolvεd in drinking watεr (400 mg/1) for two wεεkε , except one group which constituted the control group. Thε drugs wεrε administεrεd by oε , at the doεe of 10 mg/Kg, in carriεr carboxymethylcelluloεε 1% in water, 5 ml/Kg. Thus the groups, εxcεpt thε bεlow dεεcribεd control groupε, were treatεd with thε drug + L-MAME + carriεr. Thε following control groupε wεrε formεd: 1° control group: trεatmεnt: carriεr. 2° control group: trεatmεnt: carriεr + L-NAME. Thε drugε uεεd in thε experiment are thε following: diclofenac and the corresponding thioestεr with ( 4 -nitroxy)bu- tyryl pεnicillaminε (Ex. 26), piroxicam and the correεponding ester with the p- ( 4 -nitroxy)butyryloxy- ferulic acid (Ex. 25), the acetylsalicylic acid and the corresponding thioester with N-acetyl- ( 4 -nitroxy)butyrylciεteinε (Ex. 24). After two weekε from the beginning of the experiment the animals were subjected to threε consecutive injections of air by subcutaneous route , in the dorsal part of the animal , according to the following procedure: first injection: 20 ml, after threε days from thε first injεction: 10 ml. after 6 days from the first injection: the same amount of 10 ml. The animals were thεn fasted until the following morning. One hour bεforε the percutaneous injection with carragenine (2 mi of a 1% carragenine solution in water) in thε inflammatory εxudatε, the treated animalε received by os the carrier or one of the testεd compoundε dissolved or suspended in the carrier. The animals wεre sacrificed after 6 hourε from the injection of the carragenine εolution. The inflammatory exudatε was collectεd and measured to evaluate the leucocyte infiltration. In Table VI the antiinflammatory activity is expreεεεd aε % inhibition of thε lεucocyte infiltration with reεpect to the leucocytε infiltration value found in the animalε treatεd with thε carrier and pretrεatεd with L-NAME, thε % inhibition of thε gaεtrointεεtinal damage waε εvaluatεd as previously dεεcribεd in Test 1 (ex. 1), and thε % blood pressure was evaluated one hour beforε thε εacrificε and rεfεrrεd tc that of the lεt control group (treatmεnt: carrier). In this group of animals the average presεurε value waε of 108 + 10 m Hg . Table VI εhowε that the compoundε of the invention arε aε activε as thε corresponding precursors in the antiinflammatory activity test, but in the confront of the latter they reduce the damage to the cardiovascular endothelium (lower % increase of blood pressurε with rεεpεct to that of thε corrεεponding precursor), and besidεs reduce, or do not give at all, gastric damagε. EXAMPLE F6 In a second apoptosiε expεrimεnt indomethacin and the indomethacin thioester with N-acetyl- ( 4 -nitroxy)butyryl cistεinε (Ex. 3) according to the preεεnt invention werε comparεd. Thε reεultε are reportεd in Table III, and show that the compound of the invention inhibits, differεntly from the precurεor, the apoptosis induced by cumene hydroperoxidε (CIP) . EXAMPLE F7 Gastric tolerability of some drugs usεd as precursorε and of the correεponding compoundε according to the invention. The teεt for gastrointestinal damage of Example F5 was repeated but omitting thε pretrεatment of animals with L-NAME. The tεsted drugε, thεrεof adminiεtered doεεε and reεultε are reportεd in Tablε VII. From thε Table it iε drawn that gaεtropathy incidence is much lower in the groupε treatεd with thε compoundε of thε invention in the confront of the groupε treated with the correεponding precursors . EXAMPLE 27 Synthesiε of ( S ) -N-acetyl-S- [ [ 1- [ 5 - ( 2 , 5-dihydro- 5 -oxo- 3 - furanyl ) - 3 -methyl - 2 -benzofuranyl ] εthyloxy ] - 4 - oxo -butanoyl ] cyεtεinε ( 4 -nitroxy) butyl εstεr of formula wherein the precursor is benfurodil hemisuccinatε of formula (XXXI) and the precursor of 3 is N-acetylcyεtεinε (formula CVIII) - (XXXI) (CVIII) Thε compound iε εynthεtizεd according to the process described in Example 4. Yield 25%. Elementary analysiε Calculated C: 54.19% H: 5.20% N: 4.51% S: 5.17% Found C: 54.25% H: 5.22% N: 4.47% S: 5.15% EXAMPLE 28 Synthesis of (8S-cis)-10[(3 -amino, 2,3, 6 -tri -dεoxy-αr-L- lyxo-εxo pyranoεyl)oxy] -7,8,9, 10- tεtrahydro , 6,8, 11 - trihydroxy- 8 - [ [ [ 3- mεthoxy- 4 - ( 4 -nitroxybutanoyl ) phεnyl ] - 2 - trans -propenoyl -oxy] methyl- oxo] - 1 -methoxy- 5 , 12 -naphtacenedionε of formula whεrein the precursor is doxorubicin of formula (XXXII) and the precursor of B is ferulic acid of (formula DH ) (XXXII) (DH) The compound iε εynthetized according to the process described in Example 9. Yield 11%. Elementary analysis Calculated 57.88% H: 4.98% N: 3.29% Found C: 57.91% H: 5.02% N: 3.27? EXAMPLE F8 Example FI was rεpεatεd with four groups of ratε (εach group of of ten animalε), all of them receiving NEM, and orally adminiεterεd aε it follows : a. control group : the vehicle formed of an aqueous suεpεnsion 1% w/v of carboxymethylcellulose , b. one group (group b - comparativε ) administεred at the same time with 5 mg/Kg (0.014 mmoles/Kg) of indomεthacin + 2.3 mg/Kg (0.014 mmoles/Kg) of N-acetylcyεteine in thε same above vehiclε, c. onε group (group c - comparativε) adminiεtεred at the same time with 6.6 mg/Kg (0.014 mmoles/Kg) of indomethacin 4- (nitroxy)butyl εstεr, εynthetized according to the method diεclosed in WO 95/09831, + 2.3 mg/Kg (0.014 mmoles/Kg) of N-acetylcystεinε in the same above vehicle, d. one group (group d) administerεd with 8,7 mg/Kg (0.014 mmolεs/Kg) of the indomethacin thioestεr with N-acεtyl- (4- nitroxy)butyryl cisteine (rεf. Ex. 3), in thε abovε same vehicle. The results are reported in Table VIII and show that the mixtures administered respectively to groups b and c (comparatives), differently from the compound of the invention administered to group d, were almost ineffective (group b) or much less effective (group c) in reducing gastric lesions. Table I p.o. = per os; i.e. = by intracolonic route; s.c. = by subcutaneouε routε. Table II Table III Table IV J-r Table V Test 4: Screεning of thε εffectivenεss of thε listεd compounds in inhibiting radical production from DPPH. Compound % inhibition radicalε from DPPH Solvent 0 N-acetylcisteine 100 Cistεine 100 Ferulic acid 100 (L) -carnosine 80 Gεntisic acid 80 Penicillamine 100 Table VI Table VII Table VIII

Claims: CLAIMS 1. Compounds or their salts having the following gεnεral formulaε (I) and (II): A—B—C-N(0) s (I) wherein: s = is an integer εqual to 1 or 2, preferably s = 2 ; A = R— 1 - , wherein R iε the drug radical and T 1 = (CO) t or (X) t ., wherεin X = O, S, NR 1C , R lc is H or a linear or branched alkyl, having from 1 to 5 carbon atoms, or a' freε valence, t and t' are integerε and εqual to zero or 1, with the proviso that t = 1 when t' = 0; t = 0 when t' = 1; B = -T B —X 2 —T BI - wherein T B and T BI are equal or different; T B = (CO) when t = 0, T B = X when t' = 0, X being as above defined ; T BI = (CO) tx or (X) Xχ wherein tx and txx have the 0 or 1 value; with thε proviso that tx = 1 when txx = 0, and tx = 0 when txx = 1; X is as above defined; X 2 is a bivalent bridging bond as defined below; C is the bivalent -T c -Y- radical, wherein T c = (CO) when tx = 0, T c = X when txx = 0, X being as above defined; Y is an alkylenoxy group R'O wherein R' is linear or branched whεn poεεiblε C ^^ - ^ , preferably having from 1 to 6 carbon atomε , moεt preferably 2-4, or a cycloalkylene having from 5 to 7 carbon atoms, in the cycloalkylenε ring onε or more carbon atoms can be substituted by heteroatoms, the ring may havε εide chainε of R' type, R' being aε above defined; or R TIχ R- j r IIX [C] n:x — J —[C] nIIX - O- (III) I I IIX' whεrεin: nIX iε an intεgεr betweεn 0 and 3, prεfεrably 1; nllX iε an integer betwεεn 1 and 3, preferably 1; -πx, R TIX' ^ TIIX ' ^ IIX' ' equal to or different from each other are H or a linear or branched C^C^ alkyl; preferably R-π , Rχιχ ' ^ II X - ^ TIIX' are H - Y 3 is a saturated, unsaturatεd or aromatic heterocyclic ring containing at least one nitrogen atom, said ring having 5 or 6 atoms. wherein n3 is an integer from 0 to 3 and n3 ' is an integer from 1 to 3 ; wherεin n3 and n3 ' have the above mentioned meaning (CH 2 -CH-CH 2 -0) nf , I ONO (CH 2 -CH-CH 2 -0) nf ,- ONO- wherein nf ' is an integer from 1 to 6 preferably from 1 to 4; -(CH-CH 2 -0) nf - I R lf (CH ; -CH 0)nf I R If wherein R lf = H, CH 3 and nf is an integer from 1 to 6; preferably from 1 to 4; preferably Y = -R'O- wherein R' is as above defined; preferably R' is a C C 6 alkyl; A— C 1 —B j _ (II) I N(0) s wherein : ι = " cι γ ' τ cn " I wherein T CI and T CII are equal or different, T CI = (CO) when t = 0, T CI = X whεn t ' = 0 , X bεing as abovε defined; T CII = (CO) tI or (X) tII , wherein tl and til have the 0 or 1 value; with the proviso that tl = 1 when til = 0, and tl = 0 when til = 1; X iε as above defined; Y' is aε Y above dεfinεd, but with thrεε free valences instead of two, prefεrably: a -R'O- group whεrεin R' is as abovε dεfinεd, I prεfεrably an alkyl from 1 to 6 carbon atoms, most prεfεrably 2-4, or wherein n3 is an integer from 0 to 3 and n3 ' is an integer from 1 to 3; wherein n3 and n3 ' have the above mentionεd meaning; I (CH 2 -CH-CH 2 -0) nf , - I ON0 2 wherein one hydrogen atom on one of the carbon atomε iε εubεtituted by a freε valence; wherein nf ' iε an integεr from 1 to 6 preferably from 1 to 4 ; wherein onε hydrogεn atom on onε of thε carbon atoms is substituted by a free valence; -(CH-CH 2 -0) nf - i R lf wherein onε hydrogen atom on one of the carbon atomε iε substituted by a free valence; -(CH 2 -CH-0) nf - I R lf wherein R lf = H, CH 3 and nf is an integer from 1 to 6; prefεrably from 1 to 4; wherein one hydrogen atom on one of the carbon atoms is substituted by a free valence ; preferably Y' = - R'O- wherein R' is a linear or I branched C 2 -C , the oxygen which in Y' is covalently linked to the -N(0) s group is at the end of the free bond indicated in the formula of C-^ ; " T 3I I x 2a wherεin X 2a is a monovalεnt radical as defined below, T BII = (CO) when tl = 0, T BI1 = X when til = 0, X bεing as abovε defined; X 2 , bivalεnt radical is εuch that thε corrεεponding prεcurεor of B: -τ B —X 2 —T BI - meets test 4, precursor in which the T B and T BI frεε valence are each saturated with -OZ, -Z, or with -Z I -N-Z 11 , Z 1 and Z 11 being equal or I differεnt and have the Z values as defined below, dεpending on that T B and/or T BI = CO or X, in connection with the valuεs of t, t', tx and txx; X 2a monovalεnt radical , such that thε corresponding precursor of B 1 -T BII —X 2a meεts tεst 4 , prεcursor whεrein the T BII free valence is saturated with -OZ, -Z or with -Z I -N-Z 11 , Z 1 and Z 11 being equal or I or different and having the Z values as defined below, depending on that T BII = CO or X, in connection with the tl and til values; the drug A = R— T' 1 - , wherεin the freε valence is saturated as indicated hereinafter: when t ' = O with : O-Z wherein Z = H or R la , R la being a linear or branched when possible C 1 -C 10 alkyl, preferably ^-0 5 , or with ■ Z I -N-Z 11 , Z 1 and Z 11 bεing aε abovε defined, when t = 0 with -Z, wherεin Z iε aε abovε defined, with the proviεo that the drug iε not a εteroid, iε εuch to meet at leaεt one of teεtε 1-3; whεrεin teεt 1 (NEM) iε a teεt in vivo carried out on four groupε of ratε (each formed by 10 ratε), the controlε (two groups) and the treated (two groups) of which one group of the controls and one group of thε trεated respεctivεly arε administεrεd with onε dosε of 25 mg/kg s.c. of N-εthylmalεimidε (NEM), thε controls being treated with the carrier and the treatεd groups with thε carrier + the drug of formula A = R-T-^ whεrεin the freε valεnce iε saturated as above indicatεd, administεring thε drug at a dose equivalent to the maximum one tolerated by the rats that did not receive NEM, i.e. the highest dosε administrablε to the animal at which there is no manifest toxicity, i.e. such as to be symptomatologically observable; the drug complies with test 1, i.e. the drug can be used to prepare the compounds of general formula (I) and (II), when the group of rats trεated with NEM + carrier + drug shows gastrointestinal damages, or in the group treated with NEM + carrier + drug are observed gastrointestinal damages greater than those of the group treated with the carrier, or of the group treated with the carrier + drug, or of the group treated with the carrier + NEM ; whεrεin tεst 2 (CIP) is a tεεt in vitro wherein human endothelial cellε from thε umbilical vεin arε harvεstεd undεr standard conditions, thεn dividεd into two groups (εach group rεplicatεd fivε times), of which one iε treatεd with a mixture of the drug 10 "4 M concentration in the culturε mεdium, the other group with the carrier; thεn cumεne hydroperoxidε (CIP) having a 5 mM concεntration in the culture mεdium iε added to each of the two groupε; the drug meεtε tεεt 2, i.ε. thε drug can bε uεεd to prepare the compoundε of general formula (I) and (II), if a statistically significant inhibition of the apoptosis (cellular damage) inducεd by CIP is not obtainεd with p < 0.01 with rεspεct to thε group treated with the carrier and CIP; wherein test 3 (L-NAME) is a test in vivo carried out on four groups of ratε (each group formed by 10 ratε) for 4 weeks and receiving drinking water, the controls (two groups) and the treated (two groups), of which one group of the controls and of the treated respεctively receivεs in the above 4 weeks drinking water added of N-ω-nitro-L- arginine methyl eεter (L-NAME) at a concentration of 400 mg/litre, the controls in the 4 weeks being administerεd with thε carriεr and thε trεated in the 4 weeks with the carrier + the drug, administering the carrier or the drug + carrier once a day, the drug being administered at the maximum dose tolerated by the group of rats not pretreated with L-NAME, i.e., the higheεt dose administrable to animals at which no manifest toxicity appears, i.e. such aε to bε symptomatologically observable; after the said 4 wεεks, thε watεr supply is εtoppεd for 24 hourε and then εacrified, determining the blood pressure 1 hour beforε sacrifice, and after sacrifice of the rats dεtermining the plaεma glutamic pyruvic transaminase (GPT) after sacrifice, and examining the gaεtric tiεεue; the drug meεtε tεεt 3, i.e. thε drug can be used to prepare thε compounds of general formula (I) and (II), when in the group of rats treated with L-NAME + carrier + drug, greatεr hepatic damages (determinεd as highεr values of GPT) and/or gastric and/or cardiovascular damages (determinεd as highεr values of blood -prεsεure) are found in comparison respεctivεly with the group treatεd with the carrier alone, or with the group trεatεd with the carrier + drug, or with the group treatεd with thε carrier + L- NAME; thε precursorε of B or B λ with the freε valences saturated as above defined must meεt tεst 4: it is an analytical dεtεrmination carriεd out by adding portions of mεthanol solutions of thε prεcursor of B or B at a 10 "4 M concentration, to a methanol solution of DPPH (2, 2 -diphenyl- 1-picryl hydrazyl - free radical); aftεr having maintainεd thε solution at room temperature away from light for 30 minuteε, it iε rεad thε absorbance at the wave length of 517 nm of the test solution and of a solution containing only DPPH in the same amount as in the test solution; and then the inhibition induced by the precursor towards thε radical production by DPPH is calculated aε a percentage by means of the following rormu a : (1 - A S /A C )X100 whεrεin A s and A c are respεctivεly thε abεorbance valueε of thε εolution containing the teεt compound + DPPH and that of the εolution containing only DPPH; thε precurεor complies with teεt 4 whεn thε pεrcεntage of inhibition as abovε defined iε equal to or higher than 50%. Compoundε according to claim 1 wherein the precurεor compound of B or B- iε εelectεd from thε following claεεεε of compoundε : Aminoacidε, εεlεctε from thε following: L-carnoεine (formula Cl ) , anεerinε (CII), εεlenocyεteinε (CIII), sεlenomethionine (CIV), penicillamine (CV), N-acetyl - penicillamine ( CVI ) , cysteinε (CVII), N-acetyl - cystεinε (CVIII), glutathione (CIX) or its estεrε , preferably ethyl or isopropyl ester: (Cl) (CII) (CIII) (CIV) (CV) (CVI) (CVII) (CVIII) (CIX) hydroxyacids, selected from the following: gallic acid (formula DI ) , ferulic acid (DH), gentisic acid (Dili), citric acid (DIV), caffeic acid (DV) , hydro caffeic acid (DVI), p-coumaric acid (DVII), vanillic acid (DVIII), chlorogenic acid (DIX), kynurεnic acid (DX) , syringic acid (DXI): (DI) (DH) (DUD (DIV) (DV; COOH (DVI) (DVII) (DVIII) (DIX) ;DX) (DXI) Aromatic and hεterocyclic mono- and polyalcohols, selεcted from the following: nordihydroguaiaretic acid (El), quercetin (EH), catechin (EIII), ka- empferol (EIV), sulphurethyne (EV), ascorbic acid (E- VI), isoaεcorbic acid ( EVII ) , hydroquinone (EVIII), goεεypol (EIX), reductic acid (EX), methoxy- hydroquinone (EXI), hydroxyhydrcquinone (EXII), propyl gallatε (EXIII), saccharose (ΞXIV), vitamin Ξ (EXV), vitamin A ( EXVI ) , 3-quinolol (EXVII), 3- tεr-butyl-4 -hydroxyanisole (EXVIII), 3 -hydroxyflavone (EXIX), 3,5-ter-butyl-p-hydrcxyxoluene (ΞXX), p-ter- butyl phenol ( ΞXXI ) , timoloi (ΞXXII), xibornol (ΞXXIII ) , 3,5 - i-ter-butyl - -hydroxybenzyl- thio- glycolatε (EXXIV), 4 ' -hydroxybu yr nilidε (EXXV), guaiacol (EXXVI), tocol (ΞXXVII), isoεugεnol (EXXVIII), εugenol (EXXIX), pipercnyl alcohol (EXXX), allopurinol (EXXXI), conyferyl alcohol (ΞXXXII), 4- hydroxyphenetyl alcohol (EXXXIII) , ρ-courrιaric alcohol (ΞXXXIV), curcumin (EXXXV): (EH) (EIII) (EIV) (EV) (EVI) (EVI I) (EVIII) (EX) (EXI) (EXII) (EXVII) ( EXVI ) (EXVIII) ( EXXI (EXX) (EXXII) (EXXIII) (EXXIV) (EXXV) ( EXXVI ) (EXXVII) ( EXXXI ) (EXXVIII) ( EXXX ) (EXXXII) (EXXXIII) (EXXXTV) (EXXXV) aromatic and heterocyclic amines, selected from the following: N, N' -diphenyl -p-phenylenediamine (MI), ethoxyquin (Mil), thionine (Mill), hydroxyurea (M- IV) : (MI ) (M ) (Mill) (MIV) Compounds containing at least a free acid function, selected from the following: 3 , 3 ' -thiodipropionic acid (NI), fumaric acid (NH), dihydroxymaleic acid (NIH), thioctic acid (NIV), edetic acid (NV) , bilirubin (NVI), 3 , 4 -methylendioxycinnamic acid (NVII), piperonylic acid (NVIII): (NI) (NH) (NIH) (NIV) (NV) (NVII) (NVIII) 3. Compounds according to claims 1-2, wherein in formula (III) Y 3 is selεcted from the following: (Y-D (Y2) (in) (Y4) (Y5) (YS) (Y7) (Y3) Compounds according to claims 1-2, wherεin Y' ■ R'O- and Y = -R'O-, R' has 1-6 carbon atoms, . Compounds according to claims 1-4 wherein the precursor drugs of the compounds of formula (I) and (II) are εelected from the following: anti - inflammatory, analgeεic drugε, bronchodilatorε and drugs active on the cholinergic system, expεctorant -mucolytic drugs, anti-aεthmatic- antiallεrgic , antihiεtaminic drugε , ACE-inhibitorε , beta- blockεrε, antithrombotic drugε, vaεodilatorε , antidiabetic , antitumoral, antiulcεr, antihypεrlipidεmic , antibiotic, antiviral drugε, bone reabεorption inhibitorε, antidεmεntia drugs. 6. Compounds according to claim 5, whεrein the precursor drugs are selεctεd from thε following: anti- inflammatory drugs : aceclofenac, acemetacin, acetyl - salicylic acid, 5 -aminoacεtylsalicylic acid, alclofεnac, alminoprofen, amfenac, bendazac, bermoprofen, α-bisabolol, bromfenac, bromosaligenin, bucloxic acid, butibufen, carprofεn, cinmεtacin, clidanac, clopirac, sodium diclofe- nac, diflunisal, ditazol, enfenamic acid, εtodolac , eto- fenamate, felbinac, fenbufen, fεnclozic acid, fεndosal, fenoprofen, fentiazac, fepradinol, flufenamic acid, fluni- xin, flunoxaprofen, flurbiprofen, glucametacin, glycol salicylate, ibuprofen, ibuproxam, indomethacin, indoprofen, isofezolac, isoxepac, isoxicam, ketoprofen, ketorolac, lornoxicam, loxoprofen, meclofenamic acid, mefenamic acid, meloxicam, meεalamine, metiazinic acid, mofezolac, naproxen, niflumic acid, olsalazinε, oxaceprol, oxaprozin, oxyphenbutazone, parsalmide, perisoxal, phenyl acetylsalicylate, pyrazolac, piroxicam, pirprofen, prano- profen, protizinic acid, salacetamide, salicilamide 0- acεtic acid, εalicylεulphuric acid, εalsalatε, sulindac, suprofεn, suxibuzonε , tεnoxicam, tiaprofεnic acid, tia- ramide , tinoridinε, tolfεnamic acid, tolmεtin, tropεεin, xεnbucin, ximoprofen, zaltoprofen, zomεpirac, tomoxiprol ; analgεεic drugε: acetaminophen, acetaminosalol , aminoc- hlorthenoxazin, acetylsalicylic 2-amino-4 -picoline acid, acεtylsalicylεalicylic acid, anilεridinε, bεnoxaprofεn benzylmorphine , 5-bromoεalicylic acεtatε acid, bucεtin, buprεnorphin , butorphanol , capεaicinε, cinchophεn, ciramadol, clomεtacin, clonixin, codεinε, dεsomorphine , dezocine, dihydrocodeine, dihydromorphine , dimephεptanol , dipyrocetyl, eptazocine, εthoxazεnε, εthylmorphine , eugenol , floctafenine , fosfoεal, glafεninε, hydrocodone, hydromorphone , hydroxypεthidinε , ibufenac, p-la- ctophenetidε, lεvorphanol , mεptazinol, mεtazocine, metopon, morphinε, nalbuphinε, nicomorphine , norlεvorphanol , normorphine, oxycodone, oxymorphone, pen- tazocinε, phεnazocinε, phεnocoll, phenoperidine , phe- nylbutazone, phεnylsalicylate , phenylra ido1 , salicin, sa- licylamide, tiorphan, tramadol , diacerein, actarit; bronchodilators and drugs active on the cholinergic system: acefylline, albuterol, bambuterol, bamifylline, bevonium methyl sulphate, bitolterol, carbuterol , clenbuterol , chlorprenaline, dioxethedrine, difylline, ephedrine, epinεphrinε, eprozinol, etafredine, ethylnorepinephrine , etofylline, fenoterol, flutoprium bromide, hexoprenalinε, ipratropium bro idε, isoεtharine, isoprotenerol, mabuterol, metaproterenol , oxybutynin, oxi- tropium bromide, pirbuterol , procaterol , protokylol, proxyphyllinε, reproterol, rimiterol , εalmetεrol, εoterenol , tεrbutaline, 1- teobromineacetic acid, tiotro- pium bromidε, tretoquinol , tulobuterol , zaprinaεt, cyclodrine, NS-21, 2-hydroxy-2 , 2-diphenyl-N- ( 1 , 2 , 3 , 6-tetra hydro-pyridin- 4 -ylmethyl ) acεtamidε ; εxpεctorant/mucolytic drugε: ambroxol, bromhεxinε, domio- dol , εrdoεtεine, guaiacol, guaifeneεin, iodinatεd glycerol, letostεinε, mεsna, sobrεrol, stεpronin, tεrpin, tiopronin; antiaεthmatic/antiallergic antihiεtaminic drugε: acrivastine, alloclamide, amlexanox, cetirizinε, clobenzepam, chromoglycate, chromolyn, epinastine, fexofεnadinε, formoterol , histamine, hydroxyzine, levocabaεtine, lodoxamide, mabuterol, metron s, montelu- kast, nedocromil, rεpirinast, seratrodast , suplatast tosylate, tεrfεnadinε, tiaramidε, uruεhiol , bromhεxinε; ACE- inhibitors : alacεpril, benazepril, captopril, cero- napril, cilazapril, delapril, enalapril, enalaprilat, fosinopril, imidapril, lisinopril, losartan, moveltipril, naphthopidil, perindopril, quinapril, ramipril, spirapril, temocapril, trandolapril , urapidil; beta-blockerε : acebutolol , alprenolol, amosulalol , aroti- nolol , atenolol, bεtaxolol , bevantolol, bucumolol , bufeto- lol , bufuralol , bunitrolol , bupranolol , butofilol, ca- razolol, carteolol , carvedilol, celiprolol , cetamolol, dilevalol, epanolol , esmolol , indenolol , labetalol , me- pindolol , metipranolol , mεtoprolol, moprolol , nadolol , nadoxolol, nεbivolol , nifenalol, nipridalol, oxprenolol , penbutolol , pindolol , practolol , pronethalol , propranolol , sotalol, εulfinalol, talinolol, tertatolol , tilisolol, timolol, toliprolol, xibenolol ; antithrombotic and vasoactive drugs: acetorphan, acetylsalicylic acid, argatroban, bamethan, bεnfurodil hemisuccinate, benziodarone, betahistine, brovincamine , bufεniode, citicoline, clobenfurol, clopidogrel, cyclandelate, dalteparin, dipyridamole, droprenilaminε, εnoxaparin, fεndilinε, ifenprodil, iloprost, indobufen, isbogrel, iεoxsuprine, hεparin, lamifiban, midodrinε, nadroparin, nicotinyl alcohol, nylidrin, ozagrεl , pεrhexiline, phenylpropanolaminε, prεnylaminε, papa- vεrolinε, rεviparin sodium salt, ridogrεl , suloctidil, tinofedrine, tinzaparin, triflusal, xanthinol niacina- tε; antidiabεtic drugs: acarbosε, carbutamidε , glibornuride glybuthiazol (e) , miglitol, repaglinide, troglitazone, 1- butyl-3-mεtanyl-urεa, tolrεεtat, nicotinamidε; antitumoral drugs: ancitabine, anthramycin, azacitidine, azaserine, 6-azauridine, bicalutamide , carubicin, carzinophilin, chlorambucil , chlorozotocin, cytarabine, daunorubicin, defosfamide, demεcolcine, denoptεrin, 6- diazo-5-oxo-L-norleucine, docetaxel, doxifluridine, doxorubicin, droloxifenε, εdatrεxatε, eflornithine, enocitabine, epirubicin, epitiostanol , εthanidazole, etoposide, fenretinide, fludarabine, fluorouracil , gem- citabine, hexestrol, idarubicin, lonidamine, mannomustine, melphalan, menogaril, 6-mercaptopurinε, methotrexate, mitobronitol , mitolactol , mitomycins, mitoxantrone, mopidamol, mycophenolic acid, ninopterin, nogalamycin, paciitaxel, pentostatin, pirarubicin, piritrexim, plicamycin, podophyllic acid, porfimεr εodium, porfiromycin, propagermanium, puromycin, ranimuεtine, retinoic acid, roquinimex, εtreptonigrin, streptozocin, tεniposidε, tεnuazonic acid, thiamiprine, thioguanine, tomudex, topotecan, trimεtrεxatε , tubεrcidin, ubenimex, vinblaεtine, vincriεtine, vindeεinε, vinorεlbinε, zorubi - cin; antiulcεr drugε: -acεtamidocaproic acid, arbaprostil, cetraxate, cimεtidinε, εcabεt , enprostil, eεaprazole, irεogladine, misoprostol, omeprazole, ornoprostil, pantoprazole, plaunotol , rioprostil, rosaprostol, rotraxate, sofalcone, trimoproεtil ; anti -hyperlipidemic drugs: atorvastatin, cilastatin, dermostatin, fluvaεtatin, lovastatin, mεvastatin, nystatin, pεntostatin, pεpstatin, privastatin εodium salt , simvastatin; antibiotics: amdinocillin, amoxicillin, ampicillin, apal- cillin, apicyclinε, aspoxicillin, azidamfenicol , azidocil- lin, azlocillin, aztreonam, benzoylpaε, benzyl penicil- linic acid, biapenεm, bicozamycin, capreomycin, carbenicillin, carindacillin, carumonam, cefaclor, cefadroxil, cefamandole, cefatrizine, cefazedone, cefazolin, cefbupεrazonε, cεfclidin, cεfdinir, cefditoren, cefepime, cef tamεt, cεfiximε, cεf εnoxime, cefmetazole, cefminox, cefodizime, cefonicid, cefoperazone, ceforanide, cefotaxime , cefotεtan, cεfotiam, cεfoxitin, cefozopran, cefpi izole, cefpiramide, cefpirome, cefprozil, cefroxadine, cefsulodin, ceftazidime, ceftera , ceftezole, cεftibutεn, cεftiofur, cεftizoximε, ceftriaxone, cefuroxime, cefuzonam, cephacεtrilε sodium, cεphalεxin, cεphaloglycin, cephaloridine , cephalosporin C, cεphalothin, cεphapirin sodium, cephradine, chloramphenicol, chlortetracycline , cinoxacin, cyprofloxacin, clavulanic acid, clometocillin, clo- xacillin, cyclacillin, cyclosεrinε, dεmεclocycline, di- cloxacillin, epicillin, fenbεcillin, flomoxεf , floxacilli- n, hεtacillin, imipenem, lenampicillin, loracarbef , lymec- ycline, mafenidε, mεclocycline, meropenem, mεtampicillin, mεthacycline, methicillin εodium εalt, mezlocillin, mi- nocycline, moxalactam, mupirocin, yxin, negamycin, novobiocin, oxacillin, panipenem, penicillin G potassium salt, penicillin N, penicillin O, penicillin V, phenethi- cillin potassium salt, pipacycline, pipεracillin, pirli ycin, porfiromycin, propicillin, quinacillin, ritipenem, rolitetracyclinε, sancycline, sedecamycin, spεctinomycin, sulbactam, sulbenicillin, temocillin, tetracycline, ticarcillin, tigεmonam, tubercidin, azithromycin, clarithro ycin, dirithromycin, enviomycin, erythromycin, josamycin, midecamycin, iokamycin, oleando- mycin, rifabutin, rifamide, rifamycin, rifaximin, rokita- mycin, spiramycin, troleandromycin, viomycin, virginiamycin; amikacin, apramycin, arbekacin, dibekacin, dihydrostreptomycin , fortimicins, gentamicin, micronomicin, neomycin, netilmicin, paromomycin, ribostamycin, sisomicin, spectinomycin, streptomicin, tobramycin, trospectomycin;bacampicillin, cefcapene pivoxil, cefpodoxime proxetil, panipenem, pivampicillin, pivcefalεxin, sultamicillin, talampicillin; carbomycin, clindamycin, lincomycin, mikamycin, roεaramicin, ciprofloxacin, clinafloxacin, difloxacin, enoxacin, enrofloxacin, flεroxacin, flumεquinε, grεpafloxacin, lomεfloxacin, nadifloxacin, nalidixic acid, norfloxacin, ofloxacin, pazufloxacin, pefloxacin, pipemidic acid, piromidic acid, rufloxacin, sparfloxacin, tosufloxacin, trovafloxacin, clomocycline , guamεcycline, oxytetracyclinε, nifurpirinol , nifurprazine; p-aminosalicylic acid, p-aminoεalicylic acid hydrazide, clofaziminε, deoxydihydrostreptomycin, ethambutol , glyconiazide , isoniazid, opiniazide, phenyl aminosalicylate, rifampin, rifapεntinε, salinazid, 4-4'- εulfynyldianilinε , acεdiasulfonε, dapsonε, succisulfone, p-sulfanilylbenzyl amine, thiazolsulfone, acetyl εulfamethoxypyrazine, maf enide , 4 ' - ( mεthy1 sulf amoyl ) sulf anilani lide , salazosulfadimidine, sulfabenzamide , sulfacetamide, sulfachlorpyridazine, sulfachrysoidine, sulfacytine, sulfadiazine , sulfadicramide , sulfadimethoxine , sulfadoxine, sulfaethidolε, sulfaguanidine, sulfaguanole, sulfalene, sulfamεrazine, sulfameter, sulfamethazine, sulfamethizole, sulfa ethomidine, sulfamethoxazole, sulfamethoxypyridazine, sulfamethylthiazole , sulfametrole, sulfamidochrysoidine, sulfamoxole, sulfanilamide, 2-p- sulfanilylanilinoethanol , N 4 - sulfanilylsulfanilamide , sulfanilylurea, N-sulfanilyl- 3 ,4-xylamide, sulfaperine, sulfaphenazole , sulfaproxyline , sulfapyrazine , sulfapyridine, sulfasomizolε, sulfaεymazinε, εulfathiazole, εulfathiourea, εulfiεomidine, sulfisoxazolε , 4- sulfanilamido salicylic acid; negamycin, carumonan, cloxyquin, nitroxoline, arginine, metronidazole; antiviral drugε: acyclovir, amantadine, cidofovir, cytarabine , didanosinε, didεoxyadεnosinε , edoxudine, famciclovir, floxuridine, ganciclovir, idoxuridinε, indanavir, kethoxal , lamivudine, MADU, penciclovir, podophyllotoxin, ribavirin, rimantadine, saquinavir, sorivudine, stavudinε, trifluridinε, valacyclovir , vidarabinε, xεnazoic acid, zalcitabinε, zidovudine; bone reabsorption inhibitors: alendronic acid, butedronic acid, etidronic acid, oxydronic acid, pamidronic acid, risedronic acid; antidementia drugs: amiridine, lazabemide, mofegiline, salbeluzol, oxiracεtam, ipidacrinε, nebracetam, tacrine, velnacrine. 7. Compounds according to claims 5-6, wherein the precursor drugs are selected from the following: anti -inflammatory drugs: acetylsalicylic acid, 5-aminoacetylsalicylic acid, carprofen, diclofenac sodium salt, diflunisal, etodolac, flufenamic acid, flunixin, flurbiprof n, ibuprofen, indomethacin, indoprofen, keto- profen, ketorolac, lornoxicam, loxoprofen, meclofenamic acid, mefenamic acid, meloxicam, mesalaminε, naproxεn, ni- flumic acid, olsalazinε, piroxicam, salsalate, sulindac, suprofen, tenoxicam, tiaprofenic acid, tolfenamic acid, tolmetin, zomepirac, tomoxiprol; analgesic drugs: acetaminophen, acetylsalicylsalicylic acid, benoxaprofen, buprenorphinε , butorphanol, capεaicin, diacεrεinε, dihydrocodεinε , ethylmorphine , eugenol, phenylbutazone, meptazinol, morphinε , nalbuphinε, penta- zocinε, thiorphan, tramadol , actarit; bronchodilators drugs and drugs activε on the cholinergic system: albuterol, carbuterol , clenbuterol, difylline, etofylline, fenotεrol , ipratropium bromidε, mεtaprotεre- nol , oxybutynin, pirbuterol , salmεtεrol , tεrbutaline, tiotropium bromide, zaprinast , cyclodrinε, NS-21, 2- hydroxy- 2 , 2-diphεnyl-N- (1,2,3, 6-tetra hydro-pyridin-4 -yl methyl )acetamid ; εxpεctorant/mucolytic drugs: ambroxol, bromexinε , guaia- col , sobrεrol ; antiasthmatic/antiallergic antihistaminic drugs: cetirizine, chromoglycatε, hista ine, levocabastinε, lodoxamidε, montεlukast , tεrfεnadine, bromexinε; ACE- inhibitors : captopril, εnalapril, lisinopril, losar- tan, ramipril; beta blockers: alprenolol, atenolol, bupranolol, labe- talol , metipranolol , metoprolol , pindolol, propranolol , timolol; antithrombotic and vasoactivε drugs: acetylsalicylic acid, acetorphan, argatroban, clopidogrel, dalteparin, dipyridamole, enoxaparin, heparin, iloprost, midodrine, ozagrel, phenylpropanolamine, trifusal; antidiabetic drugs: tolrestat, nicotinamide; antitumoral drugs : anthramycin, daunorubicin, doxorubicin, epirubicin, fluorouracyl , methotrexate, vinblastine; antiulcer drugs: cimetidine, omeprazole, pantoprazole; antihyperlipidemic drugs: lovastatin, pravastatin sodium salt, simvaεtatin; antibiotics drugε: amoxicillin, ampicillin, aztreonam, biapεnεm, carbεnεcillin, cεfaclor, cεfadroxil, cεfamandole, cefatrizinε, cεfoxitin, clavulanic acid, dicloxacillin, imipεnem, meclocyclinε , mεthacycline, moxalactam, panipenem, sulbactam, azithromycin, erythromycin, josamycin, miokamycin, rifabutine, rifamide, rifamycin, gentamicin, paromomycin, sisomicin, bacampicillin, carbomycin, clindamycin, ciprofloxacin, clinafloxacin, difloxacin, εnrofloxacin, lomefloxacin, nadifloxacin, norfloxacin, ofloxacin, pipemidic acid, apicycline, clomocyclinε, oxytεtracycline, nifurpirinol , nifurprazine, isoniazid, rifampin, rifapentinε, dapsonε, thiazolsulfone , εulfamethoxazole , sulfamoxole, mεtronidazole, arginine; antiviral drugs: aciclovir, famciclovir, ganciclovir, penciclovir, ribavirin, vidarabine, zidovudine; bone resorption inhibitors: alendronic acid, etidronic acid, pamidronic acid. 8. Compounds or salts, or their compositions according to claims 1-7 for use as drugs. 9. Use of compounds or salts, or compositions thereof according to claims 1-7 for the preparation of drugs for the therapeutic stress -oxidative application. 10. Pharmaceutical formulations containing as active principle the compounds or their salts of claims 1-7.

Inventors: DEL SOLDATO PIERO, DEL SOLDATO, PIERO
Applicants: DEL SOLDATO PIERO, NICOX SA, DEL SOLDATO, PIERO, NICOX S.A.
Application year: 2000
Main classification: C07C203
IPC codes: A61K31, A61K38, A61P39, A61P43, C07C203, C07C211, C07C219, C07C229, C07C237, C07C327, C07D209, C07D219, C07D233, C07D277, C07D295, C07D309, C07D401, C07D405, C07D407, C07D417, C07D473, C07D495, C07D499, C07F9, C07H15