FORM 2 THE PATENTS ACT 1970 (Act 39 of 1970) COMPLETE SPECIFICATION (SECTION 10) NOVEL DIPEPTIDYL PEPTIDASE IV INHIBITORS, PHARMACEUTICAL COMPOSITIONS CONTAINING THEM, AND PROCESS FOR THEIR PREPARATION Glenmark Pharmaceuticals S.A., Chemin de la Combeta 5, 2300 La Chaux-de-Fonds, Switzerland THE FOLLOWING SPECIFICATION DESCRIBES THE NATURE OF THE INVENTION; AND THE MANNER IN WHICH IT IS PERFORMED Field of the Invention The present invention relates to dipeptidyl peptidase Iv (DPP-IV) inhibitors, pharmaceutical compositieos containing them. methods of preparing them, and methods for treating a condition that is regulated or normalized via inhibition of DPP-IV (such as Type II diabetes). Background of the Invention Diabetes generally refers to a disease process derived from multiply causative factors, and characterized by elevated levels of plasma glucose or hyperglycemia in the fasting state or after administration of glucose during an oral glucose tolerance test. Persistent or uncontrolled hyperglycemia is associated with increased and premature morbidity and mortality. Often abnormal glucose homeostasis is associated both directly and indirectly with alterations of the lipid, lipoprotein and apolipoprotein metabolism and other metabolic and hemodynamic disease. Patients with Type 2 diabetes mellitus have an increased risk of macrovasuclar and microvascular complications, including coronary heart disease, stroke, peripheral vascular disease, hypertension, nephropathy, neuropathy, and retinopathy. Therefore, therapeutic control of glucose homeostasis, lipid metabolism and hypertension are important in the clinical management and treatment of diabetes mellitus. There are two generally recognized forms of diabetes. Type I and II. In Type I diabetes (also known as insulin-dependent diabetes mellitus (IDDM)) patients produce little or no insulin, the hormone which reuiates glucose utilization. In Type II diabetes (also known as non-insulin dependent diabetes mellitus.(NIDDM')) patients often have plasma insulin levels that. are the. sarne or even elevated compared to nondiabetic lubjects; however, these patients have developed a resistance to the in,sulin stjmylaing ;ftect on glucose and lipid metabolism in the main insulin-sensitive tissues, which are muscle, liver and adipose tissues, and the plasma insulin levels, while elevated, are insufficient to overcome the pronounced insulin resistance. Insulin resistance is not primarily due to a diminished number of insulin receptors but to a post-insulin receptor binding defect that is not yet understood. This resistance to insulin responsiveness results in insufficient insulin activation of plucose uptake, oxidation and storage in muscle and inadequate insulin repression of lipolysis in adipose tissue and of glucose production and secretion in the liver. The available treatments for Type II diabetes, which have not changed substantially in many years, have recognized limitations. While physical exercise and reductions in dietary intake of calories will dramatically improve the diabetic condition, compliance with this treatment is very poor because of well-entrenched sedentary lifestyles and excess rood consumption, especially ot toods containing high amounts of satmaied fat. Increasing the plasma level of insulin bv administration of sulfonylureas (e.g. tolbutamide and glipizide) or meglitinide, which stimulate the Dancreatic B-cells to secrete nore insulin, and/or by injection of insulin when sulphonylureas or meglitinide become ineffective, can result in insulin concentrations high enough to stimulate insulin-resistance tissues. However dangerously low levels of plasma glucose can result from administration of insulin or insulin secretagogues (sulfonylureas or meglitinide), and an increased level of insulin resistance due to the even higher plasma insulin levels can occur. Biguanides can increase insulin sensitivitv resulting in some correction of hyperglycemia. However, two biguanides, phenformin and metformin, can induce lactic acidosis and nausea/diarrhea. Metformin has fewer side effects than phenformin and is often prescribed for the treatment of Type II diabetes. Glitazones (i.e., 5 benzywihriazolldlme-'2;4-diones) are a more recently described class of compounds with potential for ameliorating many symptoms of Type II diabetes. These agents substantially increase insulin sensitivity in muscle, liver and adipose tissue in several animal models of Type II diabetes resulting in partial or complete correction of the elevated plasma levels of glucose without occurrence of hypoglycemia. The glitazones that are currently marketed are agonists of the peroxisome proliferator activated receptor (PPAR), primarily the PPAR-gamma subtype. PPAR-gamma agonism is generally believed to be responsible for the improved insulin sensitization that is observed with the glitazones. Newer PPAR agonists that are being tested for treatment of Type II diabetes are agonists of the alpha, gamma or delta subtype, or a combination of these, and in many cases are chemically different from glitazones (i.e., they are not thiazolidinediones). Serious side effects (e.g. liver toxicity) have occurred with some PPAR agonists, such as troglitazone. Other treatments are under investigation, including treatment with alpha-glucosidase inhibitors (e.g., acrabose) and protein tyrosine phosphatase-IB (PTP-1B) inhibitors. Compounds that are inhibitors of the dipeptidyl peptidase-IV ("DP-IV" or "DPP-IV") enzyme are also under investigation as drugs that mayj>e useful in the treatment of diabetes, and particularly Type 11 diabetes. See, for example, WO 97/40832, WO 98/19998, U.S. Patent No. 5,939,560, Bioorg. Med. Chem. Lett. 6(10): 1163-1166 (1996), and Bioorg. Med.Chem. Lett. 6(22):2745-2748 (1996). The usefulness of DPP-IV inhibitors in the treatment of Type II diabetes is based on the fact that DPP-IV in vivo readily inactivates glucagon like peptide-1 (GLP-1) and gastric inhibitory peptide (GIP). GLP-1 and GIP are incretins and are produced when food is consumed. The incretins stimulate production of insulin. Inhibition of DPP-IV leads to decreased inactivation of the incretins, and this in turn results in increased effectiveness of the incretins in stimulating production of insulin by the pancreas. DPP-IV inhibition therefore results in an increased level of serum insulin. Advantageously, since the incretins are produced by the body only when food is consumed, DPP-IV inhibition is not expected to increase the level of insulin at inappropriate times, such as between meals, which can lead to excessively, low blood sugar (hypoglycemia). Inhibition of DPP-IV is therefore expected to increase insulin without increasing the risk of hypoglycemia, which is a dangerous side effect associated with the use of insulin secretagogues. Improved DPP-IV inhibitors are needed for better treatment of diabetes. Shown below are DPP-IV inhibitors which have reached advanced stages of human clinical trials: Formulas A, B, and C are Novartis NVP-DPP-728, Probiodrug P32/98, and Novartis NVP-LAF-237, respectively. Other anti-diabetic agents are described in WO '2003/084940, JMC (2003) 46(13):2774-2-789, WO 03/03/32/, EP 1354882 Al, U.S. -Patent No.6,011,155, WO 00/34241, and U.S. Patent No. 6,166,063. Japanese Patent Application Publication No. JP 2004-26820, International Patent Publication No. WO2002/0384541, and U.S. Patent Publication No. 2004/0072892 disclose cyanopyrrolidine derivatives having DPP-IV inhibition activity. According to US 2004/0072892, these compounds have the formula: R1 wherein: R1 is a halogen atom, a hydroxyl group, an alkoxy group having 1 to 5 carbon atoms or an alkyl group having 1 to 5 carbon atoms; R2 is a hydrogen atom, a halogen atom, a hydroxyl group, an alkoxy group having 1 to 5 carbon atoms or an alkyl group having 1 to 5 carbon atoms, or R1 and R2 together form an oxo, a hydroxyimino group, an alkoxyimino group having 1 to 5 carbon atoms or an alkylidene group having 1 to 5 carbon atoms; R3 and R4 are each a hydrogen atom, a halogen atom, a hydroxyl group, an alkoxy group having 1 to 5 carbon atoms or an alkyl group having 1 to 5 carbon atoms, or R3 and R4 together form an oxo, a hydroxyimino group, an alkoxyimino group having 1 to 5 carbon atoms or an alkylidene group having 1 to 5 carbon atoms; X is an oxygen atom or a sulfur atom; Y is -C5R6- (wherein R5 and R6 are the same or different, and are each a hydrogen atom, a halogen atom, an optionally substituted alkyl group having 1 to 10 carbon atoms or an optionally substituted alkenyl group having 2 to 10 carbon atoms), or -CR7R8-CR9R'°- (wherein R7, R8, R9 and R10 are the same or different, and each a hydrogen atom, a halogen atom or an optionally substituted alkyl group having 1 to 10 carbon atoms, or R7 and R9 together with the carbon atom to which they are attached form an optionally substituted cycloalkyl group having 3 to 8 carbon atoms, an optionally substituted cycloalkenyl group having 4 to 8 carbon atoms, an optionally substituted bicycloalkyl group having 5 to 10 carbon atoms, or an optionally substituted bicycloalkenyl group having 5 to 10 carbon atoms) and Z is a hydrogen atom or an optionally substituted alkyl group having 1 to 10 carbon atoms, or Y and Z together with the nitrogen atom to which they are attached form an optionally substituted cyclic amino group having 2 to 10 carbon atoms, or a pharmaceutically acceptable salt thereof. U.S. Patent Application Publication Nos. 2004/0121964 and 2004/0259843 X is CH2, CHF, or CF2, R is alkylcarbonyl, alkylcarbonyl, cyano, heterocyclecarbonyl, R4RsNC(0)-, B(OR6)2, (l,2,3)-dioxoborolane or 4,4,5,5-tetramethyl-(l,2,3)-dioxoborolane, Ri is alkoxyalkyl, alkyl, alkylcarbonyl, alkenyl, alkynyl, allenyl, arylalkyl, cycloalkyl, cycloalkylalkyl, cyano, haloalkyl, haloalkenyl, heterocyclealkyl, or hydroxyalkyl, R2 and R3 are independently hydrogen, alkoxyalkyl, alkyl, alkenyl, alkynyl, cycloalkyl, cycloalkylalkyl, aryl, arylalkyl, heterocycle, heterocyclealkyl, or hydoxyalkyl; or R2 and R3 taken together with the atoms to which they are attached form a particular mono or bicyclic heterocycle, and R4 and R5 are independently hydrogen, alkyl, or arylalkyl. According to the applications, these compounds inhibit DPP-IV and are useful for the prevention or treatment of diabetes (especially type II diabetes), hyperglycemia, Syndrome X, hyperinsulinemia, obesity, atherosclerosis, and various immunomodulatory diseases. International Publication No. WO 2005/023762 discloses compounds of the formula where A is a particular monocyclic or bicyclic aryl or heteroaryl group. According to the application, these compounds inhibit DPP-IV and are useful for the prevention or treatment of diabetes, hyperglycemia, syndrome X, hyperinsulinemia, obesity, satiety disorders, atherosclerosis, and various immunomodulatory diseases. Summary of the Invention The present invention relates to novel compounds useful as dipeptidyl peptidase IV (DPP-IV) inhibitors of the formula: wherein: Y is -S(0)m, -CH2-, CHF, or -CF2; m is 0, l,or2; X is a bond, C1-C5 alkyl (e.g., -CH2-), or -C(=0)-; the dotted line [—] in the carbocyclic ring represents an optional double bond; R1 is substituted or unsubstituted cycloalkyl, substituted or unsubstituted cycloalkylalkyl, substituted or unsubstituted cycloalkenyl, substituted or unsubstituted aryl, substituted or unsubstituted arylalkyl, substituted or unsubstituted heteroaryl, substituted or unsubstituted heterocyclic ring, substituted or unsubstituted heterocyclylalkyl, substituted or unsubstituted heteroarylalkyl, CN, -COOR3, CONR3R4, -OR3,-NR3R4,or NR3COR4; R2 is hydrogen, cyano, COOH, or an isostere of a carboxylic acid (such as SO3H, CONOH, B(OH)2, P03R3R,S02NR3R4, tetrazole, -COOR3, -C0NR3R4, -NR3COR4, or -COOCOR3); and R3 and R4 may be the same or different and are independently hydrogen, nitro, hydroxy, cyano, formyl, acetyl, halogen, substituted or unsubstituted amino, substituted or unsubstituted alkyl, substituted or unsubstituted alkoxy, substituted or unsubstituted alkenyl, substituted or unsubstituted alkynyl, substituted or unsubstituted cycloalkyl, substituted or unsubstituted cycloalkylalkyl, substituted or unsubstituted cycloalkenyl, substituted or unsubstituted aryl, substituted or unsubstituted arylalkyl, substituted or unsubstituted heteroaryl, substituted or unsubstituted heterocyclic ring, substituted or unsubstituted heterocyclylalkyl, substituted or unsubstituted heteroarylalkyl or a substituted or unsubstituted carboxylic acid derivative and/analogs/prodrugs,/tautomeric forms, regioisomers, stereoisomers, enantiomers, diastereomers, polymorphic solvates, N-oxides, and pharmaceutically acceptable salts thereof. According to one embodiment, -X-R1 is not -(CH2)dR5-Z-R6, wherein R5 and Z are independently -C(O)-, -NR7, -0-, or -S(0)m-, R6 is substituted or unsubstituted alkyl, substituted or unsubstituted alkenyl, substituted or unsubstituted alkynyl, substituted or unsubstituted cycloalkyl, substituted or unsubstituted cycloalkylalkyl, substituted or unsubstituted cycloalkenyl, substituted or unsubstituted aryl, substituted or unsubstituted arylalkyl, substituted or unsubstituted heteroaryl, substituted or unsubstituted heterocyclic ring, substituted or unsubstituted heterocyclylalkyl, or substituted or unsubstituted heteroarylalkyl, R7 is hydrogen, hydroxy, acetyl, substituted or unsubstituted alkyl, or substituted or unsubstituted alkoxy, m isO, l,or2, and d isO, 1, or 2. According to another embodiment, -X-R1 is not or Preferred is where X is a bond. Further preferred is where X is -CH2-. Further preferred is where X is -CH2-CH2-. Further preferred is where X is -C(=0)-. Further preferred is where Y is CH2 Further preferred is where Y is CHF. Further preferred is where R1 is chosen from cyano, substituted or unsubstituted aryl, substituted or unsubstituted heteroaryl, substituted or unsubstituted heterocyclic ring, -NR3COR4, or -NR3R4, wherein R3 and R4 may be the same or different and are independently selected from hydrogen, substituted or unsubstituted alkoxy, substituted or unsubstituted amino, substituted or unsubstituted cycloalkyl, substituted or unsubstituted aryl or substituted or unsubstituted arylalkyl. For instance, R3 and R4 may be the same or different and independently selected from hydrogen, substituted or unsubstituted alkoxy, or substituted or unsubstituted amino. Further preferred is when R1 represents -NR3R4, wherein R3 and R4 may be the same or different and are independently selected from hydrogen or the group Further preferred is when R1 represents -NR3COR4 wherein R3 and R4 may be the same or different and are independently selected from hydrogen or substituted or unsubstituted amino selected from Further preferred is where R is chosen from contd. Further preferred is where R1 is a cyano group. Further preferred is where R1 is a phenyl group. Further preferred is where R1 is a 2-methoxy-phenyl group. Further preferred is where R1 is a 3-cyano-indol-lyl group. Further preferred is where R1 is a 1,2,3,4 tetrahydro-isoquinolin-2-yl group. Further preferred is where R1 is a N-4 substituted piperazin-1-yl group. Further preferred is where the N-4 substituent in the N-4 substituted piperazin-1- is methyl. Further preferred is where the N-4 substituent in the N-4 substituted piperazin-l-yl is phenyl. Further preferred is where R is hydrogen. Further preferred is where R4 is hydrogen. Further preferred is where R4 is aniline. Further preferred is where R4 is 2,4-difluro-aniline. Further preferred is where R2 is hydrogen. Further preferred is where R2 is a cyano (-CN) group. Further preferred is where the dotted line [—] in the carbocyclic ring represents a bond Further preferred is where the carbocyclic ring of formula (I) does not contain any double bonds. The cyclopentane or cyclopentene ring in formula (I) bearing substituents at its 1 and 3 positions can fall into a cis or trans geometry. Because the carbon atoms at the 1 and 3 positions are chiral, there can be up to 2 pairs of enantiomers. Therefore, the compounds of the present invention may be prepared as a single diastereomer or a mixture of diastereomers (for example, a racemic mixture). Such single diastereomers and mixtures of diastereomers are within the scope of this invention. The compounds of the present invention may also include one or more additional asymmetrically substituted carbon atoms. This can give rise to additional stereoisomers and in each case the invention is to be understood to extend to all such stereoisomers, including enantiomers and diastereomers and their mixtures, including racemic mixtures. According to one preferred embodiment, the compound of the present invention has the formula (I-A): where Y is CH2 or CHF, and R1 is substituted or unsubstituted aryl, substituted or unsubstituted heteroaryl, substituted or unsubstituted heterocyclic ring. Preferably, R1 is a substituted or unsubstituted nitrogen containing heterocyclic ring or a substituted or unsubstituted nitrogen containing heteroaryl. More preferably, R is attached to the remainder of the compound through a nitrogen atom in the heteroaryl or heterocyclic ring. Non-limiting examples of suitable nitrogen containing heterocyclic rings, nitrogen containing heteroaryl and substituted or unsubstituted aryl groups include: According to one embodiment, Y is CH2. According to another embodiment, Y is CHF. According to a more preferred embodiment, the compound has the formula (I-B): where Y and R are defined as in the preceding paragraph. According to another more preferred embodiment, the compound has the formula (I-C): where Y and R1 are defined as in the preceding paragraph. Representative compounds of the present invention are specified below. The present invention should not be construed to be limited to them. [1] (lSR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl]-2-oxoethylamino cyclopentane-1 -carboxamide [2] (2S)-l-{2-[(3SR,lRS)-3-Cyanocyclopentylamino]acetyl}-2-pyrrolidinecarbonitrile [3] (2S)-l-{2-[(3SR,lRS)-3-Cyanomethylcyclopentylamino]acetyi}-2-pyrroIidine carbonitrile [4] (2S)-l-{2-[(3S,lR)-3-Cyanomethylcyclopentylamino]acetyl}-2-pyrrolidinecarbonitrile [5] (2S)-l-{2-[(3S,lR)-3-Cyanomethylcyclopentylamino]acetyl}-2-pyrrolidinecarbonitrile hydrochloride [6] (2S)-l-{2-[(3R,lS)-3-Cyanomethylcyclopentylamino]acetyl}-2-pyrrolidinecarbonitrile [7] (2S,4S)-l-{2-[(3S,lR)-3-Cyanomethylcyclopentylamino]acetyl}-4-fluoro-2-pyrrolidinecarbonitrile [8] (2S,4S)-l-{2-[(3R,lS)-3-Cyanomethylcyclopentylamino]acetyl}-4-fluoro-2-pyrrolidinecarbonitrile [9]3-((lR,3R)-3-{2-[(2S,4S)-2-Cyano-4-fluoropyrrolidin-l-yl]-2-oxoethylamino}cyclopentyl)propanenitrile [ 10] (2S)-1 -((1 SR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidin-1 -yl]-2-oxoethylamino}cyclopentyl-methyl)pyrrolidine-2-carboxamide [11] (2S)-l-(2-{(3SR,lRS)-3-[2S)-2-Cyanopyrrolidin-l-ylcarbonyl]cyclopentylamino]-acetyl}pyrrolidine-2-carbonitrile [12] Nl-Benzyloxy-(lSR,3RS)-3-{2-[(2S)-2-cyanopyrrolidin-l-yl]-2-oxoethylamino}-cyclopentane-1 -carboxamide [13] Nl-Phenyl-N3-((lS,3R)-3-{2-[(2S)-2-cyanopyrrolidin-l-yl]-2-oxoethy lamino } -eye lopentylmethyl )urea [14] Nl-(2,4-Difluorophenyl)-N3-((lS,3R)-3-{2-[(2S)-2-cyanopyrrolidin-l-yl]-2-oxoethyl-amino}cyclopentylmethyl)urea [15] (2S,4S)-l-{2-[(lR,3R)-3-Benzylcyclopentylamino]acetyl}-4-fluoropyrrolidin-2-yl cyanide [ 16] (2S,4S)-4-Fluoro-1 -{2-[( 1 R,3R)-3-(2-methoxybenzylcyclopentylamino]acetyl}-pyrrolidine-2-carbonitrile [17] (2S)-l-{2-[(3RS,lRS)-3-(3-Thiazolidineylmethyl)cyclopentylamino]acetyl}-pyrrolidine-2-carbonitrile [ 18] (2S)-1 -{2-[(3S, 1 R)-3-( 1,1 -Dioxo-2-isothiazolidinylmethyl)cyclopentylamino] acetyl}pyrrolidine-2-carbonitriie [ 19] (2S)-1 - {2-[(3S, 1 R)-3-Morpholinomethylcyclopentylamino] acetyl}pyrrolidine-2-carbonitrile [20] (2S)-l-{2-[(3SR,lRS)-3-(4-Methylpiperazinomethyl)cyc!opentylamino] acetyl}pyrrolidine-2-carbonitrile [21] (2S)-l-{2-[(3SR,lRS)-3-(4-Cyanopiperidinylmethyl)cyclopentylamino] acetyI}pyrrolidine-2-carbonitrile [22] (2S)-1 -{2-[(3SR, 1 RS)-3-(4-Benzylpiperazinomethyl)cyclopentylamino] acetyl} pyrrol idin-2-carbon itri le [23] (2S)-l-{2-[(lS,3R)-3-(4-Phenylpiperazinomethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitrile [24] (2S)-l-{2-[(3S,lR)-3-(2,5-dimethyl-lH-l-pyrrolylmethyl) cyclopentylamino} acetyl}-pyrrolidine-2-carbonitrile [25] (2S.4S)-1 - {2-[(3 S, 1 R)-3-(2,5-Dimethyl-1H-1 -pyrrolylmethyl) cyclopentylamino]-acetyl}-4-fluoropyrrolidine-2-carbonitrile [26] l-((lS,3R)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl]-2-oxoethylamino} cyclopenty 1 methyl)-1 H-pyrrole-2-carbonitrile [27] (2S,4S)-1 -{2-[(3SR, 1 RS)-3-(2-Cyano-1 H-pyrrol-1 -ylmethyl) cyclopentylamino)-acetyl}-4-fluoropyrrolidine-2-carbonitrile [28] (2S)-1 -{2-[( 1 S,3R)-3-( 1 H-Pyrazol-1 -ylmethyl)cyclopentylamino]acetyl} pyrrolidine-2-carbonitrile [29] (2S)-l-{2-[(3S,lR)-3-(lH-l-Imidazolylmethyl)cyclopentylamino]acetyl} pyrrolidine-2-carbonitrile [30] (2S)-1 -{2-[(3SR, 1 RS)-3-( 1 H-4-Nitro-1 -imidazolylmethyl) cyclopentylamino] acetyl }-pyrrolidine-2-carbonitrile [31 ] (2S)-1 -{2-[(3SR, 1 RS)-3-(2-Buty I-4-chloro-5-hydroxymethyI-1H-1 -imidazolylmethyl)-cyclopentylamino]acetyl}pyrrolidine-2-carbonitrile [32] 2-n-Butyl-4-chloro-l-((lSR,3RS)-3-{2-[(2S)-2-cyanopyrrolidin-l-yl]-2-oxoethyl-amino}cyclopentylmethyl)-lH-5-imidazolecarbonitrile [33] l-((lSR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl]-2-oxoethylamino} cyclopentyl-methyl)-1 H-4,5-imidazoledicarbonitrile [34] l-((lS,3R)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl]-2-oxoethylamino} cyclopentyl-methyl)-! H-4,5-imidazoledicarbonitrile [35] (2S)-l-{2-[(lS,4R)-4-(lH-l,2,4-Triazol-l-ylmethyl)-2-cyclopenty]amino] acetyl}-pyrrolidin-2-carbonitrile [36] (2S)-1 -{2-[(3SR, 1 RS)-3-( 1H-1,2,4-Triazol-l -ylmethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitrile [37] (2S)-l-{2-[(3S,lR)-3-(lH-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitri!e [38] (2S)-l-{2-[(3S,lR)-3-(lH-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl }-pyrrolidine-2-carbonitrile hydrochloride [39] (2S)-1 -{2-[(3S, 1 R)-3-( 1H-1,2,4-Triazol-1 -ylmethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitrilemaleate [40] (2S)-1 -{2-[(3R, 1 S)-3-(l H-1,2,4-Triazol-1 -ylmethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitrile [41 ] (2S,4S)-1 - {2-[(3SR, 1 RS)-3-( 1H-1,2,4-Triazol-1 -ylmethyl) cyclopentylamino]acetyl}-4-fluoropyrrolidine-2-carbonitrile [42] (2S,4S)-1 -{2-[(3 S, 1 R)-3-( 1H-1,2,4-Triazol-1 -ylmethy l)cyclopentylamino] acetyl} -4-fluoropyrrol idine-2-carbonitri le [43] (2S,4S)-l-{2-[(3S,lR)-3-(lH-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile hydrochloride [44] (2S,4S)-1 - {2-[(3S, 1 /R)-3-( 1H-1,2,4-Triazol-1 -ylmethyl) cyclopentylamino] acetyl }-4-fluoropyrrolidine-2-carbonitrile methanesulfonate [45] (25,45)-l-{2-[(3SJl/R)-3-(lH-l,2,4-Triazol-l-ylmethyi)cycIopentyiamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile oxalate [46] (25,4S)-1 -{2-[(3S,1 R)-3-( 1 /H-1,2,4-Triazol-1 -ylmethyl)cyclopentylamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile succinate [47] (25,45)-l-{2-[(35,l/R)-3-(l/H-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl }-4-fluoropyrrolidine-2-carbonitrile2-oxoglutarate [48] (2S,4S)- l-{2-[(3S,lR)-3-(l/H-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl}-4-fluoropyrrolidine-2-carbonitrilebenzoate [49] (25,45)-1 - {2-[(3S,1 R)-3-( 1H-1,2,4-Triazol-1 -ylmethyl)cyclopenty lamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile salicylate [50] (2S,4S)-l-{2-[(3S,lR)-3-(l/H-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile benzenesulfonate [51] (25,45)-l-{2-[(3S,lR)-3-(lH/-l,2,4-Triazol-l-ylmethyl)cyclopentylamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile naphthalene-1,5-disulfonic acid [52] (2S,4S)-1 -{2-[( 1 S,3R)-3-( 1H-1,2,4-Triazol-l -ylmethyl) cyclopentylamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile [53] (2S,4S)-4-Fluoro-l-{2-[(lR,3R)-3-(lH-l,2,4-Triazol-l-ylmethyl)cyclopentylamino]acetyl}pyrrolidin-2-carbonitrile [54] (4S)-3-{2-[(3S, 1 R)-3-(l H-1,2,4-Triazol-1 -yImethyl)cyclopentylamino] acetyl}-!,3-thiazolane-4-carbonitrile [55] 1 -[(3S)-3-Fluoropyrrolidin-1 -yl]-2-[( 1 S,3S)-3-( 1H-1,2,4-Triazol-1 -ylmethyl)cyclopentylamino]-1 -ethanone [56] (2S)-l-{2-[(lS,3R)-3-(2H-l,2,3-Triazol-2-ylmethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitrile [57] (2S,4S)-1 - {2-[( 1 S,3R)-3-( 1H-1,2,3-Triazol-1 -yimethy I)cyclopenty lamino] acetyl}-4-fluoropyrrolidine-2-carbonitrile [5 8] (2S,4S)-1 - {2-[( 1 S,3R)-3-(2H-1,2,3-Triazol-2-ylmethyl)cyclopentylamino]acetyl}-4-fluoropyrrolidine-2-carbonitrile [59] (2S)-l-{2-[(3S,lR)-3-[lH-l,2,3,4-Tetraazol-l -ylmethyl] cyclopentylamino] acetyl}pyrrolidine-2-carbonitrile [60] (2S)-l-{2-[(3S,lR)-3-[lH-l,2,3,4-Tetraazol-l-ylmethyl] cyclopentylamino] acetyl}pyrrolidine-2-carbonitrile maleate [61 ] (25)-1 -{2-[( 1 S,3R)-3- [1H-1,2,3,4-Tetraazol-1 -ylmethyl)cyclopentylamino] acetyl}-pyrrolidine-2-carbonitrile [62] (2S)-l-(2-{(3S,lR)-3-[5-(4-Fluorophenyl)-2H-l,2,3,4-tetrazol-2-ylmethyl] cyclopentylamino}acetyl)pyrrolidine-2-carbonitrile [63] (2S)-l-{2-[(3S,lR)-3-(2,3-Dihydro-lH-l-indolylmethyl) cyclopentylamino] acetyl}-pyrrolidine-2-carbonitriIe [64] l-((lS,3R)-3-{2-[(2S,4S)-2-Cyano-4-Fluoropyrrolidin-l-yl]-2-oxoethylamino}cyclopentylmethyl)-lH-3-indolecarbonitrile [65] (2S)-1 -{2-[(3S, 1 R)-3-(2,3-Dihydro-1 H-2-isoindolylmethyl) cyclopentylamino]acetyl}-pyrrolidine-2-carbonitrile [66] (2S,4S)-4-FIuoro-l-{2-[(3S,lR)-3-(l,2,3,4-tetrahydro-2-isoquinolinylmethyl)cyclopentylamino] acetyl}pyrrolidin-2-carbonitrile [67] (2S)-l-{2-[(lS,3R)-3-(2H-Indazol-2-ylmethyl)cyclopentylamino]acetyl} pyrrolidine-2-carbonitrile [68] (2S)-l-{2-[(lS,3R)-3-(lH-Indazol-l-ylmethyl)cyclopentylamino]acetyl} pyrrolidine-2-carbonitrile [69] (2S)-1 -{2-[(3S, 1 R)-3-( 1 H-Benzo[d]imidazol-1 -ylmethyl) cyclopenylamino] acetyI}pyrrolidine-2-carbonitrile [70] (2S)-l-{2-[(3S,lR)-3-(2H-Benzo[d][l,2,3]triazol-l-ylmethyl) cyclopentylamino] acetyl }pyrrolidine-2-carbonitrile [71] (2S)-l-{2-[(3S,lR)-3-(2H-benzo[d][l,2,3]triazol-2-ylmethyl) cyclopentylamino]acetyl}pyrrolidine-2-carbonitrile [72] l-((lSR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl]-2-oxoethylamino} cyclopentylcarboxamido)adamantine [73] l-((lSR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl)-2-oxoethylamino} cyclopentyl-carboxamido)-2,5-difluorobenzene [74] l-((lSR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidine-l-yl]-2-oxoethylamino} cyclopentyl-carboxamido)-2,4,5-trifluorobenzene [75] l-((lSR,3RS)-3-{2-[(2S)-2-Cyanopyrrolidin-l-yl)-2-oxoethylamino} cyclopentyl-carboxamido)-2-phenylbenzene and pharmaceutically acceptable salts of the foregoing compounds. Yet another embodiment is a pharmaceutical composition comprising one or more compounds of the present invention and one or more pharmaceutically acceptable excipients (e.g., one or more carriers or diluents). The present invention also includes a method of treating a condition that is regulated or normalized via inhibition of DPP-IV in a subject by administering to the subject a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to one embodiment, the present invention provides a method for: (a) treating a metabolic disorder, Type II diabetes, impaired glucose tolerance (IGT), impaired fasting glucose (IFG), food intake disorders, obesity, dyslipidemia, or functional dyspepsia (such as irritable bowel syndrome), (b) lowering blood glucose, (c) preventing or treating hyperglycemia, (d) delaying the progression of impaired glucose tolerance (IGT) to Type II diabetes, (e) delaying the progression of non-insulin requiring Type II diabetes to insulin requiring Type II diabetes, (f) increasing the number and/or the size of beta cells, (g) preventing or treating beta cell degeneration, such as apoptosis of beta cells, or (h) regulating appetite or inducing satiety. The method includes administering to the subject a therapeutically effective amount of the compound or the pharmaceutical composition of the present invention. Another embodiment is a method of treatment and/or prophylaxis of diabetes (such as non-insulin dependent diabetes mellitus (NIDDM)), impaired glucose homeostasis, impaired glucose tolerance (IGT), infertility, polycystic ovary syndrome, growth disorders, frailty, arthritis, allograft rejection in transplantation, autoimmune diseases, AIDS, allergic disorders, intestinal diseases, inflammatory bowel disease (including inflammatory bowel syndrome and chronic inflammatory bowel disease (such as Crohn's disease and ulcerative colitis)), obesity, anorexia nervosa, osteoporosis, hyperglycemia, syndrome X, diabetic complications, hyperinsulinemia, atherosclerosis (or a related disease), immunomodulatory diseases, or metabolic syndrome in a subject by administering to the subject a therapeutically effective amount of the compound or the pharmaceutical composition of the present invention. Yet another embodiment is a method for treating insulin resistant non-impaired glucose tolerance in order to prevent or delay the onset of non-insulin dependent diabetes mellitus (NIDDM) in a subject by administering to the subject a therapeutically effective amount of the compound or the pharmaceutical composition of the present invention. Yet another embodiment is a method of preparing a compound of formula (I) above by coupling a compound of the formula (where R1 and X are as defined above with respect to formula (1)) with a compound of the formula (4) (where L2 is a leaving group and R2 and Y are as defined above with respect to formula (I)) to form a compound of formula (I): Preferably, the coupling reaction is performed in an inert solvent and in the presence of a base. The coupling reaction is preferably performed at a temperature ranging from about -15°C to about 110°C. The coupling reaction is preferably performed for about 1 hour to about 7 days. The compound of formula (3) can be prepared by deprotecting a compound of the formula (where PG is a protecting group). The protected compound can be prepared by coupling a compound of the formula R'-H with a compound of the formula (1) (wherein L is a leaving group). Preferably, this coupling reaction is performed in an inert solvent and in the presence of a base. This coupling reaction is preferably performed at a temperature ranging from about -15°C to about 110°C. The coupling reaction is preferably performed for about 2 hours to about 7 days. Suitable inert solvents for the coupling reactions include, but are not limited to, tetrahydrofuran, dimethylformamide, dichloromethane, and mixtures thereof. Suitable leaving groups L1 and L include, but are not limited to, bromine, chlorine, iodine, O-toluene sulphonyls and O-methyl sulphonyls. Detailed Description of the Invention Definitions The term "aryl" refers to an aromatic radical having in the range of 6 up to 14 carbon atoms such as phenyl, naphthyl, tetrahydronapthyl, indanyl, biphenyl and the like. The term "arylalkyl" refers to an aryl group as defined above directly bonded to an alkyl group, e.g., -CH2C6H5, -C2H5C6H5 and the like. The term "heterocyclic ring" refers to a stable 3- to 15 membered ring radical which consists of carbon atoms and from one to five heteroatoms selected from the group consisting of nitrogen, phosphorus, oxygen and sulfur. For purposes of this invention, the heterocyclic ring radical may be a monocyclic, bicyclic or tricyclic ring system, which may include fused, bridged or spiro ring systems, and the nitrogen, phosphorus, carbon, oxygen or sulfur atoms in the heterocyclic ring radical may be optionally oxidized to various oxidation states. In addition, the nitrogen atom may be optionally quaternized; and the ring radical may be partially or fully saturated (i.e., heteroaromatic or heteroaryl. Examples of such heterocyclic ring radicals include, but are not limited to, azetidinyl, acridinyl, benzodioxolyl, benzodioxanyl, benzofurnyl, carbazolyl, cinnolinyl, dioxolanyl, indolizinyl, naphthyridinyl, perhydroazepinyl, phenazinyl, phenothiazinyl, phenoxazinyl, phthalazinyl, pyridyl, pteridinyl, purinyl, quinazolinyl, quinoxalinyl, quinolinyl, isoquinolinyl, tetrazoyl, imidazolyl, tetrahydroisouinolyl, piperidinyl, piperazinyl, 2-oxopiperazinyl, 2-oxopiperidinyl, 2-oxopyrrolidinyl, 2-oxoazepinyl, azepinyl, pyrrolyl, 4-piperidonyl, pyrrolidinyl, pyrazinyl, pyrimidinyl, pyridazinyl, oxazolyl, oxazolinyl, oxasolidinyl, triazolyl, indanyl, isoxazolyl, isoxasolidinyl, morpholinyl, thiazolyl, thiazolinyl, thiazolidinyl, isothiazolyl, quinuclidinyl, isothiazolidinyl, indolyl, isoindolyl, indolinyl, isoindolinyl, octahydroindolyl, octahydroisoindolyl, quinolyl, isoquinolyl, decahydroisoquinolyl, benzimidazolyl, thiadiazolyl, benzopyranyl, benzothiazolyl, benzooxazolyl, furyl, tetrahydrofurtyl, tetrahydropyranyl, thienyl, benzothienyl, thiamorpholinyl, thiamorpholinyl sulfoxide thiamorpholinyl sulfone, dioxaphospholanyl , oxadiazolyl, chromanyl, isochromanyl and the like. The heterocyclic ring radical may be attached to the main structure at any heteroatom or carbon atom that results in the creation of a stable structure. The term "heteroaryl" refers to an aromatic heterocyclic ring radical. The heteroaryl ring radical may be attached to the main structure at any heteroatom or carbon atom that results in the creation of a stable structure. The term "heteroarylalkyl" refers to a heteroaryl ring radical as defined above directly bonded to an alkyl group. The heteroarylalkyl radical may be attached to the main structure at any carbon atom from the alkyl group that results in the creation of a stable structure. The term "heterocyclyl" refers to a heterocyclic ring radical as defined above. The heterocyclyl ring radical may be attached to the main structure at any heteroatom or carbon atom that results in the creation of a stable structure. The term "heterocyclylalkyl" refers to a heterocyclic ring radical directly bonded to an alkyl group. The heterocyclylalkyl radical may be attached to the main structure at any carbon atom in the alkyl group that results in the creation of a stable structure. The term "alkyl" refers to a straight or branched hydrocarbon chain radical (of carbon and hydrogen atoms only), containing no unsaturation, having from one to eight carbon atoms, and which is attached to the rest of the molecule by a single bond, e.g., methyl, ethyl, n-propyl, 1-methylethyl (isopropyl), n-butyl, n-pentyl, 1, 1-dimethylethyl (t-butyl), and the like. The term "alkenyl" refers to an aliphatic hydrocarbon group containing a carbon-carbon double bond and which may be a straight or branched or branched chain having 2 to about 10 carbon atoms, e.g., ethenyl, 1-propenyl, 2-propenyl (allyl), iso-propenyl, 2-methyl-1-propenyl, 1-butenyl, 2-butenyl and the like. The term "alkynyl" refers to a straight or branched chain hydrocarbyl radical having at least one carbon-carbon triple bond, and having in the range of 2 up to about 12 carbon atoms (with radicals having in the range of 2 up to about 10 carbon atoms being preferred), e.g., ethynyl, propynyl, butnyl and the like. The term "alkoxy" denotes an alkyl group attached via an oxygen linkage to the rest of the molecule. Representative examples of those groups are -OCH3, -OC2H5 and the like. The term "cycloalkyl" denotes a non-aromatic mono or multicyclic ring system of 3 to about 12 carbon atoms. Non-limiting examples of monocyclic cycloalkyl groups include cyclopropyl, cyclobutyl, cyclopentyl, and cyclohexyl. Non-limiting examples of multicyclic cycloalkyl groups include perhydronapththyl, adamantyl and norbornyl groups bridged cyclic group or sprirobicyclic groups, e.g., sprio (4,4) non-2-yl. The term "cycloalkylalkyl" refers to a cyclic ring-containing radical having 3 up to about 8 carbon atoms directly attached to an alkyl group which is then attached to the main structure at any carbon from the alkyl group that results in the creation of a stable structure, such as cyclopropylmethyl, cyclobutylethyl, cyclopentylethyl, and the like. The term "cycloalkenyl" refers to a cyclic ring-containing radical having 3 up to about 8 carbon atoms with at least one carbon- carbon double bond, such as cyclopropenyl, cyclobutenyl, cyclopentenyl and the like. Unless otherwise specified, the term "substituted" as used herein refers to substitution with any one or any combination of the following substituents: hydroxy, halogen, carboxyl, cyano, nitro, oxo (=0), thio (=S), substituted or unsubstituted alkyl, substituted or unsubstituted alkoxy, substituted or unsubstituted alkenyl, substituted or unsubstituted alkynyl, substituted or unsubstituted aryl, substituted or unsubstituted arylalkyl, substituted or unsubstituted cycloalkyl, substituted or unsubstituted cycloalkenyl, substituted or unsubstituted amino, substituted or unsubstituted aryl, substituted or unsubstituted heteroaryl, substituted or unsubstituted heterocyclylalkyl ring, substituted or unsubstituted heteroarylalkyl, substituted or unsubstituted heterocyclic ring, substituted or unsubstiuted guanidine, -COORX, -C(0)Rx, -C(S)Rx, -C(0)NRxRy, -C(0)ONRxRy, -NRxCONRyRz, -N(Rx)SORy, -N(Rx)S02Ry, -(=N-N(Rx)Ry), -NRxC(0)ORy, -NRxRy, -NRxC(0)Ry, -NRxC(S)Ry, -NRxC(S)NRyRz, -SONRxRy, - S02NRxRy, -ORx, -ORxC(0)NRyRz, -ORxC(0)ORy, -OC(0)Rx, -OC(0)NRxRy, -RxNRyC(0)Rz, -Rx ORy, -RxC(0)ORy, -RxC(0)NRyRz, -RxC(0)Ry, -RxOC(0)Ry, -SRX, -SORx, -S02Rx, and -0N02, wherein RX, Ry and Rz are independently selected from hydrogen, substituted or unsubstituted alkyl, substituted or unsubstituted alkoxy, substituted or unsubstituted alkenyl, substituted or unsubstituted alkynyl, substituted or unsubstituted aryl, substituted or unsubstituted arylalkyl, substituted or unsubstituted cycloalkyl, substituted or unsubstituted cycloalkenyl, substituted or unsubstituted amino, substituted or unsubstituted aryl, substituted or unsubstituted heteroaryl, substituted heterocyclylalkyl ring, substituted or unsubstituted heteroarylalkyl, or substituted or unsubstituted heterocyclic ring. According to one embodiment, the substituents in the aforementioned "substituted" groups cannot be further substituted. For example, when the substituent on "substituted alkyl" is "substituted aryl", the substituent on "substituted aryl" cannot be "substituted alkenyl". The term "protecting group" or "PG" refers to a substituent that blocks or protects a particular functionality while permitting other functional groups on the compound to react. For example, an "amino-protecting group" is a substituent attached to an amino group that blocks or protects the amino functionality in the compound. Suitable amino-protecting groups include, but are not limited to, acetyl, trifluoroacetyl, t-butoxycarbonyl (BOC), benzyloxycarbonyl (CBz) and 9-fluorenylmethylenoxycarbonyl (Fmoc). Similarly, a "hydroxy-protecting group" refers to a substituent of a hydroxy group that blocks or protects the hydroxy functionality. Suitable hydroxy-protecting groups, but are not limited to, include acetyl and silyl. A "carboxy-protecting group" refers to a substituent of the carboxy group that blocks or protects the carboxy functionality. Suitable carboxy-protecting groups include, but are not limited to, -CH2CH2SO2Ph, cyanoethyl, 2-(trimethylsilyl)ethyl, 2-(trimethylsilyl)ethoxymethyl, 2-(p-toluene sulfonyl) ethyl, 2-(p-nitrophenylsulfenyl)ethyl, 2-(diphenylphosphino)-ethyl, nitroethyl and the like. For a general description of protecting groups and their use, see T. W, Greene, Protective Groups in Organic Synthesis, John Wiley & Sons, New York, 1991. "Treating" or "treatment" of a state, disorder or condition includes: (1) preventing or delaying the appearance of one or more clinical symptoms of the state, disorder or condition developing in a subject that may be afflicted with or predisposed to the state, disorder or condition but does not yet experience or display clinical or subclinical symptoms of the state, disorder or condition; (2) inhibiting the state, disorder or condition, i.e., arresting or reducing the development of the disease or at least one clinical or subclinical symptom thereof; or (3) relieving the disease, i.e., causing regression of the state, disorder or condition or at least one of their clinical or subclinical symptoms. The benefit to a subject to be treated is either statistically significant or at least perceptible to the subject or to the physician. The term "subject" includes mammals (especially humans) and other animals, such as domestic animals (e.g., household pets including cats and dogs) and non-domestic animals (such as wildlife). A "therapeutically effective amount" means the amount of a compound that, when administered to a subject for treating a state, disorder or condition, is sufficient to effect such treatment. The "therapeutically effective amount" will vary depending on the compound, the disease and its severity and the age, weight, physical condition and responsiveness of the subject to be treated. Pharmaceutically acceptable salts forming part of this invention include salts derived from inorganic bases (such as Li, Na, K, Ca, Mg, Fe, Cu, Zn, and Mn), salts of organic bases (such as N,N'-diacetylethylenediamine, glucamine, triethylamine, choline, hydroxide, dicyclohexylamine, metformin, benzylamine, trialkylamine, and thiamine), salts of chiral bases (such as alkylphenylamine, glycinol, and phenyl glycinol), salts of natural amino acids (such as glycine, alanine, valine, leucine, isoleucine, norleucine, tyrosine, cystine, cysteine, methionine, proline, hydroxy proline, histidine, ornithine, lysine, arginine, and serine), salts of non-natural amino acids (such as D-isomers or substituted amino acids), salts of guanidine, salts of substituted guanidine (wherein the substituents are selected from nitro, amino, alkyl, alkenyl, or alkynyl), ammonium salts, substituted ammonium salts, and aluminum salts. Other pharmaceutically acceptable salts include acid addition salts (where appropriate) such as sulphates, nitrates, phosphates, perchlorates, borates, hydrohalides, acetates (such as trifluroacetate), tartrates, maleates, citrates, fumarates, succinates, palmoates, methanesulphonates, benzoates, salicylates, benzenesulfonates, ascorbates, glycerophosphates, and ketoglutarates. Yet other pharmaceutical ly acceptable salts include, but are not limited to, quaternary ammonium salts of the compounds of the invention with alkyl halides or alkyl sulphates (such as Mel or (Me)2S04). Preferred pharmaceutically acceptable salts of the compounds of the present invention include, but are not limited to, hydrochloride, maleate, methanesulfonate, oxalate, succinate, 2-oxoglutarate, benzoate, salicylate, benzenesulfonate, and naphthalene-1,5-disulfonic acid. Pharmaceutically acceptable solvates include hydrates and other solvents of crystallization (such as alcohols). The compounds of the present invention may form solvates with standard low molecular weight solvents using methods known in the art. Pharmaceutical Compositions The pharmaceutical composition of the present invention comprises at least one compound of the present invention and a pharmaceutically acceptable excipient (such as a pharmaceutically acceptable carrier or diluent). For example, the compound of the present invention may be associated with a pharmaceutically acceptable excipient (such as a carrier or a diluent) or be diluted by a carrier, or enclosed within a carrier which can be in the form of a capsule, sachet, paper or other container. Examples of suitable carriers include, but are not limited to, water, salt solutions, alcohols, polyethylene glycols, polyhydroxyethoxylated castor oil, peanut oil, olive oil, gelatin, lactose, terra alba, sucrose, dextrin, magnesium carbonate, sugar, cyclodextrin, amylose, magnesium stearate, talc, gelatin, agar, pectin, acacia, stearic acid or lower alkyl ethers of cellulose, silicic acid, fatty acids, fatty acid amines, fatty acid monoglycerides and diglycerides, pentaerythritol fatty acid esters, polyoxyethylene, hydroxymethylcellulose and polyvinylpyrrolidone. The carrier or diluent may include a sustained release material, such as glyceryl monostearate or glyceryl distearate, alone or mixed with a wax. The pharmaceutical composition may also include one or more pharmaceutically acceptable auxiliary agents, wetting agents, emulsifying agents, suspending agents, preserving agents, salts for influencing oxmetic pressure, buffers, sweetening agents, flavoring agents, colorants, or any combination of the foregoing. The pharmaceutical composition of the invention may be formulated so as to provide quick, sustained, or delayed release of the active ingredient after administration to the subject by employing procedures known in the art. The pharmaceutical compositions of the present invention may be prepared by conventional techniques, e.g., as described in Remington: The Science and Practice of Pharmacy. 20th Ed., 2003 (Lippincott Williams & Wilkins). For example, the active compound can be mixed with a carrier, or diluted by a carrier, or enclosed within a carrier, which may be in the form of a ampoule, capsule, sachet, paper, or other container. When the carrier serves as a diluent, it may be a solid, semi-solid, or liquid material that acts as a vehicle, excipient, or medium for the active compound. The active compound can be adsorbed on a granular solid container, for example, in a sachet. The pharmaceutical compositions may be in conventional forms, for example capsules, tablets, aerosols, solutions, suspensions or products for topical applications. The route of administration may be any route which effectively transports the active compound of the invention which inhibits the enzymatic activity of DPP-IV to the appropriate or desired site of action. Suitable routes of administration include, but are not limited to, oral, nasal, pulmonary, buccal, subdermal, intradermal, transdermal, parenteral, rectal, depot, subcutaneous, intravenous, intraurethral, intramuscular, intranasal, ophthalmic (such as with an ophthalmic solution) or topical (such as with a topical ointment). The oral route is preferred. Solid oral formulations include, but are not limited to, tablets, capsules (soft or hard gelatin), dragees (containing the active ingredient in powder or pellet form), troches and lozenges. Tablets, dragees, or capsules having talc and/or a carbohydrate carrier or binder or the like are particularly suitable for oral application. Preferable carriers for tablets, dragees, or capsules include lactose, cornstarch, and/or potato starch. A syrup or elixir can be used in cases where a sweetened vehicle can be employed. A typical tablet that may be prepared by conventional tabletting techniques may contain: (1) Core: Active compound (as free compound or salt thereof), 250 mg colloidal silicon dioxide (Aerosil®), 1.5 mg microcrystalline cellulose (Avicel®), 70 mg modified cellulose gum (Ac-Di-Sol®), and 7.5 mg magnesium stearate; (2) Coating: HPMC, approx. 9 mg Mywacett 9-40 T, and approx. 0.9 mg acylated monoglyceride (used as plasticizer for film coating). Liquid formulations include, but are not limited to, syrups, emulsions, soft gelatin and sterile injectable liquids, such as aqueous or non-aqueous liquid suspensions or solutions For parenteral application, particularly suitable are injectable solutions or suspensions, preferably aqueous solutions with the active compound dissolved in polyhydroxylated castor oil. Methods of Treatment The present invention also includes a method of treatins a condition that is regulated or normalized via inhibition of DPP-IV in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to one embodiment, the present invention provides a method of treating a metabolic disorder in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to another embodiment, the present invention provides a method for lowering blood glucose in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating Type II diabetes in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating impaired glucose tolerance (IGT) in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating impaired fasting glucose (IFG) in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of preventing or treating hyperglycemia in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of delaying the progression of impaired glucose tolerance (IGT) to Type II diabetes in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of delaying the progression of non-insulin requiring Type II diabetes to insulin requiring Type II diabetes in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of increasing the number and/or the size of beta cells in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of preventing or treating beta cell degeneration, such as apoptosis of beta cells, in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating food intake disorders in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating obesity in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of regulating appetite or inducing satiety in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating dyslipidemia in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method of treating functional dyspepsia, such as irritable bowel syndrome, in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. According to yet another embodiment, the present invention provides a method for the treatment and/or prophylaxis of a disease selected from diabetes, non-insulin dependent diabetes mellitus, impaired glucose tolerance, inflammatory bowel disease, ulcerative colitis, Crohn's disease, obesity, and metabolic syndrome in a subject by administering a therapeutically effective amount of a compound or pharmaceutical composition of the present invention. The compounds of the present invention may be administered to a mammal, especially a human in need of such treatment, prevention, elimination, alleviation or amelioration of the various diseases as mentioned above, e.g., Type II diabetes, IGT, IFG, obesity, appetite regulation or as a blood glucose lowering agent. The compounds of the invention are effective over a wide dosage range. For example, in the treatment of adult humans, dosages from about 0.05 to about 1000 mg, preferably from about 0.1 to about 500 mg, per day may be used. A most preferable dosage is about 0.5 mg to about 250 mg per day. In choosing a regimen for patients it may frequently be necessary to begin with a higher dosage and when the condition is under control to reduce the dosage. The exact dosage will depend upon the mode of administration, on the therapy desired, form in which administered, the subject to be treated and the body weight of the subject to be treated. The compounds of the present invention can be dispensed in unit dosage form comprising from about 0.05 to about 1000 mg of active ingredient together with a pharmaceutically acceptable carrier per unit dosage. Dosage forms suitable for oral, nasal, pulmonal or transdermal administration can comprise from about 0.05 mg to about 1000 mg, preferably from about 0.5 mg to about 250 mg, of the compound(s) admixed with a pharmaceutically acceptable carrier or diluent. The present invention also encompasses prodrugs of a compound of the invention, which on administration undergo chemical conversion oy metabonc processes before becoming active pharmacological substances. In general, such prodrugs will be functional derivatives of a compound of the invention, which are readily convertible in vivo into a compound of the invention. Conventional procedures for the selection and preparation of suitable prodrug derivatives are described, for example, in Design of Prodrugs, ed. H. Bundgaard, Elsevier, 1985. The invention also encompasses active metabolites of a compound of the invention. Methods of Preparing the Compounds of the Invention The compounds of the present invention may be synthesized according to the general scheme shown below: General Scheme wherein L and L2 are leaving groups (such as bromide, chlorine, iodine, O-toluene sulphonyls and O-methyl sulphonyls) and PG is a protecting group (such as -BOC or -Cbz). The compounds of formula (I) can be prepared by methods known in the art. One such approach is shown in the general synthetic scheme above. An intermediate of formula (1) can be coupled with a mono-protected bifunctional intermediate of formula (2). The coupled product can then be deprotected to yield an intermediate of formula (3). Compounds of formula (I) can be obtained by coupling intermediates of formulas (3) and (4). Preferably, each coupling reaction is performed in the presence of a base. Suitable bases include, but are not limited to, tertiary amines (e.g., triethylamine), carbonates (e.g., K2CO3), hydroxides, and mixtures thereof. The coupling reactions are typically performed in an inert solvent, such as tetrahydrofuran, dimethylformamide, dichloromethane, and mixtures thereof. The coupling sequence of the fragments (l)-(4) can be altered and the compounds of general formula I can be obtained by other methods known in the art. A compound of formula (I) having a particular stereochemistry for the cyclopentane or cyclopentene ring can be prepared from an optically active 1- amino cyclopentane or 1-aminocyclopentene of formula (2). The optically active compound of formula (2) may be obtained by resolution, asymmetric synthesis, or other method known in the art. The compounds of the present invention can be isolated and/or purified, such as by methods known in the art. For example, the compounds can be isolated and/or purified by distilling off the solvent in vacuum and recrystallizing the residue obtained from a suitable solvent or subjecting it to a purification method, such as column chromatography on a suitable support material. Salts can be obtained by dissolving the free compound in a suitable solvent, e.g., in a chlorinated hydrocarbon (e.g., methylene chloride, chloroform, 1,2-dichloroethane, carbontetrachloride, and the like ) or a low molecular weight aliphatic alcohol (e.g., ethanol or isopropanol), which contains the desired acid or base, or to which the desired acid or base is then added. The salts can then be obtained by filtering, re-precipitating, precipitating with a non-solvent for the addition salt or by evaporating the solvent. Salts obtained can be converted to the free base by basification or by acidification into the free compounds which, in turn can be converted into other salts. The compounds can be prepared in pure or substantially pure form by methods known in the art, such as crystallization using solvents such as pentane, diethyl ether, isopropyl ether, chloroform, dichloromethane, ethyl acetate, acetone, methanol, ethanol, isopropanol, water or their combinations, or column chromatography using alumina or silica gel and eluting the column with solvents such as hexane, petroleum ether (pet.ether), chloroform, ethyl acetate, acetone, methanol or their combinations. Polymorphs of a compound of formula (I) forming part of this invention may b prepared by crystallization of the compound under various conditions (e.g., by varyin temperature of crystallization and/or the rate of cooling) and with various solvents. Fc example, polymorphs may be obtained by heating or melting the compound followed by gradual or fast cooling. The presence of polymorphs may be determined by solid probe NMR spectroscopy, IR spectroscopy, differential scanning calorimetry, and powder X-ray diffraction. The invention is described in detail in the examples given below which are provided by way of illustration only and therefore should not be construed to limit the scope of the invention. Intermediates Step 1: (±)-2-N-BOC-Azabicyclo[2,2,l]hept-5-ene-3-one: A solution of di-tert-butyl dicarbonate (144 g, 660.5 mmol) in THF (100 ml) was added (20 min) to a stirred solution of (±)-2-azabicyclo[2,2,l]hept-5-ene-3-one (60 g, 549.8 mmol), triethylamine (83.5 g, 824.6 mmol) and 4-dimethylaminopyridine (6.7 g, 54.8 mmol) in THF (500 ml) at room temperature. The reaction mixture was stirred for another 4 h at room temperature. The solvent was evaporated under reduced pressure and the residue was diluted with EtOAc (800 ml) and washed with water (3 x 500 ml) and brine (400 ml). The EtOAc extract was dried (Na2S04) and evaporated under reduced pressure to give 115 g of the compound as a white solid; IR (KBr) 2979, 1755, 1705, 1455, 1331, 1305, 1149, 1117 cm"'; 'H NMR (CDCI3, 300 MHz) S 1.50 (s, 9H), 2,13-2.16 (m, 1H), 2.33-2.37 (m, 1H), 3.38-3.40 (m, 1H), 4.94-4.96 (m, 1H), 6.64-6.66 (m, 1H), 6.88-6.90 (m, 1H). Step 2: cis-(+)-4-N-BOC-Aminocyclopent^-ene-l-carboxylic acid: To a stirred solution of Step 1 intermediate (30.0 g, 143.3 mmol) in THF (100 ml) was added \N sodium hydroxide (300 ml) and the mixture was stirred at 40 °C for 20 h. The reaction mixture was cooled to 0 °C and acidified to pH 3.5 with IN hydrochloric acid. The mixture was extracted with dichloromethane (3 x 200 ml) and the combined extracts were washed with water (2 x 300 ml), brine (300 ml) and dried (Na2SO4). The solvent was evaporated under reduced pressure to give 31.5 g of the product as a white solid; IR (KBr) 3408, 3222, 2982, 1724, 1681, 1504, 1392 cm'1; !H NMR (CDC13, 300 MHz) 6 1.45 (s, 9H), 1.87-2.03 (m, 1H), 2.37-2.60 (m, 1H), 3.49 (brs, 1H), 4.60 (brs, 1H), 4.49 (brs, 1H), 5.90 (brs, 2H), 9.01 (brs, 1H). Method A: To a solution of Intermediate 1 (15 g, 66.0 mmol) in methanol (100 ml) was added 5 % Pd/C (1.0 g) and the mixture was maintained under hydrogen pressure (40 psi) for 2 h at room temperature. The catalyst was then filtered off and the filtrate was concentrated under reduced pressure to give 14.9 g of the product as a white solid; IR (KBr) 3304, 3249, 3098, 2978, 1705, 1646, 1403, 1164 cm'1; ]H NMR (CDC13, 300 MHz) 5 1.42 (s, 9 H), 1.53-2.20 (m, 5H), 2.11-2.35 (m, 1H), 2.73-3.01 (m, 1H), 4.05 (brs, 1H), 4.86 (brs, 1H). Method B: Step 1: cis-(±)-2-N-BOC-Azabicyclo[2,2,l]heptane-3-one: To a solution of cis-(±)-2-N-BOC-Azabicyclo[2,2,l]hept-5-ene-3-one (18.0 g, 86.02 mmol) obtained from Intermediate 1, Step 1, in EtOAc (180 ml) was added 5 % Pd/C (1.5 g) and the mixture was maintained under hydrogen pressure (40 psi) for 2 h at room temperature. The catalyst was then filtered off and the filtrate was concentrated under reduced pressure to give 18.1 g (99.6 %) of the compound as a white solid; IR (KBr) 2982, 1754, 1708, 1349, 1316, 1217, 1155, 1096,921 cm"1; 'H NMR (CDC13, 300 MHz) 8 1.42 (d, J= 10.2 Hz, 1H), 1.52 (s, 9H), 1.73-1.96 (m, 5H), 2.86 (brs, 1H), 4.53 (brs, 1H). Step 2: cis-(±)-3-N-BOC-Aminocyclopentane-l-carboxylic acid: To a stirred solution of Step 1 intermediate (9.0 g, 42.60 mmol) in THF (45 ml) was added IN sodium hydroxide (90 ml) and the mixture was stirred at 50 °C for 24 h. The reaction mixture was cooled to 0 °C and acidified to pH 3.5 with 1 N hydrochloric acid. The mixture was extracted with dichloromethane (3 x 100 ml) and the combined extracts were washed with water (2 x 100 ml), brine (100 ml) and dried (Na2SO4). The solvent was evaporated under reduced pressure to give 9.5 g (97 %) of the product as a white solid. The product isolated was identical in all respects with that obtained from Method A Method A: Sodium borohydride (1.43 g, 37.8 mmol) was added to a stirred solution of (±)-2-iV-BOC-Azabicyclo[2,2,I]-heptane-3-one (8.0 g, 37.86 mmol) obtained from Step 1, Method B of Intermediate 2 in 10 % aqueous THF (100 ml) at 0 °C. A second lot of sodium borohydride (1.43 g, 37.8 mmol) was added after 0.5 h at the same temperature and the mixture was stirred at 0-10 °C for 4 h. The excess reagent was quenched with IN HC1 and the reaction mixture was acidified to pH 5.0. The mixture was extracted with ethyl acetate (3 x 200 ml) and the combined organic extracts were washed with water (3 x 200 ml) brine (200 ml) and dried (Na2S04). The solvent was evaporated under reduced pressure to give 6.9 g (85 %) of the compound as a white solid; IR (KBr) 3361, 2969, 1683, 1524, 1366, 1271, 1172, 1017 cm"1; *H NMR (CDC13, 300 MHz) 8 1.11-1.16 (m, 1H), 1.40-1.53 (m, 2H), 1.44 (s, 9H), 1.71-1.79 (m, 1H), 1.87-1.95 (m, 1H), 2.15-2.01 (m, 2H), 3.57 (t, J = 5.1 Hz, 2H), 3.94 (brs, 1H), 4.73 (brs, 1H). Method B: Ethyl chloroformate (4.73 g, 43.58 mmol) was added to a stirred solution of Intermediate 2 (10 g, 43.66 mmol) and triethylamine (4.42 g, 43.76 mmol) in dry THF (100 ml) at 0 °C over 5 min under a nitrogen atmosphere. The reaction mixture was stirred for another 30 min at the same temperature. It was then filtered to remove the precipitated triethylamine hydrochloride. The filtrate containing the mixed anhydride was slowly added to a stirred suspension of NaBfy (4.95 g, 130.84 mmol) in 20 % aqueous THF (100 ml) maintained at 10 °C. The mixture was stirred for another 30 min at the same temperature and then acidified with \N HC1 to pH 4. The mixture was extracted with EtOAc (3 x 200 ml) and the organic layer was washed with 2 N NaOH solution (2 x 250 ml), water (2 x 250 ml) and brine (300 ml). The solvent was evaporated under reduced pressure to give 7.01 (75 %) of the alcohol as a white solid. IR and *H NMR spectra of the product were identical in all respects with the compound obtained from Method A. Methanesulfonyl chloride (15.23 g, 0.13 mol) was added to a stirred and cooled (10 °C) solution of Intermediate 3 (26 g, 0.12 mol) and triethylamine (15 g, 0.148 mol) in dry dichloromethane (150 ml) under a nitrogen atmosphere. The mixture was stirred at the same temperature for 15 min and then diluted with water (150 ml). The organic and aqueous layers were separated. The aqueous layer was extracted with dichloromethane (100 ml) and the combined organic extracts were washed with water, brine and dried (Na2S04). The solvent was concentrated under reduced pressure to give 35.4 g of the product as a white solid; IR (KBr) 3361, 2969, 2870, 1678, 1529, 1349, 1286, 1252, 1167, 1052, 973 cm'1; 'H NMR (CDC13, 300 MHz) 5 1.11-1.20 (m, 1H), 1.41-1.56 (m, 2H), 1.44 (s, 9H), 1.75-1.88 (m, 1H), 1.94-1.98 (m, 1H), 2.01-2.94 (m, 2H), 3.02 (s, 3H), 3.95 (brs, 1H), 4.15 (d, J = 6.6 Hz, 2H), 4.53 (brs, 1H). Method A:Step 1: (45',li?)-(+)-4-N-BOC-Aminocyclopent-2-ene-l-carboxylic acid: This intermediate was prepared by the optical resolution of Intermediate 1 using (S)-(-)-phenyl ethylamine in a mixture of isopropanol and ethanol; [α]o + 48.0 ° (c = 1.0, MeOH). Step 2: Ethyl chloroformate (2.86 g, 26.4 mmol) was added to a well stirred solution of Intermediate 1 (5.0 g, 22.0 mmol) and triethylamine (3.34 g, 33.0 mmol) in dry THF (50 ml) at 0 °C over 5 min under a nitrogen atmosphere. The reaction mixture was stirred for another 30 min at the same temperature. It was then filtered to remove the precipitated triethylamine hydrochloride. The filtrate containing the mixed anhydride was slowly added to a stirred suspension of NaBH4 (2.50 g, 66.0 mmol) in 20 % aqueous THF (20 ml) maintained at 10 °C. The mixture was stirred for another 30 min at the same temperature and then acidified with \N HC1 to pH 4. The mixture was extracted with EtOAc and the organic layer was washed with 2 N NaOH, brine and dried (Na2SO4). The solvent was evaporated under reduced pressure to give 4.0 g of the alcohol as a white solid; IR (KBr) 3316, 1958, 1681, 1538, 1370, 1250, 1166, 1039, 997 cm'1; 1H NMR (CDC13, 300 MHz) 8 1.34-1.42 (m, 1H), 1.44 (s, 9H), 2.44-2.51 (m, 1H), 2.83 (brs, 1H), 3.51-3.68 (m, 2H), 4.72 (brs, 1H), 4.88 (brs, 1H), 5.72-5.82 (m, 2H). Method B:Step 1: (15,4/2)-(+)-2-A^-BOC-Azabicyclo[2,2,l]hept-5-ene-3-one: This inter¬mediate was synthesized from (liS,47?)-(+)-2-Azabicyclo[2,2, l]hept-5-ene-3-one (10.0 g, 91.74 mmol) and di-ter/-butyl dicarbonate (26 g, 119.26 mmol) using triethylamine (13.92 g, 137.5 mmol) and 4-dimethylaminopyridine (1.1 g, 9.17 mmol) in THF (50 ml) as described in Intermediate 1, Step 1 to give 19.3 g of the compound as a white solid; IR and *H NMR spectra of the product were identical with that of the racemic product from Intermediate 1, Step 1. Step 2: Sodium borohydride (2.71 g, 71.69 mmol) was added to a stirred solution of Step 1 intermediate (15.0 g, 71.69 mmol) in 10 % aqueous THF (50 ml) at 0 °C. A second lot of sodium borohydride (2.71 g, 71.69 mmol) was added after 0.5 h at the same temperature and the mixture was stirred at 0-10 °C for 4 h. The excess reagent was quenched with IN HC1 and the reaction mixture was acidified to pH 5.0. The mixture was extracted with ethyl acetate and the combined organic extracts were washed with water, brine and dried (Na2S04). The solvent was evaporated under reduced pressure to give 13.30 g (87 %) of the product as a white solid. IR and lH NMR spectra of the product were identical in all respects with the compound obtained from Method A. Methanesulfonyl chloride (6.45 g, 56.27 mmol) was added to a stirred and cooled (10 °C) solution of Intermediate 5 (10.0 g, 46.89 mmol) and triethylamine (7.12 g, 70.33 mmol) in dry dichloromethane (50 ml) under a nitrogen atmosphere. The mixture was stirred at the same temperature for 15 min and then diluted with water. The organic and aqueous layers were separated. The aqueous layer was extracted with dichloromethane and the combined organic extracts were washed with water, brine and dried (Na2SO4). The solvent was removed under reduced pressure to give 12.9 g of the compound as a white solid; IR (KBr) 3352, 2984, 1678, 1515, 1343, 1239, 1168, 1060, 979 cm"1; 'H NMR (CDC13, 300 MHz) 5 1.31-1.42 (m, 2H), 1.44 (s, 9H), 2.54-2.61 (m, 1H), 3.08 (s, 3H), 4.13 (dd,.7=4.2, 1.5 Hz, 2H), 4.61 (brs, 1H), 4.72 (brs, 1H), 5.75-5.82 (m, 2H). Method A: Step 1: (lfl,4S)-(+)-2-./V-BOC-Azabicyclo[2,2,l]heptan-3-one: Step 1 inter¬mediate, from Method B, Intermediate 5 (9.0 g, 43.26 mmol) was hydrogenated using 5 % Pd/C (1.0 g) as described in Method B, Intermediate 2 to give 9.0 g of the product as a white solid; IR and 'H NMR spectra were identical with that of the racemic product. Step2:(liS,3#)-(+)-3-Af-BOC-Arninocyclopentane-l-carboxylic acid: Hydrolytic cleavage of Step 1 intermediate (8.5 g, 40.26 mmol) as described in Intermediate 2, Method B, Step 2 gave the desired product as a white solid. IR and *H NMR spectra were identical with that of the racemic intermediate; [(X]D + 12.2 ° (c = 1.0, MeOH). Method B: Step 1: (45,li?)-(+)-4-jV-BOC-Aminocyclopent-2-ene-l-carboxylic acid: This intermediate was prepared by the optical resolution of Intermediate 1 using (5)-(-)-phenyl ethylamine in a mixture of isopropanol and ethanol; [O]D + 48.0 ° (c = 1.0, MeOH). Step 2: (lS,3/?)-(+)-3-Af-BOC-Aminocyclopentane-l-carboxylic acid: To a solution of Step 1 intermediate, from Method A, Intermediate 5 (8.0 g, 35.2 mmol) in ethyl acetate (150 ml) was added 5 % Pd/C (1.0 g) and the mixture was maintained under hydrogen pressure (40 psi) for 3 h at room temperature to give 8.0 g of the product as a white solid, which was identical in all respects with the product obtained from Method A. Method A: This intermediate was prepared by the reductive cleavage of (1R,4S)-(+)-2-N-BOC-Azabicyclo[2,2,l]heptan-3-one (8.0 g, 37.86 mmol) (Step 1 intermediate, Method A, Intermediate 7) with sodium borohydride (2.86 g, 75.6 mmol) in 10 % aqueous THF (100 ml) as described in Intermediate 3, Method A to give 6.95 g (85 %) of the product as a white solid; [