Reaction SMILES: NCCC1N=CNC=1.[CH2:9]1[C@@H:13]([OH:14])[C@H:12](/[CH:15]=[CH:16]/[C@@H:17]([OH:24])[CH2:18][CH2:19][CH2:20][CH2:21][CH2:22][OH:23])[C@@H:11]([CH2:25]/[CH:26]=[CH:27]\[CH2:28][CH2:29][CH2:30][C:31]([OH:33])=[O:32])[C@H:10]1[OH:34]>>[CH2:9]1[C:10](=[O:34])[C@H:11]([CH2:25]/[CH:26]=[CH:27]\[CH2:28][CH2:29][CH2:30][C:31]([OH:33])=[O:32])[C@@H:12](/[CH:15]=[CH:16]/[C@@H:17]([OH:24])[CH2:18][CH2:19][CH2:20][CH2:21][CH2:22][OH:23])[C@@H:13]1[OH:14].[CH2:9]1[C:10](=[O:34])[C@H:11]([CH2:25][CH2:26][CH2:27][CH2:28][CH2:29][CH2:30][C:31]([OH:33])=[O:32])[C@@H:12](/[CH:15]=[CH:16]/[C@@H:17]([OH:24])[CH2:18][CH2:19][CH2:20][CH2:21][CH2:22][OH:23])[C@@H:13]1[OH:14]
Reactant: O=C(O)CCC/C=C\C[C@@H]1[C@@H](/C=C/[C@@H](O)CCCCCO)[C@H](O)C[C@@H]1O
Agent: NCCc1c[nH]cn1
Product: O=C(O)CCC/C=C\C[C@H]1C(=O)C[C@@H](O)[C@@H]1/C=C/[C@@H](O)CCCCCO
Product: O=C(O)CCCCCC[C@H]1C(=O)C[C@@H](O)[C@@H]1/C=C/[C@@H](O)CCCCCO

Procedure:
The prostaglandin analogues of general formula VII and the cyclodextrin clathrates and, when R in formula VII represents a hydrogen atom, their non-toxic salts, possess the valuable pharmacological properties typical of prostaglandins in a selective fashion including, in particular, hypotensive activity, inhibitory activity on gastric acid secretion and gastric ulceration, stimulatory activity on uterine contraction, inhibitory activity on blood platelet aggregation, bronchodilator activity and luteolytic activity at doses which do not induce, in general, diarrhoea as an undesired side-effect, and are useful in the treatment of hypertension, in the treatment of gastric ulceration, in the induction of labour in pregnant female mammals, in the treatment of disorders of the peripheral circulation, in the prevention and treatment of cerebral thrombosis and myocardial infarction, in the treatment of asthma and in the control of oestrus in female mammals. For example, in standard laboratory screening tests, (1) by intravenous administration to the allobarbital-anaesthetized dog, 20-hydroxy-PGE2 produces falls in blood pressure of 18 mm.Hg and 50 mm.Hg respectively lasting 4 minutes and 14 minutes respectively at doses of 20 and 50 μg./kg. animal body weight respectively, 16(ξ)-methyl-20-hydroxy-PGE1 produces falls in blood pressure of 12 mm.Hg, 38 mm.Hg and 52 mm.Hg. respectively, lasting 3 minutes, 12 minutes and 19 minutes, respectively, at doses of 0.2, 0.5 and 1.0 μg./kg. animal body weight, respectively, 16(ξ)-methyl-20-hydroxy-PGE2 produces falls in blood pressure of 14 mm.Hg and 36 mm.Hg, respectively, lasting 23 minutes and 54 minutes, respectively, at doses of 2.0 and 10.0 μg./kg. animal body weight, respectively, 20-hydroxy-13,14-dihydro-PGE1 produces falls in blood pressure of 22 mm.Hg and 40 mm.Hg, respectively, lasting 12 minutes and 24 minutes, respectively, at doses of 5.0 and 10.0 μg./kg. animal body weight, respectively, and 20-hydroxy-PGE1 produces falls in blood pressure of 14 mm.Hg and 28 mm.Hg, respectively, each lasting 5 minutes at doses, respectively, of 2.0 and 5.0 μg./kg. animal body weight, respectively; (2)(a) in stress ulceration of rats produced according to the method of Takagi and Okabe [Jap. J. Pharmac, 18, 9-18, (1968)], by oral administration, 20-hydroxy-PGE2 produces 56.12% and 60.25% inhibitions, respectively, of stress ulceration at doses of 1.0 and 2.0 mg./kg. animal body weight, respectively, 16(ξ)-methyl-20-hydroxy-PGE1 produces 68.87% and 78.85% inhibitions, respectively, of stress ulceration at doses of 0.1 and 0.2 mg./kg. animal body weight, respectively, and 20-hydroxy-13,14-dihydro-PGE1 produces 42.14% and 47.13% inhibitions, respectively, of stress ulceration at doses of 1.0 and 2.0 mg./kg. animal body weight, respectively; (b) against gastric ulceration in rats induced by the subcutaneous administration of indomethacin, the oral administration of 20-hydroxy-PGE2 and 20-hydroxy-PGE1 produce inhibitions of 32% and 41%, respectively, at a dose of 100 μg./kg. animal body weight; (3) oral perfusion of 20-hydroxy-PGE2 at a dose of 20 μg./kg. animal body weight/minute for 1 hour (total dose 1200 μg./kg. animal body weight) produces 35% inhibition of gastric acid secretion in male Wistar rats in which gastric acid secretion has been stimulated by the intravenous infusion of pentagastrin at a dose of 100 ng./kg. animal body weight/minute; (4) 20-hydroxy-PGE2 stimulates uterine contraction in the pregnant rat at doses of 10-15 μg./kg. animal body weight by intravenous administration; (5) against adenosine diphosphate-induced blood platelet aggregation in platelet-rich plasma of rats, 16(ξ)-methyl-20-hydroxy-PGE1 produces 50% inhibition of aggregation at a concentration of 9.0 × 10-2 μg./ml. and 20-hydroxy-13,14-dihydro-PGE1 produces 50% inhibition of aggregation at a concentration of 7.0 × 10-1 μg./ml.; (6) on guinea pig isolated tracheal muscle 20-hydroxy-PGE1 produces 50% relaxation of histamine-induced contraction of 4 out of 7 preparations at the dose of 10-6.28 g./ml., 20-hydroxy-PGE2 produces 50% relaxation of contraction of 5 out of 6 preparations at the dose of 10-6.02 g./ml. and 16(ξ)-methyl-20-hydroxy-PGE1 methyl ester produces 50% relaxation of contraction of 5 out of 5 preparations at the dose of 10-5.09 g./ml. (7) by intravenous administration, in anaesthetized guinea pigs in which an increase in resistance in the respiratory tract was induced by the administration of histamine, as determined by the method of Konzett and Rossler [Arch. exp. Path. Pharmak; 195, 71-74, (1940)], 20-hydroxy-PGE1 produces inhibitions of the histamine induces bronchoconstriction of 68% and 88%, respectively, at doses of 0.1 and 0.5 μg./kg. animal body weight, respectively; (8) by inhalation in an aerosol, convulsions induced by the inhalation of a histamine-containing aerosol in the conscious guinea pig are delayed by 16(ξ)-methyl-20-hydroxy-PGE1 leading to increases in the preconvulsion time of 81%, 130% and 143%, respectively, at doses of 1.0, 3.0 and 10.0 μg./ml. of aerosol, respectively; likewise 20-hydroxy-13,14-dihydro-PGE1 increases the preconvulsion time by 106% and 161%, respectively, at doses of 10.0 and 100 μg./ml. of aerosol, respectively, 16(ξ)-methyl-20-hydroxy-PGE2 increases the preconvulsion time by 39%, 88%, 129% and 162%, respectively, at doses of 1.0, 3.0, 10.0 and 30.0 μg./ml. of aerosol, respectively, 16(ξ)-methyl-20-hydroxy-PGE1 methyl ester increases the preconvulsion time by 76%, 119% and 191%, respectively, at doses of 3.0, 10.0 and 30.0 μg./ml. of aerosol, respectively, and 16(ξ)-methyl-20-hydroxy-PGE1 triethanolamine salt increases the preconvulsion time by 71%, 161% and 161%, respectively, at doses of 3.0, 10.0 and 30.0μg./ml. of aerosol, respectively; (9) by oral administration, against convulsions, induced by the inhalation of a histamine-containing aerosol by the conscious guinea pig, 16(ξ)-methyl-20-hydroxy-PGE1 increases the preconvulsion time by 92%, 111% and 276%, respectively, at doses of 10.0, 30.0 and 100 μg./kg. animal body weight, respectively, and increases the preconvulsion time by 100% at a dose of 15.5 μg./kg. animal body weight; (10) by subcutaneous administration to the pregnant hamster on the 4th day of pregnancy, 20-hydroxy-PGF2α and 20-hydroxy-15-epi-PGF2α induce abortion in 50% of the animals at doses of 200 and 330 μg./kg. animal body weight, respectively; (11) the doses of 20-hydroxy-PGE2 and 20-hydroxy-PGE1 which produce diarrhoea in 50% of mice (ED50) by oral administration are, respectively, 12.4 and 19.5 mg./kg. animal body weight; and (12) by oral administration to the morphine-constipated mouse, 20-hydroxy-PGE2, 20-hydroxy-PGE1 and 20-hydroxy-13,14-dihydro-PGE1 induce the production of faeces at doses of ≈ 1000, 1000 and 1000 μg./kg. animal body weight, respectively, 20-hydroxy-PGF2α induces a 13% production of faeces at a dose of 1000 μg./kg. animal body weight and 20-hydroxy-15-epi-PGF2α dose not induce the production of faeces at a dose of 1000 μg./kg. animal body weight.