1-SUBSTITUTED-1-AMINOMETHYL-CYCLOALKANE DERIVATIVES (=GABAPENTIN ANALOGUES), THEIR PREPARATION AND THEIR USE IN THE TREATMENT OF NEUROLOGICAL DISORDERS

Abstract: Novel amines of formulas (1), (1C), (1F), (1G) and (1H) or a pharmaceutical acceptable salt thereof wherein n is an integer of from 0 to 2; m is an integer of from 0 to 3; R is sulfonamide, amide, phosphonic acid, heterocycle, sulfonic acid, or hydroxamic acid; A' is a bridged ring selected from (1), (2), (3), (4), (5) wherein ␣ is the point of attachment; Z1 to Z4 are each independently selected from hydrogen and methyl; o is an integer of from 1 to 4; and p is an integer of from 0 to 2. In formula (1) above R cannot be sulfonic acid when m is 2 and n is 1 are disclosed and are useful as agents in the treatment of epilepsy, faintness attacks, hypokinesia, cranial disorders, neurodegenerative disorders, depression, anxiety, panic, pain, neuropathological disorders, inflammatory diseases, and gastrointestinal disorders, especially irritable bowel syndrome.

Description: 1-SUBSTITUTED-l-AMINOMETHYL-CYCLOALKANE DERIVATIVES (=GABAPENTIN ANALOGUES ) , THEIR PREPARATION AND THEIR USE IN THE TREATMENT OF NEUROLOGICAL DISORDERS BACKGROUND OF THE INVENTION Compounds of formula H 2 N-CH 2 -C-CH 2 -COOR j (CH 2 ) n wherein Rj is hydrogen or a lower alkyl radical and n is 4, 5, or 6 are known in United States Patent Number 4,024,175 and its divisional United States Patent Number 4,087,544. The uses disclosed are: protective effect against cramp induced by thiosemicarbazide; protective action against cardiazole cramp; the cerebral diseases, epilepsy, faintness attacks, hypokinesia, and cranial traumas; and improvement in cerebral functions. The compounds are useful in geriatric patients. The patents are hereby incorporated by reference. Compounds of formula R 3 R 2 I I H 2 NCH-C-CH 2 COOH I Ri wherein R\ is a straight or branched alkyl group having from 1 to 6 carbon atoms, phenyl, or cycloalkyl having from 3 to 6 carbon atoms; R 2 is hydrogen or methyl; and R3 is hydrogen, methyl, or carboxyl are known in United States Patent Number 5,563,175 and various divisionals. These patents are hereby incorporated by reference. SUMMARY OF THE INVENTION The compounds of the instant invention are novel amines and their pharmaceutically acceptable salts useful in a variety of disorders. The disorders include: epilepsy, faintness attacks, hypokinesia, cranial disorders, neurodegenerative disorders, depression, anxiety, panic, pain, neuropathological disorders, inflammatory diseases, and gastrointestinal disorders, especially irritable bowel syndrome. The compounds of the invention are those of formulas 1, IC, IF, IG, and 1H below. Preferred compounds are those wherein R is a sulfonamide selected from -NHSO R 15 or -SO NHR 15 wherein R 15 is straight or branched alkyl or trifluoromethyl. Especially preferred is N-[2-(l-aminomethyl-cyclohexyl)-ethyl]- methanesulfonamide. Other preferred compounds are those wherein R is a phosphonic acid, -PO 3 H 2 . Especially preferred are (l-aminomethyl-cyclohexylmethyl)-phosphonic acid and (2-aminomethyl-4-methyl-pentyl)-phosphonic acid. Other preferred compounds are those wherein R is a heterocycle selected from: Especially preferred are C-[l-(lH-tetrazol-5-ylmethyl)cyclohexyl]- methylamine and 4-methyl-2-( lH-tetrazol-5-ylmethyl)-pentylamine. DETAILED DESCRIPTION OF THE INVENTION The amines of the instant invention are compounds of formulas 1, IC, IF, IG, and 1H and the pharmaceutically acceptable salts thereof. The compounds of the invention are those of formula IC IF IG in or a pharmaceutically acceptable salt thereof wherein: n is an integer of from 0 to 2; m is an integer of from 0 to 3; R is sulfonamide, amide, phosphonic acid, heterocycle, sulfonic acid, or hydroxamic acid; A' is a bridged ring selected from (1) (2) (3) (4) (5) wherein is the point of attachment; Z IO ZA are each independently selected from hydrogen and methyl; o is an integer of from 1 to 4; and p is an integer of from 0 to 2. In Formula 1 above R cannot be sulfonic acid when m is 2 and n is i. (Suman-Chaulan N., et al., European Journal of Pharmacology, 1993;244:293-301.) Preferred compounds of the invention are: ( l-Aminomethyl-cyclohexylmethyl)-phosphonic acid; ( lR-trans)( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)-phosphonic acid; (trans)( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-phosphonic acid; (1 R-trans)( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-phosphonic acid; ( 1 S-cis)( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-phosphonic acid; ( 1 S-trans)( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-phosphonic acid; ( 1 R-cis)( 1 - Aminomethyl-3-methyl-cyclopentylmethyl)-phosphonic acid; ( 1 α,3α,4α)( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-phosphonic acid; (lα,3β,4β)(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-phosphonic acid; (R)( 1 -Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-phosphonic acid; (S)( 1 -Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-phosphonic acid; ( 1 -Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-phosphonic acid; 2-( 1 - Aminomethyl-cyclohexyl)-N-hydroxy-acetamide; (lS-trans)2-(l-Aminomethyl-3-methyl-cyclohexyl)-N-hydroxy-acetamide; (trans)2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-N-hydroxy- acetamide; (lS-cis)2-(l-Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy-acetamide; (lR-trans)2-(l-Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy- acetamide; (lR-cis)2-(l-Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy-acetamide; (lS-trans)2-(l-Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy- acetamide; ( 1 α,3α,4α)2-( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)-N-hydroxy- acetamide; ( 1 α,3 β,4β)2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-N-hydroxy- acetamide; (S)2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-N-hydroxy-acetamide; (R)2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-N-hydroxy-acetamide; 2-( 1 -Aminomethyl-3,3-dimethyl-cyclobutyl)-N-hydroxy-acetamide; N-[2-( 1 -Aminomethyl-cyclohexyl)-ethyl]-methanesulfonamide; ( 1 S-cis)N- [2-( 1 - Aminomethyl-3 -methyl -cyclohexyl)-ethyl] - methanesulf onamide ; (trans)N-[2-( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)-ethyl]- methanesulfonamide; ( 1 S-cis)N-[2-( 1 - Aminomethyl-3-methyl-cyclopentyl)-ethyl]- methanesulf onamide; ( 1 R-trans)N- [2-( 1 - Aminomethyl-3-methyl-cyclopentyl)-ethyl] - methanesulfonamide; ( 1 R-cis)N- [2-( 1 - Aminomethyl-3-methyl-cyclopentyl)-ethyl] - methanesulfonamide ; (lS-cis)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]- methanesulf onamide ; ( 1 α,3 α,4α)N-[2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-ethyl] - methanesulfonamide ; ( 1 α,3 β,4β)N-[2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-ethyl]- methanesulfonamide; (S)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]- methanesulfonamide; (R)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]- methanesulfonamide ; N- [2-( 1 - Aminomethyl-3 ,3-dimethyl-cyclobutyl)-ethyl] - methanesulfonamide; 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]oxadiazol-5-one; (lS-cis)3-(l-Aminomethyl-3-methyl-cyclohexylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; (trans)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; (lR-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; ( lR-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; ( 1 S-trans)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2 ,4] oxadiazol-5 -one ; (lα,3α,4α)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; ( 1 ,3 β,4β)3-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; (S)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; (R)3-( l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; 3-( l-Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-4H-[ 1 ,2,4]oxadiazol- 5-one; 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]oxadiazole-5-thione; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (trans)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (lS-cis)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; (lR-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (lR-cis)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; ( 1 S-trans)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (lα,3α,4α)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; (lα,3β,4β)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; (S)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (R)3-( 1 -Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; 3-( 1 -Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-4H-[ 1 ,2,4]oxadiazole- 5-thione; C-[l-(lH-Tetrazol-5-ylmethyl)-cyclohexyl]-methylamine; ( 1 S-cis)C- [3-Methyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclohexyl] - methylamine; (trans)C-[3,4-Dimethyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; ( 1 S-cis)C-[3-Methyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; ( 1 R-trans)C- [3-Methyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl] - methylamine; (lR-cis)C-[3-Methyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; ( 1 S-trans)C- [3-Methyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; (lα,3α,4α)C-[3,4-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; (1 ,3 β,4β)C- [3 ,4-Dimethyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl] - methylamine; (S)C-[3,3-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; (R)C- [3 ,3-Dimethyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; C-[3,3-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclobutyl]-methylamine; N-[2-(l-Aminomethyl-cyclohexyl)-ethyl]-C,C,C-trifluoro- methanesulf onamide ; ( 1 S-cis)N-[2-( 1 -Aminomethyl-3-methyl-cyclohexyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (trans)N-[2-(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (lR-cis)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (lS-trans)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (lS-cis)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (lR-trans)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (lα,3α,4α)N-[2-(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-ethyl]- C,C,C-trifluoro-methanesulfonamide; (lα,3β,4β)N-[2-(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (S)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (R)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; N-[2-(l-Aminomethyl-3,3-dimethyl-cyclobutyl)-ethyl]-C,C,C-trifluoro- methanesulf onamide ; 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]thiadiazol-5-one; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (trans)3-( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; ( lR-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (lS-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]thiadiazol-5-one; (lR-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; ( 1 α,3α,4α)3-( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (lα,3β,4β)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (S)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (R)3-( 1 -Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; 3-(l-Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-4H-[l,2,4]thiadiazol- 5 -one; C-[l-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- cyclohexyl]-methylamine; (lS-cis)C-[3-Methyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4- ylmethyl)-cyclohexyl] -methylamine; (trans)C-[3,4-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol- 4-ylmethyl)-cyclopentyl]-methylamine; ( 1 S-cis)C-[3-Methyl- 1 -(2-oxo-2,3-dihydro-2λ 4 -[ 1 ,2,3 ,5]oxathiadiazol-4- ylmethyl)-cyclopentyl]-methylamine; (lR-trans)C-[3-Methyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol- 4-ylmethyl)-cycloρentyl]-methylamine; (lR-cis)C-[3-Methyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4- ylmethyl)-cyclopentyl]-methylamine; (lS-trans)C-[3-Methyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4- ylmethyl)-cyclopentyl]-methylamine; ( 1 α,3 α,4α)C- [3 ,4-Dimethyl- 1 -(2-oxo-2,3-dihydro-2λ 4 - [ 1 ,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (lα,3β,4β)C-[3,4-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 - [ 1 ,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (S)C-[3,3-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4- ylmethyl)-cyclopentyl]-methylamine; (R)C-[3,3-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4- ylmethyl)-cyclopentyl] -methylamine ; C-[3,3-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4- ylmethyl)-cyclobutyl] -methylamine; (l-Aminomethyl-cyclohexyl)-methanesulfonamide; (lR-trans)(l-Aminomethyl-3-methyl-cyclohexyl)-methanesulfonamide; (trans)(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-methanesulfonamide; ( 1 S-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonamide; (lR-cis)(l-Aminomethyl-3-methyl-cyclopentyl)-methanesulfonamide; (1 R-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonamide; ( 1 S-cis)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonamide; ( 1 α,3 β,4β)( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)- methanesulf onamide ; ( 1 α,3 α,4α)( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)- methanesulfonamide; (R)(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-methanesulfonamide; (S)(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-methanesulfonamide; (l-Aminomethyl-3,3-dimethyl-cyclobutyl)-methanesulfonamide; ( 1 - Aminomethyl-cyclohexyl)-methanesulfonic acid; (lR-trans) (l-Aminomethyl-3-methyl-cyclohexyl)-methanesulfonic acid; (trans)( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)-methanesulfonic acid; ( 1 S-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; ( 1 S-cis)( 1 - Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; ( lR-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; (lR-cis)(l-Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; ( 1 ,3β,4β)( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)-methanesulfonic acid; (lα,3α,4α)(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-methanesulfonic acid; (R)(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-methanesulfonic acid; (S)(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-methanesulfonic acid; (l-Aminomethyl-3,3-dimethyl-cyclobutyl)-methanesulfonic acid; ( l-Aminomethyl-cyclopentylmethyl)-phosphonic acid; 2-( 1 - Aminomethyl-cyclopentyl)-N-hydroxy-acetamide; N-[2-( 1 -Aminomethyl-cyclopentyl)-ethyl]-methanesulfonamide; 3-( 1 - Aminomethyl-cyclopentylmethyl)-4H-[ 1 ,2,4]oxadiazol-5-one; 3-( 1 -Aminomethyl-cyclopentylmethyl)-4H-[ 1 ,2,4]oxadiazole-5-thione; C-[ l-( lH-Tetrazol-5-ylmethyl)-cyclopentyl]-methylamine; N-[2-(l-Aminomethyl-cyclopentyl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; 3-(l-Aminomethyl-cyclopentylmethyl)-4H-[l,2,4]thiadiazol-5-one; C-[l-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- cyclopentylj-methylamine; ( 1 -Aminomethyl-cyclopentyl)-methanesulfonamide; ( 1 -Aminomethyl-cyclopentyl)-methanesulfonic acid; (9-Aminomethyl-bicyclo[3.3. l]non-9-ylmethyl)-phosphonic acid; 2-(9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-N-hydroxy-acetamide; N-[2-(9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-ethyl]- methanesulfonamide; 3-(9-Aminomethyl-bicyclo[3.3.1]non-9-ylmethyl)-4H-[l,2,4]oxadiazol-5- one; 3-(9-Aminomethyl-bicyclo[3.3.1]non-9-ylmethyl)-4H-[l,2,4]oxadiazole-5- thione; C-[9-(lH-Tetrazol-5-ylmethyl)-bicyclo[3.3.1]non-9-yl]-methylamine; N-[2-(9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; 3-(9-Aminomethyl-bicyclo[3.3.1]non-9-ylmethyl)-4H-[l,2,4]thiadiazol-5- one; C-[9-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- bicyclo[3.3.1]non-9-yl]-methylamine; (9- Aminomethyl-bicyclo [3.3.1] non-9-yl)-methanesulfonamide ; (9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-methanesulfonic acid; (2-Aminomethyl-adamantan-2-ylmethyl)-phosphonic acid; 2-(2-Aminomethyl-adamantan-2-yl)-N-hydroxy-acetamide; N-[2-(2-Aminomethyl-adamantan-2-yl)-ethyl]-methanesulfonamide; 3-(2-Aminomethyl-adamantan-2-ylmethyl)-4H-[l,2,4]oxadiazol-5-one; 3-(2- Aminomethyl-adamantan-2-ylmethyl)-4H-[ 1 ,2,4]oxadiazole-5-thione; C-[2-(lH-Tetrazol-5-ylmethyl)-adamantan-2-yl]-methylamine; N-[2-(2-Aminomethyl-adamantan-2-yl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; 3-(2-Aminomethyl-adamantan-2-ylmethyl)-4H-[l,2,4]thiadiazol-5-one; C-[2-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- adamantan-2-yl]-methylamine; (2-Aminomethyl-adamantan-2-yl)-methanesulfonamide; (2-Aminomethyl-adamantan-2-yl)-methanesulfonic acid; ( 1 -Aminomethyl-cycloheptylmethyl)-phosphonic acid; 2-( 1 -Aminomethyl-cycloheptyl)-N-hydroxy-acetamide; N-[2-(l -Aminomethyl-cycloheptyl)-ethyl] -methanesulfonamide ; 3-(l-Aminomethyl-cycloheptylmethyl)-4H-[l,2,4]oxadiazol-5-one; 3-(l-Aminomethyl-cycloheptylmethyl)-4H-[l,2,4]oxadiazole-5-thione; C-[l-(lH-Tetrazol-5-ylmethyl)-cycloheptyl]-methylamine; N-[2-(l-Aminomethyl-cycloheptyl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; C-[l-(2-Oxo-2,3-dihydro-2 14-[l,2,3,5]oxathiadiazol-4-ylmethyl)- cycloheptyl]-methylamine; ( 1 -Aminomethyl-cycloheptyl)-methanesulfonamide; and ( 1 - Aminomethyl-cycloheptyl)-methanesulfonic acid. Since amino acids are amphoteric, pharmacologically compatible salts can be salts of appropriate inorganic or organic acids, for example, hydrochloric, sulphuric, phosphoric, acetic, oxalic, lactic, citric, malic, salicylic, malonic, maleic, succinic, methanesulfonic acid, and ascorbic. Starting from corresponding hydroxides or carbonates, salts with alkali metals or alkaline earth metals, for example, sodium, potassium, magnesium, or calcium are formed. Salts with quaternary ammonium ions can also be prepared with, for example, the tetramethyl-ammonium ion. The carboxyl group of the amino acids can be esterified by known means. Certain of the compounds of the present invention can exist in unsolvated forms as well as solvated forms, including hydrated forms. In general, the solvated forms, including hydrated forms, are equivalent to unsolvated forms and are intended to be encompassed within the scope of the present invention. Novel intermediates useful in the preparation of the final compounds are included in the invention. The terms used to define the invention are as described below. Sulfonamides are those of formula -NHSO 2 Rl5 or -SO NHRl5 wherein Rl5 is a straight or branched alkyl group of from 1 to 6 carbons or a trifluoromethyl. Amides are compounds of formula -NHCOR12 wherein R^ is straight or branched alkyl of from 1 to 6 carbons, benzyl, and phenyl. Phosphonic acids are -PO3H 2 . Sulfonic acids are -SO3H . Hydroxamic acid is . Heterocycles are groups of from 1 to 2 rings, with from 1 to 6 heteroatoms selected from oxygen, nitrogen, and sulfur. Preferred heterocycles are The term alkyl is a straight or branched group of from 1 to 11 carbon atoms including but not limited to methyl, ethyl, propyl, n-propyl, isopropyl, butyl, 2-butyl, tert-butyl, pentyl, hexyl, and n-hexyl, heptyl, octyl, nonyl, decyl, and undecyl except as where otherwise stated. The cycloalkyl groups are from 3 to 8 carbons and are cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, and cyclooctyl unless otherwise stated. The benzyl and phenyl groups may be unsubstituted or substituted by from 1 to 3 substituents selected from hydroxy, carboxy, carboalkoxy, halogen, CF3, nitro, alkyl, and alkoxy. Preferred are halogens. Alkoxy is as defined above for alkyl. Halogen is fluorine, chlorine, and bromine and preferred are fluorine and chlorine. Carboalkoxy is -COOalkyl wherein alkyl is as described above. Preferred are carbomethoxy and carboethoxy. Certain of the compounds of the present invention can exist in unsolvated forms as well as solvated forms, including hydrated forms. In general, the solvated forms, including hydrated forms, are equivalent to unsolvated forms and are intended to be encompassed within the scope of the present invention. Certain of the compounds of the present invention possess one or more chiral centers and each center may exist in the R(D) or S(L) configuration. The present invention includes all enantiomeric and epimeric forms as well as the appropriate mixtures thereof. The radioligand binding assay using [^H] gabapentin and the α δ subunit derived from porcine brain tissue was used ("The Novel Anti-convulsant Drug, Gabapentin, Binds to the α 2 δ Subunit of a Calcium Channel", Gee N.S., et al., J. Biol. Chem., 1996;271(10):5768-5776). The compounds of the invention show good binding affinity to the α 2 δ subunit. Gabapentin (Neurontin®) is about 0.10 to 0.12 μM in this assay. Since the compounds of the instant invention also bind to the subunit, they are expected to exhibit pharmacologic properties comparable to gabapentin. For example, as agents for convulsions, anxiety, and pain. TABLE 1 Example α2δ Pain Model Assay % MPE IC 50 (nM) 1 Hour 2 Hours 1 Hour 2 Hours C-[ l-(lH-Tetrazol-5-ylmethyl)- 0.203 na na 60 100 cyclohexyl]-methylamine; hydrochloride 3-( 1 - Aminomethyl-cyclohexylmethyl)- 0.17 80.6 76.1 20 40 4H-[ 1 ,2,4]oxadiazol-5-one; hydrochloride C-[9-(lH-Tetrazol-5-ylmethyl)-2- 4.37 adamantyl]-methylamine; hydrochloride C-[9-( 1 H-Tetrazol-5-ylmethyl)- 3.7 bicyclo[3.3.1]non-9-yl]- methylamine; hydrochloride 3-( 1 - Aminomethyl-cyclohexylmethyl)- 4.22 0 0 4H-[ 1 ,2,4]oxadiazol-5-thione; hydrochloride Trans C-[ 1 -( 1 H-Tetrazol-5-ylmethyl)- 0.108 3,4-dimethylcyclopentyl]- methylamine; hydrochloride N-[2-( 1 -Aminomethy 1-cyclohexyl)- >10 0.3 -0.9 0 ethylj-methanesulfonamide N-f 2-( 1 -Aminomethyl-cyclohexyl)- >10 1.6 -4.8 0 ethy 1] -t-butylamide N-[2-(l-Aminomethyl-cyclohexyl)- >10 ethyl]-malonamic acid N-[2-(l-Aminomethyl-cyclohexyI)- >10 ethyl]-3-phenyl-propionamide; hydrochloride N-[2-( 1 -Aminomethyl-cyclohexyl)- >10 ethyl]-2-phenyl-acetamide; hydrochloride Gabapentin 0.14 49.9 19.9 100 100 3-( 1 -Aminomethyl-cyclohexylmethyl)-4H-[ 1 ,2,4]oxadiazol-5-one; hydrochloride was active in the carrageenan induced hyperalgesia assay. When dosed at 30 mg/kg orally in the rat, the compound increased paw withdrawal latency by 80.6% at 1 hour and 76% at 2 hours. By comparison, gabapentin at this dose caused a 49.9% increase at 1 hour and only a 19.9% increase at 2 hours. Thus, the former compound appears to have an antihyperalgesic effect of longer duration than gabapentin. C-[l-(lH-Tetrazol-5-ylmethyl)-cyclohexyl]-methylamine hydrochloride, when tested in the DBA2 audiogenic seizure model at 10 mg/kg after oral dosing, gave 60% protection after 1 hour postdose, 100% protection after 2 hours postdose, 100% protection after 4 hours postdose, and 80% after 6 hours postdose. In the same assay, gabapentin, dosed at 10 mg/kg orally, gave no significant response. At 30 mg/kg it gave 100% protection at 2 hours postdose. The compounds of the invention are related to Neurontin®, a marketed drug effective in the treatment of epilepsy. Neurontin® is l-(aminomethyl)- cyclohexaneacetic acid of structural formula The compounds of the invention are also expected to be useful in the treatment of epilepsy. The present invention also relates to therapeutic use of the compounds of the mimetic as agents for neurodegenerative disorders. Such neurodegenerative disorders are, for example, Alzheimer's disease, Huntington's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis, and epilepsy. The present invention also covers treating neurodegenerative disorders termed acute brain injury. These include but are not limited to: stroke, head trauma, and asphyxia. Stroke refers to a cerebral vascular disease and may also be referred to as a cerebral vascular incident (CVA) and includes acute thromboembolic stroke. Stroke includes both focal and global ischemia. Also, included are transient cerebral ischemic attacks and other cerebral vascular problems accompanied by cerebral ischemia such as in a patient undergoing carotid endarterectomy specifically or other cerebrovascular or vascular surgical procedures in general, or diagnostic vascular procedures including cerebral angiography and the like. Pain refers to acute as well as chronic pain. Acute pain is usually short-lived and is associated with hyperactivity of the sympathetic nervous system. Examples are postoperative pain and allodynia. Chronic pain is usually defined as pain persisting from 3 to 6 months and includes somatogenic pains and psychogenic pains. Other pain is nociceptive. Still other pain is caused by injury or infection of peripheral sensory nerves. It includes, but is not limited to pain from peripheral nerve trauma, herpes virus infection, diabetes mellitus, causalgia, plexus avulsion, neuroma, limb amputation, and vasculitis. Neuropathic pain is also caused by nerve damage from chronic alcoholism, human immunodeficiency virus infection, hypothyroidism, uremia, or vitamin deficiencies. Neuropathic pain includes, but is not limited to pain caused by nerve injury such as, for example, the pain diabetics suffer from. Psychogenic pain is that which occurs without an organic origin such as low back pain, atypical facial pain, and chronic headache. Other types of pain are: inflammatory pain, osteoarthritic pain, trigeminal neuralgia, cancer pain, diabetic neuropathy, restless leg syndrome, acute herpetic and postherpetic neuralgia, causalgia, brachial plexus avulsion, occipital neuralgia, gout, phantom limb, burn, and other forms of neuralgia, neuropathic and idiopathic pain syndrome. Other incidents are head trauma, spinal cord trauma, or injury from general anoxia, hypoxia, hypoglycemia, and hypotension as well as similar injuries seen during procedures from embole, hyperfusion, and hypoxia. The compounds of the instant invention will be useful in gastrointestinal disorders, for example, irritable bowel syndrome (IBS). The instant invention would be useful in a range of incidents, for example, during cardiac bypass surgery, in incidents of intracranial hemorrhage, in perinatal asphyxia, in cardiac arrest, and status epilepticus. A skilled physician will be able to determine the appropriate situation in which subjects are susceptible to or at risk of, for example, stroke as well as suffering from stroke for administration by methods of the present invention. The compounds of the invention are also expected to be useful in the treatment of depression. Depression can be the result of organic disease, secondary to stress associated with personal loss, or idiopathic in origin. There is a strong tendency for familial occurrence of some forms of depression suggesting a mechanistic cause for at least some forms of depression. The diagnosis of depression is made primarily by quantification of alterations in patients' mood. These evaluations of mood are generally performed by a physician or quantified by a neuropsychologist using validated rating scales, such as the Hamilton Depression Rating Scale or the Brief Psychiatric Rating Scale. Numerous other scales have been developed to quantify and measure the degree of mood alterations in patients with depression, such as insomnia, difficulty with concentration, lack of energy, feelings of worthlessness, and guilt. The standards for diagnosis of depression as well as all psychiatric diagnoses are collected in the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) referred to as the DSM-IV-R manual published by the American Psychiatric Association, 1994. GABA is an inhibitory neurotransmitter with the central nervous system. Within the general context of inhibition, it seems likely that GAB A-mimetics might decrease or inhibit cerebral function and might therefore slow function and decrease mood leading to depression. The compounds of the instant invention may produce an anticonvulsant effect through the increase of newly created GABA at the synaptic junction. If gabapentin does indeed increase GABA levels or the effectiveness of GABA at the synaptic junction, then it could be classified as a GABA-mimetic and might decrease or inhibit cerebral function and might, therefore, slow function and decrease mood leading to depression. The fact that a GABA agonist or GABA-mimetic might work just the opposite way by increasing mood and thus, be an antidepressant, is a new concept, different from the prevailing opinion of GABA activity heretofore. The compounds of the instant invention are also expected to be useful in the treatment of anxiety and of panic as demonstrated by means of standard pharmacological procedures. MATERIAL AND METHODS Carrageenin-Induced Hyperalgesia Nociceptive pressure thresholds were measured in the rat paw pressure test using an analgesymeter (Randall-Sellitto Method: Randall L.O., Sellitto J.J., A method for measurement of analgesic activity on inflamed tissue. Arch. Int. Pharmacodvn., 4:409-419 (1957)). Male Sprague-Dawley rats (70-90 g) were trained on this apparatus before the test day. Pressure was gradually applied to the hind paw of each rat and nociceptive thresholds were determined as the pressure (g) required to elicit paw withdrawal. A cutoff point of 250 g was used to prevent any tissue damage to the paw. On the test day, two to three baseline measurements were taken before animals were administered 100 μL of 2% carrageenin by intraplantar injection into the right hind paw. Nociceptive thresholds were taken again 3 hours after carrageenin to establish that animals were exhibiting hyperalgesia. Animals were dosed with either gabapentin (3-300 mg/kg, s.c), morphine (3 mg/kg, s.c), or saline at 3.5 hours after carrageenin and nociceptive thresholds were examined at 4, 4.5, and 5 hours post carrageenin. Semicarbazide-Induced Tonic Seizures Tonic seizures in mice are induced by subcutaneous administration of semicarbazide (750 mg/kg). The latency to the tonic extension of forepaws is noted. Any mice not convulsing within 2.0 hours after semicarbazide are considered protected and given a maximum latency score of 120 minutes. Animals Male Hooded Lister rats (200-250 g) are obtained from Interfauna (Huntingdon, UK) and male TO mice (20-25 g) are obtained from Bantin and Kingman (Hull, UK). Both rodent species are housed in groups of six. Ten Common Marmosets (Callithrix Jacchus) weighing between 280 and 360 g, bred at Manchester University Medical School (Manchester, UK) are housed in pairs. All animals are housed under a 12-hour light/dark cycle (lights on at 07.00 hour) and with food and water ad libitum. Drug Administration Drugs are administered either intraperitoneally (IP) or subcutaneously (SC) 40 minutes before the test in a volume of 1 mL/kg for rats and marmosets and 10 mL/kg for mice. Mouse Light/Dark Box The apparatus is an open-topped box, 45 cm long, 27 cm wide, and 27 cm high, divided into a small (2/5) and a large (3/5) area by a partition that extended 20 cm above the walls (Costall B., et al., Exploration of mice in a black and white box: validation as a model of anxiety. Pharmacol. Biochem. Behav., 32:777-785 (1989)). There is a 7.5 x 7.5 cm opening in the center of the partition at floor level. The small compartment is painted black and the large compartment white. The white compartment is illuminated by a 60-W tungsten bulb. The laboratory is illuminated by red light. Each mouse is tested by placing it in the center of the white area and allowing it to explore the novel environment for 5 minutes. The time spent in the illuminated side is measured (Kilfoil T., et al., Effects of anxiolytic and anxiogenic drugs on exploratory activity in a simple model of anxiety in mice. Neuropharmacol.. 28:901-905 (1989)). Rat Elevated X-Maze A standard elevated X-maze (Handley S.L., et al., Effects of alpha- adrenoceptor agonists and antagonists in a maze-exploration model of 'fear'- motivated behavior. Naunyn-Schiedeberg's Arch. Pharmacol., 327:1-5 (1984)), was automated as previously described (Field, et al., Automation of the rat elevated X-maze test of anxiety. Br. J. Pharmacol., 102(Suppl):304P (1991)). The animals are placed on the center of the X-maze facing one of the open arms. For determining anxiolytic effects the entries and time spent on the end half sections of the open arms is measured during the 5-minute test period (Costall, et al., Use of the elevated plus maze to assess anxiolytic potential in the rat. Br. J. Pharmacol., 96(Suppl):312P (1989)). Marmoset Human Threat Test The total number of body postures exhibited by the animal towards the threat stimulus (a human standing approximately 0.5 m away from the marmoset cage and staring into the eyes of the marmoset) is recorded during the 2-minute test period. The body postures scored are slit stares, tail postures, scent marking of the cage/perches, piloerection, retreats, and arching of the back. Each animal is exposed to the threat stimulus twice on the test day before and after drug treatment. The difference between the two scores is analyzed using one-way analysis of variance followed by Dunnett's t-test. All drug treatments are carried out SC at least 2 hours after the first (control) threat. The pretreatment time for each compound is 40 minutes. Rat Conflict Test Rats are trained to press levers for food reward in operant chambers. The schedule consists of alternations of four 4-minute unpunished periods on variable interval of 30 seconds signaled by chamber lights on and three 3-minute punished periods on fixed ratio 5 (by footshock concomitant to food delivery) signaled by chamber lights off. The degree of footshock is adjusted for each rat to obtain approximately 80% to 90% suppression of responding in comparison with unpunished responding. Rats receive saline vehicle on training days. The compounds of the instant invention are also expected to be useful in the treatment of pain and phobic disorders (Am. J. Pain Manag., 5:7-9 (1995)). The compounds of the instant invention are also expected to be useful in treating the symptoms of manic, acute or chronic, single upside, or recurring depression. They are also expected to be useful in treating and/or preventing bipolar disorder (United States Patent Number 5,510,381). TNBS-Induced Chronic Visceral Allodynia In Rats Injections of trinitrobenzene sulfonic (TNBS) into the colon have been found to induce chronic colitis. In human, digestive disorders are often associated with visceral pain. In these pathologies, the visceral pain threshold is decreased indicating a visceral hypersensitivity. Consequently, this study was designed to evaluate the effect of injection of TNBS into the colon on visceral pain threshold in a experimental model of colonic distension. Animals and Surgery Male Sprague-Dawley rats (Janvier, Le Genest-St-Ilse, France) weighing 340-400 g are used. The animals are housed 3 per cage in a regulated environment (20 ± FC, 50 ± 5% humidity, with light 8:00 am to 8:00 pm). Under anesthesia (ketamine 80 mg/kg i.p; acepromazin 12 mg/kg ip), the injection of TNBS (50 mg/kg) or saline (1.5 mL/kg) is performed into the proximal colon (1 cm from the cecum). After the surgery, animals are individually housed in polypropylene cages and kept in a regulated environment (20 + 1°C, 50 ± 5% humidity, with light 8:00 am to 8:00 pm) during 7 days. Experimental Procedure At Day 7 after TNBS administration, a balloon (5-6 cm length) is inserted by anus and kept in position (tip of balloon 5 cm from the anus) by taping the catheter to the base of the tail. The balloon is progressively inflated by step of 5 mm Hg, from 0 to 75 mm Hg, each step of inflation lasting 30 seconds. Each cycle of colonic distension is controlled by a standard barostat (ABS, St-Die, France). The threshold corresponds to the pressure which produced the first abdominal contraction and the cycle of distension is then discontinued. The colonic threshold (pressure expressed in mm Hg) is determined after performance of four cycles of distension on the same animal. Determination of the Activity of the Compound Data is analyzed by comparing test compound-treated group with TNBS- treated group and control group. Mean and sem are calculated for each group. The antiallodynic activity of the compound is calculated as follows: Activity (%) = (group C - group T) / (group A - group T) Group C: mean of the colonic threshold in the control group Group T: mean of the colonic threshold in the TNBS -treated group Group A: mean of the colonic threshold in the test compound-treated group Statistical Analysis Statistical significance between each group was determined by using a one-way ANOVA followed by Student's unpaired t-test. Differences were considered statistically significant at p <0.05. Compounds TNBS is dissolved in EtOH 30% and injected under a volume of 0.5 mL/rat. TNBS is purchased from Fluka. Oral administration of the test compound or its vehicle is performed 1 hour before the colonic distension cycle. Sub-cutaneous administration of the test compound or its vehicle is performed 30 minutes before the colonic distension cycle. The compounds of the present invention can be prepared and administered in a wide variety of oral and parenteral dosage forms. Thus, the compounds of the present invention can be administered by injection, that is, intravenously, intramuscularly, intracutaneously, subcutaneously, intraduodenally, or intraperitoneally. Also, the compounds of the present invention can be administered by inhalation, for example, intranasally. Additionally, the compounds of the present invention can be administered transdermally. It will be obvious to those skilled in the art that the following dosage forms may comprise as the active component, either a compound of Formula I or a corresponding pharmaceutically acceptable salt of a compound of Formula I. For preparing pharmaceutical compositions from the compounds of the present invention, pharmaceutically acceptable carriers can be either solid or liquid. Solid form preparations include powders, tablets, pills, capsules, cachets, suppositories, and dispersible granules. A solid carrier can be one or more substances which may also act as diluents, flavoring agents, binders, preservatives, tablet disintegrating agents, or an encapsulating material. In powders, the carrier is a finely divided solid which is in a mixture with the finely divided active component. In tablets, the active component is mixed with the carrier having the necessary binding properties in suitable proportions and compacted in the shape and size desired. The powders and tablets preferably contain from five or ten to about seventy percent of the active compound. Suitable carriers are magnesium carbonate, magnesium stearate, talc, sugar, lactose, pectin, dextrin, starch, gelatin, tragacanth, methylcellulose, sodium carboxymethylcellulose, a low melting wax, cocoa butter, and the like. The term "preparation" is intended to include the formulation of the active compound with encapsulating material as a carrier providing a capsule in which the active component with or without other carriers, is surrounded by a carrier, which is thus in association with it. Similarly, cachets and lozenges are included. Tablets, powders, capsules, pills, cachets, and lozenges can be used as solid dosage forms suitable for oral administration. For preparing suppositories, a low melting wax, such as a mixture of fatty acid glycerides or cocoa butter, is first melted and the active component is dispersed homogeneously therein, as by stirring. The molten homogenous mixture is then poured into convenient sized molds, allowed to cool, and thereby to solidify. Liquid form preparations include solutions, suspensions, and emulsions, for example, water or water propylene glycol solutions. For parenteral injection liquid preparations can be formulated in solution in aqueous polyethylene glycol solution. Aqueous solutions suitable for oral use can be prepared by dissolving the active component in water and adding suitable colorants, flavors, stabilizing and thickening agents as desired. Aqueous suspensions suitable for oral use can be made by dispersing the finely divided active component in water with viscous material, such as natural or synthetic gums, resins, methylcellulose, sodium carboxymethylcellulose, and other well-known suspending agents. Also included are solid form preparations which are intended to be converted, shortly before use, to liquid form preparations for oral administration. Such liquid forms include solutions, suspensions, and emulsions. These preparations may contain, in addition to the active component, colorants, flavors, stabilizers, buffers, artificial and natural sweeteners, dispersants, thickeners, solubilizing agents, and the like. The pharmaceutical preparation is preferably in unit dosage form. In such form the preparation is subdivided into unit doses containing appropriate quantities of the active component. The unit dosage form can be a packaged preparation, the package containing discrete quantities of preparation, such as packeted tablets, capsules, and powders in vials or ampoules. Also, the unit dosage form can be a capsule, tablet, cachet, or lozenge itself, or it can be the appropriate number of any of these in packaged form. The quantity of active component in a unit dose preparation may be varied or adjusted from 0.1 mg to 1 g according to the particular application and the potency of the active component. In medical use the drug may be administered three times daily as, for example, capsules of 100 or 300 mg. The composition can, if desired, also contain other compatible therapeutic agents. In therapeutic use, the compounds utilized in the pharmaceutical method of this invention are administered at the initial dosage of about 0.01 mg to about 100 mg/kg daily. A daily dose range of about 0.01 mg to about 100 mg/kg is preferred. The dosages, however, may be varied depending upon the requirements of the patient, the severity of the condition being treated, and the compound being employed. Determination of the proper dosage for a particular situation is within the skill of the art. Generally, treatment is initiated with smaller dosages which are less than the optimum dose of the compound. Thereafter, the dosage is increased by small increments until the optimum effect under the circumstances is reached. For convenience, the total daily dosage may be divided and administered in portions during the day, if desired. Sulfonamides of the instant invention can be synthesized by the general route outlined in Scheme 1. Scheme 1 Reagents: (i) Diethylcyanomethyl phosphonate, NaH, tetrahydrofuran; (ii) Nitromethane, tetrabutylammonium fluoride, tetrahydrofuran; (iii) Borane methyl sulphide, toluene; (iv) Triethylamine, R^SO 2 Cl, tetrahydrofuran; (v) 10% Pd-C, hydrogen gas, methanol. Tetrazoles can be synthesized by the general route outlined in Scheme 2. Scheme 2 Reagents: (i) Trimethylsilylazide, Trimethylaluminium (2M in hexanes), toluene; (ii) Raney Nickel, Methanol. Amides can be synthesized by the general route outlined in Scheme 3. Scheme 3 Reagents: (i) Diethylcyanomethyl phosphonate, NaH, tetrahydrofuran; (ii) Nitromethane, tetrabutylammonium fluoride, tetrahydrofuran; (iii) Borane methyl sulphide, toluene; (iv) Triethylamine, Rl^COCl, tetrahydrofuran; (v) 10% Pd-C, hydrogen gas, methanol. Heterocycles such as can be synthesized by the general route outlined in Scheme 4. Scheme 4 (i) NH 2 OH HCl, Et 3 N; (ii) iBuOCOCl, pyridine followed by reflux in xylene; (iii) Fe/HCl. Compound 1 [(l-Nitromethyl-cyclohexyl)acetonitrile] can be treated with hydroxylamine hydrochloride in the presence of a base such as triethylamine to give compound 2. The heterocyclic compound 3 can be prepared from compound 2 by treatment with iso-butyl chloroformate in the presence of a base such as pyridine followed by reflux in a solvent such as xylene. The nitro compound (compound 3) can be converted to the required amine by reduction, for example, with iron and hydrochloric acid. Heterocycles such as can be synthesized by the general route outlined in Scheme 5a. Scheme 5a Heterocycles such as 10 can be synthesized by the general route outlined in Scheme 5b. Scheme 5b 10 Heterocycles such as can be synthesized by the general route shown in Scheme 6 below: Scheme 6 (i) NH 2 OH-HCl, Et 3 N; (ii) 1 , 1 '-thiocarbonyldiimidazole followed by DBU or DBN; (iii) Fe/HCl. Compound 1 [(Nitromethyl-cyclohexyl)acetonitrile] can be treated with hydroxylamine hydrochloride in the presence of a base such as triethylamine to give compound 2. The heterocyclic compound 3 can be prepared from compound 2 by treatment with 1 , l'-thiocarbonyldiimidazole followed by a base such as l,8-diazabicyclo-[4,5,0]-undec-7-ene (DBU) or l,5-diazabicyclo[2.2.2]octane] (DBN). The nitro compound (compound 3) can be converted to the required amine by reduction, for example, with iron and hydrochloric acid. Heterocycles such as can be synthesized following the general route as shown in Scheme 7. Scheme 7 (i) NH 2 OH HCl, Et 3 N; (ii) 1 , l'-thiocarbonyldiimidazole followed by silica gel or BF3-OEt ; (iii) Fe/HCl. Compound 1 [(Nitromethyl-cyclohexyl)acetonitrile] can be treated with hydroxylamine hydrochloride in the presence of a base such as triethylamine to give compound 2. The heterocyclic compound 3 can be prepared from compound 2 by treatment with 1, l'-thiocarbonyldiimidazole followed by treatment with silica gel or boron trifluoride etherate. The nitro compound (compound 3) can be converted to the required amine by reduction, for example, with iron and hydrochloric acid. Heterocycles such as can be synthesized following the general route outlined in Scheme 8: Scheme 8 (i) NH 2 OH HCl, Et 3 N; (ϋ) Pyridine, SOCl 2 ; (iϋ) Fe/HCl. Compound 1 [(Nitromethyl-cyclohexyl)acetonitrile] can be treated with hydroxylamine hydrochloride in the presence of a base such as triethylamine to give compound 2. The heterocyclic compound 3 can be prepared from compound 2 by treatment with thionyl chloride in the presence of a base such as pyridine. The nitro compound (compound 3) can be converted to the required amine by reduction, for example, with iron and hydrochloric acid. The following examples are illustrative of the instant invention; they are not intended to limit the scope. EXAMPLE 1 (6) (5) ( 4 ) Reagents: (i) Diethylcyanomethyl phosphonate, NaH, tetrahydrofuran; (ii) Nitromethane, tetrabutylammonium fluoride, tetrahydrofuran; (iii) Borane methyl sulphide, toluene; (iv) Triethylamine, methanesulphonyl chloride, tetrahydrofuran; (v) 10% Pd-C, hydrogen gas, methanol then HCl. Cyclohexylidene-acetonitrile (2) Sodium hydride (60% in oil, 0.80 g, 20 mmol) was suspended in 50 mL tetrahydrofuran and chilled in ice under nitrogen. Diethylcyanomethyl phosphonate (3.85 g, 22 mmol) was added dropwise in 10 mL tetrahydrofuran and stirring continued for 15 minutes to give a clear solution. Cyclohexanone (1.90 g, 19 mol) was added in 5 mL tetrahydrofuran and the reaction mixture allowed to warm up to room temperature. The liquor was decanted and the residue washed three times with ether. The liquor and washings were combined, washed with dilute hydrochloric acid and water, dried over magnesium sulphate, filtered, and evaporated to dryness. The residue was purified by chromatography on silica eluting with heptane/ethyl acetate 4: 1 to give the required product as a colorless oil (1.5 g, 67%). iH NMR 400 MHz (CDCI3): 6 1.50 (m, 6H), 2.25 (t, J = 5.6 Hz, 2H), 2.49 (t, J = 6.8 Hz, 2H), 5.04 (s, IH). IR vmax 2933, 2859, 2217, 1633, 1449 (l-Nitromethyl-cyclohexyl)-acetonitrile (3) The nitrile (compound 2, 0.78 g, 6.44 mmol), nitromethane (0.80 g, 13.11 mmol) and tetrabutyl ammonium fluoride (1.0 M in tetrahydrofuran, 10 mL, 10 mmol) were heated in 20 mL tetrahydrofuran to 70°C overnight. The reaction mixture was diluted with ethyl acetate and washed with dilute hydrochloric acid and water, dried over magnesium sulphate, filtered, and evaporated to dryness. The residue was purified by chromatography on silica eluting with heptane/ethyl acetate 3:1 to give the required product as a yellow oil (0.83 g, 71%). iH NMR 400 MHz (CDCI3): δ 1.57 (s, 10H), 2.63 (s, 2H), 4.52 (s, 2H). Analysis calculated for C9H13N 2 O 2 : C, 59.32; H, 7.74; N, 15.37. Found: C, 59.40; H, 7.65; N, 15.18. 2-(l-Nitromethyl-cyclohexyl)-ethylamine (4) Borane methyl sulphide (2.0 M in toluene, 1.3 mL, 2.6 mmol) was added to compound 3 (0.4 g, 2.2 mmol) in toluene (10 mL) under nitrogen. After heating to 60°C for 3 hours, the mixture was allowed to cool, and 15 mL methanol was added followed by 15 mL 4 M HCl in dioxan. After reflux for 1 hour, the mixture was evaporated to dryness. Crystallization from ethyl acetate gave the required product as colorless crystals (0.23 g, 47%); mp 170-173°C. iH NMR 400 MHz (d 6 -DMSO): δ 1.30-1.50 (m, 10H), 1.64-1.69 (m, 2H), 2.82-2.86 (m, 2H), 4.57 (s, 2H), 7.89 (s, 3H). Analysis calculated for C9H1 8 N 2 O2«HC1*0.2H 2 O: C, 47.77; H, 8.64: N, 12.38. Found: C, 47.80; H, 8.66; N, 12.64. N-[2-(l-Nitromethyl-cyclohexyl)-ethyI]-methanesulfonamide (5) Triethylamine (0.64 g, 6.3 mmol) was added dropwise to a mixture of the amine hydrochloride salt (compound 4, 0.70 g, 3.1 mmol) and methane sulfonyl chloride (0.36 g, 6.3 mmol) in tetrahydrofuran (35 mL). After stirring at room temperature for 2 hours, the mixture was filtered, diluted with ethyl acetate, and washed with dilute hydrochloric acid, saturated sodium bicarbonate solution, and water, dried over magnesium sulphate, filtered, and evaporated to dryness. The residue was crystallized from ethyl acetate/heptane to give colorless crystals (0.39 g, 47%); mp 86-88°C. !H NMR 400 MHz (d 6 -DMSO): δ 1.35-1.50 (m, 10H), 1.55-1.60 (m, 2H), 2.89 (s, 3H), 2.99-3.06 (m, 2H), 4.55 (s, 2H), 6.93 (t, J = 6 Hz, IH). Analysis calculated for CioH 2 oN 2 O4S: C, 45.44; H, 7.63; N, 10.60; S, 12.13. Found: C, 45.77; H, 7.64; N, 10.58; S, 12.17. N-[2-(l-Aminomethyl-cyclohexyI)-ethyl]-methanesulfonamide hydrochloride (6) Ten percent Palladium on carbon was added under nitrogen to a solution of compound 5 (0.35 g, 1.3 mmol) in methanol (50 mL). The mixture was shaken under 40 psi hydrogen for 6 hours and then filtered through keiselguhr. The filtrate was evaporated to dryness. 4N HCl in dioxan was added followed by ether to give the product as a colorless crystalline solid (0.33 g, 92%); mp 196-199°C. l U NMR 400 MHz (d 6 -DMSO): δ 1.25-1.45 (m, 10H), 1.55-1.60 (m, 5H), 2.70-2.75 (m, 2H), 2.90-2.95 (m, 5H), 6.86 (t, J = 6.0 Hz, IH), 7.86 (bs, 3H). Analysis calculated for Cι oH 22 N 2 O 2 S«HCl » 0.25H 2 O: C, 43.63; H, 8.60; N, 10.17. Found: C, 43.43; H, 8.64; N, 9.95. EXAMPLE 2 (1) (2) (3) Reagents: (i) Trimethylsilylazide, trimethylaluminium (2 M in hexanes), toluene; (ii) Raney Nickel, hydrogen gas, methanol then HCl. l-(lH-Tetrazol-5-ylmethyl)-cyclohexanecarbonitrile (2) To a soluton of the bis nitrile (Griffiths G., Mettler H., Mills L.S., and Previdoli F., Helv. Chim. Acta. 74:309 (1991)) (1.48 g, 10 mmol) in toluene (20 mL) under nitrogen was added trimethylsilylazide (1.15 g, 10 mmol) followed by trimethylaluminium (5 mL, 2.0 M in hexanes, 10 mmol). After heating to 90°C overnight, the mixture was allowed to cool and added carefully to ethyl acetate, ice and 6N hydrochloric acid. The aqueous phase was extracted with ethyl acetate, and the extracts washed with water, dried over magnesium sulphate, and evaporated to dryness. Crystallization gave the required compound (158 mg, 8%). C-[l-(lH-Tetrazol-5-ylmethyl)-cyclohexyl]-methylamine hydrochloride (3) The tetrazole (compound 8, 158 mg, 0.83 mmol) in methanol was added to a washed suspension of Raney nickel in methanol. The mixture was shaken under 40 psi hydrogen for 3.5 hours and then filtered to remove the catalyst and evaporated to dryness. The residue was partitioned between ethyl acetate and dilute hydrochloric acid. The aqueous phase was separated and evaporated to dryness. Recrystallization from methanol/ether gave the required product (44 mg, 23%); mp l76-179°C. iH NMR 400 MHz (d 6 -DMSO): δ 1.20-1.60 (m, 10H), 2.84 (s, 2H), 3.07 (s, 2H), 8.06 (bs, 3H). EXAMPLE 3 (1) (2) (3) (4) (5) (6) Reagents: (i) Diethylcyanomethyl phosphonate, NaH, tetrahydrofuran; (ii) Nitromethane, tetrabutylammonium fluoride, tetrahydrofuran; (iii) Borane methyl sulphide, toluene; (iv) Triethylamine, acetyl chloride, tetrahydrofuran; (v) 10% Pd-C, hydrogen gas, methanol then HCl Cyclohexylidene-acetonitrile (2) Sodium hydride (60% in oil, 0.80 g, 20 mmol) was suspended in 50 mL tetrahydrofuran and chilled in ice under nitrogen. Diethylcyanomethyl phosphonate (3.85 g, 22 mmol) was added dropwise in 10 mL tetrahydrofuran and stirring continued for 15 minutes to give a clear solution. Cyclohexanone (1.90 g, 19 mmol) was added in 5 mL tetrahydrofuran and the reaction mixture allowed to warm up to room temperature. The liquor was decanted and the residue washed three times with ether. The liquor and washings were combined, washed with dilute hydrochloric acid and water, dried over magnesium sulphate, filtered, and evaporated to dryness. The residue was purified by chromatography on silica eluting with heptane/ethyl acetate 4: 1 to give the required product as a colorless oil (1.5 g, 67%). iH NMR 400 MHz (CDC1 3 ): δ 1.50 (m, 6H), 2.25 (t, J = 5.6 Hz, 2H), 2.49 (t, J = 6.8 Hz, 2H), 5.04 (s, IH). IR vmax 2933, 2859, 2217, 1633, 1449. (l-Nitromethyl-cyclohexyl)-acetonitrile (3) The nitrile (compound 2, 0.78 g, 6.44 mmol), nitromethane (0.80 g, 13.11 mmol) and tetrabutyl ammonium fluoride (1.0 M in tetrahydrofuran, 10 mL, 10 mmol) were heated in 20 mL tetrahydrofuran to 70°C overnight. The reaction mixture was diluted with ethyl acetate and washed with dilute hydrochloric acid and water, dried over magnesium sulphate, filtered, and evaporated to dryness. The residue was purified by chromatography on silica eluting with heptane/ethyl acetate 3: 1 to give the required product as a yellow oil (0.83 g, 71%). iH NMR 400 MHz (CDCI3): δ 1.57 (s, 10H), 2.63 (s, 2H), 4.52 (s, 2H). Analysis calculated for C9Hi3N 2 O 2 : C, 59.32; H, 7.74; N, 15.37. Found: C, 59.40; H, 7.65; N, 15.18. 2-(l-NitromethyI-cyclohexyl)-ethylamine (4) Borane methyl sulphide (2.0 M in toluene, 1.3 mL, 2.6 mmol) was added to compound 3 (0.4 g, 2.2 mmol) in toluene (10 mL) under nitrogen. After heating to 60°C for 3 hours, the mixture was allowed to cool, and 15 mL methanol was added followed by 15 mL 4 M HCl in dioxan. After reflux for 1 hour, the mixture was evaporated to dryness. Crystallization from ethyl acetate gave the required product as colorless crystals (0.23 g, 47%); mp 170-173°C. *H NMR 400 MHz (d 6 -DMSO): δ 1.30-1.50 (m, 10H), 1.64-1.69 (m, 2H), 2.82-2.86 (m, 2H), 4.57 (s, 2H), 7.89 (s, 3H). Analysis calculated for C9H 1 8 N2θ 2 «HCl'0.2H 2 O: C, 47.77; H, 8.64; N, 12.38. Found: C, 47.80; H, 8.66; N, 12.64. N-[2-(l-Nitro ethyl-cyclohexyl)-ethyI]-acetamide (5) The amine hydrochloride salt (compound 4, 0.50 g, 2.25 mmol) was reacted with acetyl chloride (0.20 g, 2.55 mmol) and triethylamine (0.45 g, 4.45 mmol) in tetrahydrofuran following the procedure described in Example 1, Step 4. Purification by chromatography on silica eluting with ethyl acetate gave the required product as a crystalline solid (0.35 g, 69%); mp 68-70°C. iH NMR 400 MHz (CDCI3): δ 1.40-1.60 (m, 10H), 1.60-1.65 (m, 2H), 1.98 (s, 3H), 3.30-3.40 (m, 2H), 4.40 (s, 2H), 5.59 (bs, IH). N-[2-(l-Aminomethyl-cyclohexyl)-ethyl]-acetamide hydrochloride (6) Compound 5 (0.30 g, 1.3 mmol) was hydrogenated in the presence of 10% palladium on carbon following the procedure described in Example 1 , Step 5 to give the product as the hydrochloride salt (0.35 g, 100%). *H NMR 400 MHz (d 6 -DMSO): δ 1.20-1.40 (m, 10H), 1.40-1.50 (m, 2H), 1.81 (s, 3H), 2.75 (q, J = 6.0 Hz, 2H), 2.95-3.05 (m, 2H), 7.99 (bs, 3H), 8.06 (t, J = 4.8 Hz, IH). IR vmax 3265, 2929, 1628, 1553, 1446, 1373, 1298. EXAMPLE 4 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]oxadiazol-5-one; hydrochloride [l-(tert-Butoxycarbonylamino-methyl)-cyclohexyl]-acetic acid (2) A solution of Gabapentin (1) (9.37g, 0.0547 mol) in 125 mL IN NaOH and 50 mL THF was cooled to 0°C and a solution of di-tert-butyl dicarbonate (13.1 g, 0.06 mol) in 200 mL THF was slowly added. The reaction mixture was stirred at room temperature 2 hours and concentrated on a rotary evaporator to remove THF. The concentrate was saturated with KH2PO4 and extracted 3X EtOAc. The EtOAc extracts were washed 2X brine and dried over MgSOφ Evaporation yielded 14.8 g (100%) white solid, mp 109-111°C. 1HNMR (CDCI3) δ 1.2-1.4 (m, 19H), 2.27 (s, 2H), 3.11 (d, 2H, J = 6.84 Hz), 4.95 (broad, IH). MS (APCI) m z 272 (M + 1). Analysis calculated for C, 61.97; H, 9.29; N, 5.16. Found: C, 62.36; H, 9.27; N, 5.19. (l-Carbamoylmethyl-cyclohexylmethyl)-carbamic acid tert-butyl ester (3) [l-(tert-Butoxycarbonylamino-methyl)-cyclohexyl] -acetic acid (2) (152 g, 0.56 mol) was taken up in 1 L THF and triethylamine (66.2 g, 0.65 mol) and cooled to -10°C. Over a 1-hour period, isobutyraldehyde was added (84.7 g, 0.62 mol), and the heterogeneous mixture was stirred at 0°C for 15 minutes. Ammonia gas was bubbled into the cold reaction mixture for 30 minutes, and the mixture was allowed to warm to room temperature. After 16 hours stirring, the reaction mixture was evaporated to dryness on a rotary evaporator, and the residue was taken up in water, extracted 3X EtOAc, washed 2X brine and dried over MgSO4- Evaporation yielded an oil which was crystallized from pentane to yield 116.5 g (77%) white crystals; mp 123-125°C. 1HNMR (CDC1 3 ) δ 1.2-1.6 (m, 19H), 2.12 (s, 2H), 3.13 (d, 2H, J = 7.08 Hz), 4.97 (s, IH), 5.43 (s, IH), 7.34 (s, IH). MS (APCI) 271 m/z. (M +1). Analysis calculated for C 14^6^03: C, 62.19; H, 9.69; N, 10.36. Found: C, 62.00; H, 9.72; N, 9.96. (l-Cyanomethyl-cyclohexylmethyl)-carbamic acid tert-butyl ester (4) Cyanuric chloride (39.5 g, 0.214 mol) was added to (1-carbamoylmethyl- cyclohexylmethyl)-carbamic acid tert-butyl ester (3) (116 g, 0.429 mol) in 400 mL DMF. An ice-water bath was used to moderate the exotherm, and the reaction mixture was stirred at room temperature for 1.5 hours. The mixture was poured into ice-water containing 120 g (1.43 mol) NaHCO3 and was extracted 4X EtOAc. The extracts were washed IX water, 2X brine and dried over Na 2 SO4. Evaporation yielded an oil which was taken up in 3: 1 hexane/EtOAc and filtered through silica gel. Evaporation yielded white crystals (86.5 g, 80%); mp 54-58°C. iHNMR (CDCI3) δ 1.3-1.5 (m, 19H), 2.30 (s, 2H), 3.15 (d, 2h, J = 7.00 Hz), 4.60 (broad, IH). MS (APCI) m/z 253 (M + 1). Analysis calculated for Ci4H 2 4N O 2 : C, 66.63; H, 9.59; N, 11.10. Found: C, 66.64; H, 9.52; N, 10.80. [l-(N-Hydroxycarbamimidoylmethyl)-cyclohexylmethyl]-carbamic acid tert- butyl ester (5) A suspension of hydroxylamine hydrochloride (69.5 g, 1.00 mol) in DMSO (300 mL) was cooled in ice-water, and triethylamine (106.7 g, 1.05 mol) was added. The resulting exotherm brought the temperature to 20°C. The mixture was stirred at this temperature 15 minutes, and triethylamine hydrochloride was filtered off and washed with THF. The filtrate was concentrated to remove THF, and (l-cyanomethyl-cyclohexylmethyl)-carbamic acid tert-butyl ester (4) (50.4 g, 0.2 mol) was added, and the mixture was heated at 75°C for 15 hours. After cooling, the reaction mixture was diluted with water ( 1 L) and extracted 3X EtOAc. The EtOAc extracts were washed IX saturated KH 2 PO4, IX saturated NaHCO3 , 2X brine and dried over Na 2 SO4- Evaporation yielded a gummy solid which was triturated in Et 2 O to give white crystals, 25.2 g (44%); mp 125-127°C. iHNMR (CDCI3) δ 1.3-1.5 (m 19H), 1.99 (s, 2H), 3.12 (d, 2H J = 6.84 Hz), 4.93 (t, IH, J = 6.84 Hz), 5.40 (s, IH). MS (APCI) m/z 286 (M + 1). Analysis calculated for C14H27N3O3: C, 58.92; H, 9.54; N, 14.72. Found: C, 58.96; H, 9.80; N, 14.65. BOC-Gabapentin amidoxime carbamate (6) A solution of [l-(N-Hydroxycarbamimidoylmethyl)-cyclohexylmethyl]- carbamic acid tert-butyl ester (5) (25.1 g, 0.088 mol) and pyridine (7.82 g, 0.099 mol) in DMF (200 mL) was cooled in ice-water as isobutyraldehyde (12.32 g, 0.09 mol) was added dropwise. After 15 minutes, the bath was removed and the mixture was stirred at room temperature 2 hours, diluted with water, and extracted 3X EtOAc. The extracts were washed IX water, 2X brine and dried over N 2 SO4. Evaporation yielded an oil, 34 g (100%) which was used without further purification. MS (APCI) m/z 386 (M + l). [l-(5-Oxo-4,5-dihydro-[l,2,4]oxadiazoI-3-ylmethyl)-cyclohexylmethyl]- carbamic acid tert-butyl (7) BOC-Gabapentin amidoxime carbamate (33.88 g, 0.088 mol) was taken up in xylene (250 mL) and heated under reflux 2.5 hours. The xylene was evaporated off and the residue taken up in Et 2 O and extracted 3X 75 mL IN NaOH. The alkaline extracts were acidified with saturated KH PO4 and extracted 3X Et 2 O. The Et 2 O extracts were washed IX saturated KH 2 PO4 2X brine and dried over Na 2 SO4. Evaporation yielded 17.9 g (65%) of a cream-colored solid, mp 140-143°C. iHNMR (CDC1 3 ) δ 1.0-1.6 (m, 19H), 2.42 (s, 2H), 3.00 (d, 2H, J = 7.32 Hz), 4.86 (t, IH, J = 7.08 Hz), 11.30 (s, IH). MS (APCI) m/z 312 (M + 1). Analysis calculated for C\ 5H25N3O4: C, 57.86; H, 8.09; N, 13.49. Found: C, 58.21; H, 8.31; N, 13.30. 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]oxadiazol-5-one; hydrochloride (8) A solution of BOC-Gabapentin oxadiazolone (17.7 g, 0.0568 mol) in 4 M HCl in dioxane (200 mL) was allowed to stand 1.5 hours. Concentration to half volume followed by addition of Et 2 O gave a precipitate which was filtered off and recrystalhzed from MeOH to give white crystals (12.98 g, 92.7%), mp 209-212°C. iHNMR (DMSO-d 6 ) δ 1.2-1.5 (m, 10H), 2.64 (s, 4H), 2.79 (s, 2H), 7.98 (s, 3H), 12.35 (s, IH). MS (APCI) m/z 212 (M +1). Analysis calculated for C10H17N3O2 HCI: C, 48.49; H, 7.32; N, 16.96; Cl, 14.31. Found: C, 48.71; H, 7.18; N, 17.03; Cl, 14.32. EXAMPLE 5 [l-(5-Thioxo-4,5-dihydro-[l,2,4]oxadiazol-3-ylmethyl)-cyclohexylmethyI]- carbamic acid tert-butyl ester (9) A mixture of [l-(N-Hydroxycarbamimidoylmethyl)-cyclohexylmethyl]- carbamic acid tert-butyl ester (4.85 g, 0.017 mol), 90% 1, l'- thiocarbonyldiimidazole (3.96 g, 0.02 mol) and DBU (10.39 g, 0.068 mol) in MeCN (150 mL) was stirred at room temperature 19 hours. The reaction mixture was evaporated to dryness, suspended in saturated KH2PO4 and extracted 3X EtOAc. The EtOAc extracts were washed 2X saturated KH2PO4, 2X brine and dried over Na2SO4. Evaporation followed by filtration through silica gel, eluting with 3: 1 EtOAc/hexane yielded, upon evaporation, a solid which was recrystalhzed from Et2θ/hexane to give a pale pink solid, 2.6 g (47%), mp 160-161°C. iHNMR (CDCI3) δ 1.1-1.6 (m, 19H), 2.53 (s, 2H), 3.00 (d, 2H, J = 7.33 Hz), 4.90 (t, IH, J = 7.08 Hz), 12.88 (s, IH). MS (APCI) m/z 328 (M + l). Analysis calculated for C 15H25N3O3S : C, 55.02; H, 7.70; N, 12.83; S, 9.79. Found: C, 55.34; H, 7.80; N, 12.72; S, 9.43. 3-(l-Aminomethyl-cyclohexylmethyI)-4H-[l,2,4]oxadiazole-5-thione; hydrochloride (10) [l-(5-Thioxo-4,5-dihydro-[l,2,4]oxadiazol-3-ylmethyI)-cyclohexylmethyl]- carbamic acid tert-butyl ester (9) (2.5 g, 0.0076 mol) was taken up in 4 M HCl in 1,4-dioxane (75 mL) and stirred at room temperature. The precipitate which formed was filtered off and recrystalhzed from MeOH- Et2θ to yield 1.31 g (66%) white solid, mp 210-212°C. iHNMR (DMSO-d 6 ) δ 1.2-1.5 (m, 10H), 2.79-2.85 (m, 4H), 7.99 (s, 3H). MS (APCI) m/z 228 (M +1). Analysis calculated for C, 45.53; H, 6.88; N, 15.93; S, 12.16; Cl, 13.44. Found: C, 45.92; H, 6.71; N, 15.83; S, 11.81; Cl, 13.48. EXAMPLE 6 Reagents: (i) Trimethylsilylazide, dibutyl tin oxide, toluene (ii) Nickel catalyst, Methanol Synthesis of 9-(lH-Tetrazol-5-ylmethyl)-bicyclo[3.3.1]nonane-9-carbonitrile (2) To a solution of the bis nitrile (ref WO 9733859) (1.2 g, 6.38 mmol) in toluene (10 mL) was added trimethylsilylazide (1.48 g, 12.87 mmol) followed by dibutyl tin oxide (0.16 g, 0.64 mmol). After heating to 95° for 3 days the mixture was diluted with ethyl acetate, washed with IN HCl and water, dried over magnesium sulphate, and evaporated to dryness. Crystallization gave the required compound (0.3 g, 20%); mp 189-191°C. 400 MHz NMR (d 6 -DMSO) δ 1.50-1.70 (m, 4H), 1.75-2.10 (m, 10H), 3.48 (s, 2H). Synthesis of C-[9-(lH-TetrazoI-5-ylmethyI)-bicyclo[3.3.1]non-9-yl]- methylamine hydrochloride (3) The tetrazole obtained in Step 1 (0.60 g, 2.59 mmol) in methanol (100 mL) was added to a washed suspension of nickel catalyst in methanol. The mixture was shaken under 40 psi hydrogen overnight and then filtered to remove the catalyst and evaporated to dryness. The residue was dissolved in methanol and ethereal hydrogen chloride added. Addition of ether and filtration gave the required product (0.19 g, 22%). mp 232-236°C. 400 MHz NMR (d6-DMSO) δ 1.40-1.70 (m, 8H), 1.75-1.95 (m, 4H), 2.05-2.15 (m, 2H), 3.13 (s, 2H), 3.29 (s, 2H), 8.0 (bs, 3H). EXAMPLE 7 (1 ) (2) (3) (4) (5) Reagents: (i) Ethylcyanoacetate, NaH, THF; (ii) KCN, EtOH, water, reflux; (iii) Trimethylsilylazide, dibutyltin oxide, toluene; (iv) Nickel catalyst, Methanol Synthesis of 2-(lH-Tetrazol-5-ylmethyl)-adamantane-2-carbonitrile (4) Prepared in the same manner as 9-(lH-Tetrazol-5-ylmethyl)- bicyclo[3.3.1]nonane-9-carbonitrile in Example 4. Synthesis of C-[2-(lH-Tetrazol-5-ylmethyl)-adamantan-2-yl]-methylamine hydrochloride (5) The nitrile obtained in Step 3 was prepared in an analogous manner to (0.47 g, 1.9 mmol) was shaken with nickel catalyst (one spatula full, washed) under 50 psi hydrogen overnight. Filtration through kieselguhr and evaporation followed by treatment with methanol and ethereal hydrogen chloride gave the required product which was crystallized from methanol and acetonitrile (25 mg, 5%); mp 250-252°C. 400 MHz NMR δ 1.49 (s, 2H), 1.54 (d, J = 13.7 Hz, 2H), 1.59 (d, J = 13.7 Hz), 1.67 (s, 2H), 1.83 (s, IH), 1.90 (s, IH), 1.97 (d, J = 12.9 Hz, 2H), 2.19 (d, J = 12.7 Hz, 2H), 3.15 (s, 2H), 3.34 (s, obscured by water), 7.99 (bs, 3H). Mass Spec ES+ 248 (100%, (M+H)+). EXAMPLE 8 (1) (2) Reagents: (i) Ethyl cyanoacetate, ammonium acetate, acetic acid, toluene (ii) Potassium cyanide, aqueous ethanol (iii) Trimethylsilylazide, dibutyltin oxide, toluene (iv) nickel catalyst, methanol Synthesis of (trans)Cyano-(3,4-dimethyl-cyclopentylidene)-acetic acid ethyl ester (2) Trans-3,4-dimethyl cyclopentanone (2.91 g, 25.94 mmol), ethyl cyanoacetate (2.93 g, 25.93 mmol), ammonium acetate (0.20 g, 2.60 mmol), and acetic acid (0.31 g, 5.17 mmol) were heated together in refluxing toluene under a Dean-Starck trap for 24 hours. After cooling and filtration through kieselguhr, evaporation gave the required product as an off-white solid (5.0 g, 93%). 400 MHz NMR δ 1.08 (d, J = 6.0 Hz, 3H), 1.09 (d, J = 6.4 Hz, 3H), 1.34 (t, J = 7.2 Hz, 3H), 1.55-1.70 (m, 2H), 2.30-2.45 (m, 2H), 3.08 (dd, J = 20.0 Hz, 8.0 Hz, IH), 3.43 (dd, J = 20.0 Hz, 7.0 Hz, IH), 4.26 (q, J = 7.1 Hz, 2H). Mass Spec ES+ 208.19 (M+H)+, 225.19, 230.16 (100%, (M+Na)+). Synthesis of (trans)l-CyanomethyI-3,4-dimethyl-cyclopentanecarbonitrile (3) The product from Step 1 (5.0 g, 24.1 mmol) was refluxed with potassium cyanide (1.57 g, 24.2 mmol) in ethanol/ 10% water (50 mL) overnight. Evaporation to dryness and purification by chromatography eluting with ethyl acetate/heptane 1:1 gave the required product as a yellow oil 2.9 g (74%). tic rf 0.45 ethyl acetate/heptane 1: 1. 400 MHz NMR δ 1.05 (d, J = 8.4 Hz, 3H), 1.07 (d, J = 8.8 Hz, 3H), 1.49 (dd, J = 13.2, 11.6 Hz, IH), 1.60-1.70 (m, IH), 1.75-1.90 (m, IH), 1.96 (dd, J = 13.6, 14.8 Hz, IH), 2.19 (dd, J = 14.0, 8.4 Hz, IH), 2.48 (dd, J = 13.2, 6.4 Hz, IH), 2.73 (s, 2H). Synthesis of (trans)3,4-Dimethyl-l-(lH-tetrazol-5-ylmethyl)- cyclopentanecarbonitrile (4) The bis-nitrile from Step 2 (1.62 g, 10 mmol) was heated with trimethylsilyl azide (2.84 g, 24.7 mmol) and di-butyl tin oxide (0.24 g, 0.96 mmol) in toluene (50 mL) to 100°C overnight. The reaction mixture was diluted with ethyl acetate and washed with dilute hydrochloric acid and water. The solution was dried over magnesium sulphate and evaporated to dryness. Purification by chromatography eluting with ethyl acetate gave the required product as a colorless oil 0.94 g, (46%). Mass Spec ES+ 206.23 (M+H)+ 228.26 (M+Na)+. 400 MHz NMR CDCI3 δ 1.04 (d, J = 7.2 Hz, 3H), 1.05 (d, J = 6.4 Hz), 1.56 (dd, J = 11.6, 11.6 Hz, IH), 1.55-1.65 (m, IH), 1.65-1.75 (m, IH), 1.83 (dd, J = 13.6, 9.2 Hz, IH), 2.27 (dd, J = 14.0, 8.0 Hz), 2.35 (dd, J = 13.0, 6.8 Hz, IH), 3.36 (s, 2H). Synthesis of (trans)C-[3,4-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine hydrochloride (5) The tetrazole obtained in Step 3 (0.90 g, 0.44 mmol) and nickel catalyst (one spatula full, washed) were shaken together in methanol (200 mL) overnight. The mixture was filtered through kieselguhr and evaporated to dryness. The residue was treated with methanol and ethereal hydrogen chloride and then stirred with di-tertiarybutyl dicarbonate (0.80 g, 3.67 mmol) and sodium bicarbonate (0.80 g, 9.52 mmol) in aqueous dioxan (1:1, 20 mL) overnight. The mixture was diluted with ethyl acetate and the aqueous phase separated, acidified, and extracted 3X with ethyl acetate. The extracts were dried over magnesium sulphate, filtered and evaporated to give a colorless oil. This oil was stirred with 4 M hydrogen chloride in dioxan (5 mL) overnight and then evaporated to dryness to give the required product 0.24 g (76%). 400 MHz dg-DMSO δ 0.88 (d, J = 6.4 Hz, 3H), 0.89 (d, J = 5.6 Hz, 3H), 1.15-1.25 (m, 3H), 1.35-1.45 (m, IH), 1.70-1.80 (m, 2H), 2.82 (d, J = 13.2 Hz, IH), 2.89 (d, J = 13.2 Hz, IH), 3.04 (d, J = 15.2 Hz, IH), 3.05 (d, J = 15.2 Hz, IH). Mass Spec ES+ 210 100%, (M+H)+. Elemental analysis calculated for Ci ()Hi9N5-HCl-0.5H 2 O: C, 47.14; H, 8.31; N, 27.49. Found: C, 47.23; H, 7.97; N, 27.16.

Claims: CLAIMS The compounds of the invention are those of formula IC IF IG IH or a pharmaceutically acceptable salt thereof wherein: n is an integer of from 0 to 2; m is an integer of from 0 to 3; R is sulfonamide, amide, phosphonic acid, heterocycle, sulfonic acid, or hydroxamic acid; R\ to R 14 are each independently selected from hydrogen or straight or branched alkyl of from 1 to 6 carbons, unsubstituted or substituted benzyl or phenyl which substituents are selected from halogen, alkyl, alkoxy, hydroxy, carboxy, carboalkoxy, trifluoromethyl, and nitro; A' is a bridged ring selected from (1) (2) (3) ( ) (5) wherein f is the point of attachment; Z\ to ZA are each independently selected from hydrogen and methyl; o is an integer of from 1 to 4; and p is an integer of from 0 to 2 with the proviso that in formula 1 R is not -SO3H when m is 2 and n is 1. A compound according to Claim 1 wherein the formula is 1, m is 2, and 3. A compound according to Claim 1 wherein R is a sulfonamide selected from -NHSO 2 R15 0 r -SO 2 NHRl5 wherein Rl5 is straight or branched alkyl or trifluoromethyl. 4. A compound according to Claim 1 named N-[2-(l-aminomethyl- cyclohexyl)-ethyl]-methanesulfonamide. 5. A compound according to Claim 1 wherein R is a phosphonic acid, -PO 3 H 2 . 6. A compound according to Claim 1 and selected from (1-aminomethyl- cyclohexylmethyl)-phosphonic acid and (2-aminomethyl-4-methyl- pentyl)-phosphonic acid. 7. A compound according to Claim 1 wherein R is a heterocycle selected from 8. A compound according to Claim 1 and selected from C-[l-(lH-tetrazol-5- ylmethyl)cyclohexyl]-methylamine, and 4-methyl-2-(lH-tetrazol- 5-ylmethyl)-pentylamine. 9. A compound according to Claim 1 and selected from: ( 1 -Aminomethyl-cyclohexylmethyl)-phosphonic acid; ( 1 R-trans)( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)- phosphonic acid; (trans)( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentylmethyl)- phosphonic acid; ( 1 R-trans)( 1 - Aminomethyl-3-methyl-cyclopentylmethyl)- phosphonic acid; ( 1 S-cis)( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-phosphonic acid; (1 S-trans)( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)- phosphonic acid; ( 1 R-cis)( 1 - Aminomethyl-3-methyl-cyclopentylmethyl)-phosphonic acid; ( 1 ,3 ,4α)( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- phosphonic acid; (l ,3β,4β)(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- phosphonic acid; (R)(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-phosphonic acid; (S)(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-phosphonic acid; ( 1 - Aminomethyl-3 ,3 -dimethyl-cyclobutylmethyl)-phosphonic acid; 2-( 1 -Aminomethyl-cyclohexyl)-N-hydroxy-acetamide; ( 1 S-trans)2-( 1 -Aminomethyl-3-methyl-cyclohexyl)-N-hydroxy- acetamide; (trans)2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-N-hydroxy- acetamide; ( 1 S-cis)2-( 1 -Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy- acetamide; ( lR-trans)2-( l-Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy- acetamide; ( 1 R-cis)2-( 1 - Aminomethyl-3 -methyl-cyclopentyl)-N-hydroxy- acetamide; ( 1 S-trans)2-( 1 -Aminomethyl-3-methyl-cyclopentyl)-N-hydroxy- acetamide; ( 1 α,3α,4α)2-( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)-N- hydroxy-acetamide; ( 1 α,3 β,4β)2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-N- hydroxy-acetamide; (S)2-( 1 -Aminomethyl-3,3-dimethyl-cyclopentyl)-N-hydroxy- acetamide; (R)2-( 1 -Aminomethyl-3,3-dimethyl-cyclopentyl)-N-hydroxy- acetamide; 2-( 1 -Aminomethyl-3,3-dimethyl-cyclobutyl)-N-hydroxy- acetamide; N-[2-( 1 -Aminomethyl-cyclohexyl)-ethyl] -methanesulfonamide; (lS-cis)N-[2-(l-Aminomethyl-3-methyl-cyclohexyl)-ethyl]- methanesulfonamide ; (trans)N- [2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)-ethyl] - methanesulfonamide; ( 1 S-cis)N- [2-( 1 - Aminomethyl-3-methyl-cyclopentyl)-ethyl]- methanesulfonamide; ( 1 R-trans)N- [2-( 1 - Aminomethyl-3-methyl-cyclopentyl)-ethyl] - methanesulfonamide ; ( lR-cis)N-[2-( 1 -Aminomethyl-3-methyl-cyclopentyl)-ethyl]- methanesulf onamide; ( 1 S-cis)N-[2-( 1 - Aminomethyl-3-methyl-cyclopentyl)-ethyl]- methanesulfonamide ; ( lα,3α,4α)N-[2-( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)- ethylj-methanesulfonamide; ( 1 α,3 β,4β)N- [2-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentyl)- ethyl]-methanesulfonamide; (S)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]- methanesulf onamide; (R)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]- methanesulf onamide ; N-[2-(l-Aminomethyl-3,3-dimethyl-cyclobutyl)-ethyl]- methanesulfonamide; 3-( l-Aminomethyl-cyclohexylmethyl)-4H-[ 1 ,2,4]oxadiazol-5-one; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; (trans)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; ( 1 S-cis)3-( 1 - Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; (lR-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; ( lR-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; ( 1 S-trans)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; (lα,3α,4α)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- 4H-[ 1 ,2,4]oxadiazol-5-one; (1 ,3β,4β)3-( 1 - Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- 4H-[ 1 ,2,4]oxadiazol-5-one; (S)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazol-5-one; (R)3-( 1 -Aminomethyl-3 ,3-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazol-5-one; 3-(l-Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-4H- [l,2,4]oxadiazol-5-one; 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]oxadiazole-5- thione; (1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (trans)3-( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; ( lR-trans)3-( l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; (lR-cis)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; (lS-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; (lα,3α,4α)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- 4H-[l,2,4]oxadiazole-5-thione; (lα,3β,4β)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- 4H-[l,2,4]oxadiazole-5-thione; (S)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [l,2,4]oxadiazole-5-thione; (R)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; 3-(l-Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; C-[ 1 -( lH-Tetrazol-5-ylmethyl)-cyclohexyl]-methylamine; (lS-cis)C-[3-Methyl-l-(lH-tetrazol-5-ylmethyl)-cyclohexyl]- methylamine; (trans)C-[3,4-Dimethyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; ( 1 S-cis)C-[3-Methyl- 1 -( lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; ( 1 R-trans)C- [3-Methyl- 1 -( 1 H-tetrazol-5-ylmethyl)-cyclopentyl] - methylamine; (lR-cis)C-[3-Methyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; (lS-trans)C-[3-Methyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; ( 1 α,3α,4α)C-[3,4-Dimethyl- 1 -(lH-tetrazol-5-ylmethyl)- cyclopentyl] -methylamine ; (lα,3β,4β)C-[3,4-Dimethyl-l-(lH-tetrazol-5-ylmethyl)- cyclopentylj-methylamine; (S)C-[3,3-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; (R)C-[3,3-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclopentyl]- methylamine; C-[3,3-Dimethyl-l-(lH-tetrazol-5-ylmethyl)-cyclobutyl]- methylamine; N-[2-(l-Aminomethyl-cyclohexy])-ethyl]-C,C,C-trifluoro- methanesulfonamide; (lS-cis)N-[2-(l-Aminomethyl-3-methyl-cyclohexyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (trans)N-[2-(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-ethyl]- C,C,C-trifluoro-methanesulfonamide; ( 1 R-cis)N-[2-( 1 -Aminomethyl-3-methyl-cyclopentyl)-ethyl] - C,C,C-trifluoro-methanesulfonamide; (1 S-trans)N-[2-( 1 -Aminomethyl-3-methyl-cyclopentyl)-ethyl]- C,C,C-trifluoro-methanesulfonamide; (lS-cis)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]- C,C,C-trifluoro-methanesulfonamide; (lR-trans)N-[2-(l-Aminomethyl-3-methyl-cyclopentyl)-ethyl]- C,C,C-trifluoro-methanesulfonamide; ( l ,3α,4α)N-[2-( l-Aminomethyl-3,4-dimethyl-cyclopentyl)- ethyl]-C,C,C-trifluoro-methanesulfonamide; ( 1 α,3β,4β)N-[2-( l-Aminomethyl-3,4-dimethyl-cyclopentyl)- ethyl]-C,C,C-trifluoro-methanesulfonamide; (S)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; (R)N-[2-(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; N-[2-(l-Aminomethyl-3,3-dimethyl-cyclobutyl)-ethyl]-C,C,C- trifluoro-methanesulfonamide; 3-(l-Aminomethyl-cyclohexylmethyl)-4H-[l,2,4]thiadiazol-5-one; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclohexylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (trans)3-( 1 - Aminomethyl-3 ,4-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (1 R-cis)3-( 1 - Aminomethyl-3 -methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; ( 1 S-trans)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; ( 1 S-cis)3-( 1 -Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [l,2,4]thiadiazol-5-one; (lR-trans)3-(l-Aminomethyl-3-methyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; ( 1 α,3α,4α)3-( 1 -Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- 4H-[ 1 ,2,4]thiadiazol-5-one; (lα,3β,4β)3-(l-Aminomethyl-3,4-dimethyl-cyclopentylmethyl)- 4H-[ 1 ,2,4]thiadiazol-5-one; (S)3-(l-Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; (R)3-( 1 -Aminomethyl-3,3-dimethyl-cyclopentylmethyl)-4H- [l,2,4]thiadiazol-5-one; 3-( 1 -Aminomethyl-3,3-dimethyl-cyclobutylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; C-[l-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- cyclohexylj-methylamine; ( 1 S-cis)C-[3-Methyl- 1 -(2-oxo-2,3-dihydro-2λ 4 - [ 1 ,2,3,5]oxathiadiazol-4-ylmethyl)-cyclohexyl]-methylamine; (trans)C-[3,4-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; ( 1 S-cis)C-[3-Methyl- 1 -(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (lR-trans)C-[3-Methyl-l-(2-oxo-2,3-dihydro-2λ 4 - [ 1 ,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; ( lR-cis)C-[3-Methyl- 1 -(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (lS-trans)C-[3-Methyl-l-(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; ( 1 α,3 ,4α)C-[3 ,4-Dimethyl- 1 -(2-oxo-2,3-dihydro-2λ 4 - [ 1 ,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (l ,3β,4β)C-[3,4-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (S)C-[3,3-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; (R)C-[3,3-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 - [l,2,3,5]oxathiadiazol-4-ylmethyl)-cyclopentyl]-methylamine; C-[3,3-Dimethyl-l-(2-oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol- 4-ylmethyl)-cyclobutyl]-methylamine; (l-Aminomethyl-cyclohexyl)-methanesulfonamide; ( 1 R-trans)( 1 -Aminomethyl-3-methyl-cyclohexyl)- methanesulf onamide; (trans)( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)- methanesulfonamide; (1 S-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)- methanesulf onamide ; (lR-cis)(l-Aminomethyl-3-methyl-cyclopentyl)- methanesulfonamide; (lR-trans)(l-Aminomethyl-3-methyl-cyclopentyl)- methanesulfonamide; ( 1 S-cis)( 1 -Aminomethyl-3-methyl-cyclopentyl)- methanesulf onamide ; (lα,3β,4β)(l-Aminomethyl-3,4-dimethyl-cyclopentyl)- methanesulf onamide ; ( 1 α,3α,4α)( 1 -Aminomethyl-3 ,4-dimethyl-cyclopentyl)- methanesulf onamide; (R)( 1 -Aminomethyl-3 ,3-dimethyl-cyclopentyl)- methanesulfonamide ; (S)( 1 -Aminomethyl-3,3-dimethyl-cyclopentyl)- methanesulfonamide; (1 -Aminomethyl-3,3-dimethyl-cyclobutyl)-methanesulfonamide; ( 1 -Aminomethyl-cyclohexyl)-methanesulfonic acid; ( 1 R-trans) ( 1 - Aminomethyl-3 -methyl-cyclohexyl)-methanesulfonic acid; (trans)(l-Aminomethyl-3,4-dimethyl-cyclopentyl)-methanesulfonic acid; ( 1 S-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; ( 1 S-cis)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; (1 R-trans)( 1 -Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; ( 1 R-cis)( 1 - Aminomethyl-3-methyl-cyclopentyl)-methanesulfonic acid; ( 1 α,3β,4β)( 1 -Aminomethyl-3,4-dimethyl-cyclopentyl)- methanesulfonic acid; (lα,3α,4α)(l-Aminomethyl-3,4-dimethyl-cyclopentyl)- methanesulfonic acid; (R)(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-methanesulfonic acid; (S)(l-Aminomethyl-3,3-dimethyl-cyclopentyl)-methanesulfonic acid; ( 1 -Aminomethyl-3,3-dimethyl-cyclobutyl)-methanesulfonic acid; ( 1 -Aminomethyl-cyclopentylmethyl)-phosphonic acid; 2-(l-Aminomethyl-cyclopentyl)-N-hydroxy-acetamide; N-[2-(l-Aminomethyl-cyclopentyl)-ethyl]-methanesulfonamide; 3-(l-Aminomethyl-cyclopentylmethyl)-4H-[l,2,4]oxadiazol-5-one; 3-(l-Aminomethyl-cyclopentylmethyl)-4H-[l,2,4]oxadiazole-5- thione; C-[ 1 -( lH-Tetrazol-5-ylmethyl)-cyclopentyl]-methylamine; N-[2-(l-Aminomethyl-cyclopentyl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; 3-(l-Aminomethyl-cyclopentylmethyl)-4H-[l,2,4]thiadiazol-5-one; C-[l-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- cyclopentyl]-methylamine; ( 1 -Aminomethyl-cyclopentyl)-methanesulfonamide; (l-Aminomethyl-cyclopentyl)-methanesulfonic acid; (9-Aminomethyl-bicyclo[3.3. l]non-9-ylmethyl)-phosphonic acid; 2-(9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-N-hydroxy-acetamide; N-[2-(9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-ethyl]- methanesulf onamide ; 3-(9-Aminomethyl-bicyclo[3.3. l]non-9-ylmethyl)-4H- [l,2,4]oxadiazol-5-one; 3-(9-Aminomethyl-bicyclo[3.3.1]non-9-ylmethyl)-4H- [ 1 ,2,4]oxadiazole-5-thione; C-[9-(lH-Tetrazol-5-ylmethyl)-bicyclo[3.3.1]non-9-yl]- methylamine; N-[2-(9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-ethyl]-C,C,C- trifluoro-methanesulf onamide ; 3-(9-Aminomethyl-bicyclo[3.3.1 ]non-9-ylmethyl)-4H- [ 1 ,2,4]thiadiazol-5-one; C-[9-(2-Oxo-2,3-dihydro-2λ 4 -[ 1 ,2,3,5]oxathiadiazol-4-ylmethyl)- bicyclo[3.3.1]non-9-yl]-methylamine; (9-Aminomethyl-bicyclo[3.3.1]non-9-yl)-methanesulfonamide; (9-Aminomethyl-bicyclo[3.3. l]non-9-yl)-methanesulfonic acid; (2-Aminomethyl-adamantan-2-ylmethyl)-phosphonic acid; 2-(2-Aminomethyl-adamantan-2-yl)-N-hydroxy-acetamide; N-[2-(2-Aminomethyl-adamantan-2-yl)-ethyl]- methanesulf onamide ; 3-(2-Aminomethyl-adamantan-2-ylmethyl)-4H-[ 1 ,2,4]oxadiazol-5- one; 3-(2-Aminomethyl-adamantan-2-ylmethyl)-4H-[l,2,4]oxadiazole- 5-thione; C- [2-( 1 H-Tetrazol-5-ylmethyl)-adamantan-2-yl] -methylamine ; N-[2-(2-Aminomethyl-adamantan-2-yl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; 3-(2-Aminomethyl-adamantan-2-ylmethyl)-4H-[l,2,4]thiadiazol-5- one; C-[2-(2-Oxo-2,3-dihydro-2λ 4 -[l,2,3,5]oxathiadiazol-4-ylmethyl)- adamantan-2-yl] -methylamine ; (2-Aminomethyl-adamantan-2-yl)-methanesulfonamide; (2-Aminomethyl-adamantan-2-yl)-methanesulfonic acid ( 1 -Aminomethyl-cycloheptylmethyl)-phosphonic acid; 2-( 1 - Aminomethyl-cycloheptyl)-N-hydroxy-acetamide ; N-[2-( 1 -Aminomethyl-cycloheptyl)-ethyl]-methanesulfonamide; 3-( l-Aminomethyl-cycloheptylmethyl)-4H-[ 1 ,2,4]oxadiazol-5-one; 3-( 1 - Aminomethyl-cycloheptylmethyl)-4H-[ 1 ,2,4]oxadiazole-5- thione; C-[ 1 -( lH-Tetrazol-5-ylmethyl)-cycloheptyl]-methylamine; N-[2-(l-Aminomethyl-cycloheptyl)-ethyl]-C,C,C-trifluoro- methanesulfonamide; C-[l-(2-Oxo-2,3-dihydro-2 14-[l,2,3,5]oxathiadiazol-4-ylmethyl)- cycloheptyl] -methylamine ; (l-Aminomethyl-cycloheptyl)-methanesulfonamide; and ( l-Aminomethyl-cycloheptyl)-methanesulfonic acid. 10. A pharmaceutical composition comprising a therapeutically effective amount of a compound according to Claim 1 and a pharmaceutically acceptable carrier. 11. A method for treating epilepsy comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 12. A method for treating faintness attacks, hypokinesia, and cranial disorders comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 13. A method for treating neurodegenerative disorders comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 14. A method for treating depression comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 15. A method for treating anxiety comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 16. A method for treating panic comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 17. A method for treating pain comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 18. A method for treating neuropathological disorders comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 19. A method for treating gastrointestinal damage comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 20. A method for treating inflammation comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment. 21. A method for treating irritable bowel syndrome comprising administering a therapeutically effective amount of a compound according to Claim 1 to a mammal in need of said treatment.

Inventors: BRYANS JUSTIN STEPHEN, CAPIRIS THOMAS, HORWELL DAVID CHRISTOPHER, KNEEN CLARE OCTAVIA, WUSTROW DAVID JUERGEN, BRYANS, JUSTIN, STEPHEN, CAPIRIS, THOMAS, HORWELL, DAVID, CHRISTOPHER, KNEEN, CLARE, OCTAVIA, WUSTROW, DAVID, JUERGEN
Applicants: BRYANS JUSTIN STEPHEN, CAPIRIS THOMAS, HORWELL DAVID CHRISTOPHER, KNEEN CLARE OCTAVIA, WARNER LAMBERT CO, WUSTROW DAVID JUERGEN, BRYANS, JUSTIN, STEPHEN, CAPIRIS, THOMAS, HORWELL, DAVID, CHRISTOPHER, KNEEN, CLARE, OCTAVIA, WARNER-LAMBERT COMPANY, WUSTROW, DAVID, JUERGEN
Application year: 1998
Main classification: C07D257
IPC codes: A61K31, A61P1, A61P25, A61P29, C07C233, C07C239, C07C259, C07C309, C07C311, C07D257, C07D271, C07D285, C07D291, C07F9