Field of Invention The present invention relates to novel quinoline compounds of formula (I) and their pharmaceutically acceptable salts, for treatment of various disorders that are related to 5-HT4 receptor agonists. Background of the Invention 5-HT4 receptor (5-HT4R), belonging to serotonin (5-HT) receptor superfamily is positively coupled to adenylate cyclase thereby increasing the cAMP production. 5-HT4Rs are widely expressed throughout the body, but in all species studied so far the highest density of 5-HT4R is observed in the brain regions associated with learning like cortex and hippocampus (Lezoualc'h, F. et. al. The Serotonin Receptors: From Molecular Pharmacology to Human Therapeutics, The Humana Press, Chapter 15, 2006, 459 - 479). Brain microdialysis has shown increased release of acetylcholine in the rat frontal cortex and hippocampus following intracerebroventricular injection of 5-HT4R agonists (Journal of Pharmacology and Experimental Therapeutics, 2001, 296(3), 676 - 682). Behavioral studies in animal models of learning and memory also support the role of 5-HT4R in cognition. Interestingly, 5-HT4R also regulates the production of the neurotoxic amyloid P-peptide (A(J), which is one of the major pathogenetic pathways in Alzheimer's disease (Experimental Neurology, 2007, 203(1), 274 - 278). Indeed, 5-HT4R agonists can stimulate the non-amyloidogenic pathway leading to the release of the soluble form of the amyloid precursor protein (sAPPa), which in contrast to Ap, has putative neurotrophic and neuroprotective properties (Journal biological chemistry, 2001, 276(48), 44881 - 44888). 5-HT4 receptors are, therefore, an exciting potential target for the treatment of Alzheimer's disease symptomatology and pathology (Experimental Neurology, 2007, 205(2), 325 - 329). Besides this neurodegenerative disorder, 5-HT4R has been described as having mood modulating properties, and these features might be exploited for the treatment of depression (Neuron, 2007, 55(5), 712 - 725). Thus, 5-HT4R agonists are found to have potential for the treatment of dementia related disorders such as alzheimer's disease, schizpherenia, attention deficit hyperactivity disorder, huntington's disease, parkinson's disease and several other psychiatric disorders (Behavioral brain research, 1996, 73(1-2), 249 - 52; Schizophrenia Bulletin, 2007, 33 (5), 1100 - 1119 and Neuroscience & Medicine, 2011, 2, 87 - 92) and pain (Neuroscience, 2011,174,224 - 233). 5-HT4R agonists also have utility in the treatment of gastrointestinal disorders, especially those associated with reduced esophageal, gastric motility disorders, dyspepsia condition, functional dyspepsia, conditions associated with constipation and irritable bowel syndrome (IBS) and esophagitis (Expert Opinion on Investigational Drugs, 2010, 19(6), 765-775). Patent publications WO9410174, WO9408994, WO2005049608, WO2006090224, WO2011099305, WO2011101774, US20080207690 and US200802692I1 disclosed some 5-HT4 receptor compounds. While several 5-HT4 receptor agonists/partial agonists have been disclosed in the literature, no compound, either agonist or partial agonist targeting 5-HT4 receptor is launched in the market until now for treatments of dementia related disorers. Thereofore, there is need and scope to discover new 5-HT4 receptor agonists/partial agonists with novel chemical structures for treatment of dementia related disorders. Our quest for finding novel and potent ligands as 5-HT4 agonists/partial agonists had resulted in the discovery of quinoline compounds of the formula (I) which are demonstrating very high affinity and agonist activity towards 5-HT4R with other druggable properties like adequate brain penetration, good oral bioavailability, activity in animal models of cognition, ability to increase cortical sAPPa levels in mice brain significantly and decreasing the levels of Api^o and Ap^ levels in the rat brain. Therefore, it is an object of this invention to provide compounds, which are useful as therapeutic agents in the treatment of disorders that are affected by the 5-HT4 receptor agonists. Summary of the Invention The present invention relates to novel 5-HT4 receptor agonists of formula (I), ; or a pharmaceutically acceptable salt thereof, wherein, "X" is hydrogen or halogen; "v/wvr" is a bond representing racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen;. R2 is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 3, both inclusive. The compounds of formula (I) may involve below mentioned embodiments. It is to be understood that the embodiments below are illustrative of the present invention and are not intended to limit the claims to the specific embodiment's exemplied. According to one embodiment, there is provided a compound of the formula (la): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; ">AA^" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; R( is hydrogen, hydroxy or halogen; R4 is alkyl, cycloalkyl or cycloalkylalkyl; "m" is an integer ranging from 0 to 1, both inclusive. According to one embodiment, there is provided a compound of the formula (Ib-1): or a pharmaceutical^ acceptable salt thereof, wherein, "X" is halogen; '\A/WP" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive. According to one embodiment, there is provided a compound of the formula (Ib-2): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "i^w" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to I, both inclusive. According to one embodiment, there is provided a compound of the formula (Ic-1): —^ or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "JVW" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Rt is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive. According to one embodiment, there is provided a compound of the formula (Ic-2): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "VAAAP" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive. According to one embodiment, there is provided a compound of the formula (Ic-3): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "VA/W*" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive. According to one embodiment, there is provided a compound of the formula (Ic-4): or a pharmaceutical^ acceptable salt thereof, wherein, "X" is halogen; "v/vrv/xn" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive. According to one embodiment, there is provided a compound of the formula (Id-1): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "v/vw^" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; According to one embodiment, mere is provided a compound of the formula (Id-2): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; 'Wwn" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to I, both inclusive; According to one embodiment, there is provided a compound of the formula (Ie-1): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "V/VWP" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 3, both inclusive; According to one embodiment, there is provided a compound of the formula (Ie-2): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "v/wvr>" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 3, both inclusive; According to one embodiment, there is provided a compound of the formula (Ie-3): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "*/wv>" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 3, both inclusive; The present invention relates to use of a therapeutically effective amount of compound of formula (I), to manufacture a medicament in the treatment of various disorders that are related to 5-HT4 receptor agonists. Specifically, the compounds of this invention are useful in the treatment of various disorders such as alzheimer's disease, schizpherenia, attention deficit hyperactivity disorder, huntington's disease, parkinson's disease, psychiatric disorders or gastrointestinal disease and symptoms thereof. In another aspect, the invention relates to pharmaceutical compositions containing a therapeutically effective amount of at least one compound of formula (I), and their pharmaceutically acceptable salts thereof, in admixture with pharmaceutical acceptable excipient. In still another aspect, the invention relates to methods for using compounds of formula (I). In yet another aspect, the invention further relates to the process for preparing compounds of formula (I) and their pharmaceutically acceptable salts. Representative compounds of the present invention include those specified below and their pharmaceutically acceptable salts. The present invention should not be construed to be limited to them. 5-Ammo^-chloro-A^-{[l^tetrahyoVo-2H-pyran^-ylmethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide hemifumarate; 5-Amino-6-chloro-A^-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Ammo^-chloro-Ar-[l^tetrahyato-2//-pyran^ (R,S)5-Amino-6-chloro-A^-{[l-(tetrahydro-3-fiiranylmethyI)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; (R,S) 5-Amino-6-chloro-iV-{[ 1 -(tetrahydro-2-ftiranylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-JV-{[l-(tetrahydro-2//-pyran-4-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-Ar-{[3-(tetrahydro-3-furanylmethyl)-3-azabicyclo[3.l.0]hex-6-yl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-A'-{[3-isobutyl-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)- tartarate; 5-Amino-6-chloro-JV-{[3-cyclopropylmethyI-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[3-isopropyl-3-azabicycIo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)- tartarate; 5-Amino-6-fluoro-A^- {[ 1 -(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl] methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-AL{[l-(tetrahydro-2H-pyran-4-ylmethyl)-3-pyrrolidinyl] methyl} qutnoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-iV-{tl-(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; (Exo)5^Amino-6-chloro-A':{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide; 5-Amino-6-chloro-A'-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide (exo/endo mixture); 5-Amino-6-bromo-iV- {[ 1 -(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl] methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-bromo-A':-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Ammo^-chloroW-{[Ktetrahydro-2-fiiranylmethyl)-4-piperidmyl]methyl}quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-fluoro-Ar-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Ammo^-chloro-A4[4-fluoro-l-(tetrahydro-2H-py^ carboxamide L(+)-tartarate; (R,S) 5-Ammo^^hloro-iV-{[4-fluoro-l, 2.89 - 2.94 (2H, m), 2.96 - 2.99 (1H, m), 4.03 - 4.14 (1H, m), 6.90 (2H, bs), 7.50 - 7.53 (1H, m), 8.49 (1H, s), 8.65 - 8.68 (1H, m), 8.89 - 8.90 (1H, m), 10.90 - 10.91 (1H, d); Mass (m/z): 305.3 (M+H)\ 307.3 (M+H)+. Preparation 4: Preparation of 5-Amino-6-chloro-/V-{[3-azabicyclo[3.1.0|hex-6-yl|methyl} quinoline-8-carboxamide NH2 Step (i): Preparation of (3-Aza bicycIo[3.1.0]hex-6-yl) methanol Hydrogen gas was passed into a stirred solution of (3-benzyl-3-azabicyclo[3.1.0]hex-6-yl)methanol (15.50 grams, 0.076 mole) and palladium hydroxide (7.75 grams, 50 % w/w) in methanol (150 mL) over a period of 6 hours, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was filtered through celite bed and the filtrate was concentrated under vacuum to afford the title compound. Yield: 8.20 grams (69 %). 'H - NMR (8 ppm): 0.89 - 0.96 (1H, m), 1.35 - 1.42 (2H, m), 2.05 - 2.07 (2H, m), 2.85 - 2.88 (2H, m), 2.98 - 3.01 (2H, m), 3.50 - 3.52 (1H, m), 3.94 - 3.96 (1H, m); Mass (m/z): 114.3 (M+H)+. Step (ii): Preparation of tert-butyl 6-hydroxymethyl-3-azabicyclo[3.l.0|hexane-3-carboxylate Di-tert-butyl dicarbonate (16.96 grams, 0.077 mole) was added to a solution of (3-aza bicyclo[3.l.0]hex-6-yl) methanol (8.00 grams, 0.070 mole, obtained in above step) and triethylamine (11.40 grams, 0.112 mole) in dichloromethane (150 mL) at 10 °C. The reaction mass was stirred for 2 hours at 10 °C, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was washed with chilled water (50 mL), brine solution (50 mL) and dried over sodium sulphate. The organic phase was concentrated under vacuum to obtain a crude residue, which was further purified by flash chromatography using ethyl acetate:n-hexane (50:50) to afford the title compound. Yield: 7.84 grams (52 %). 'H - NMR (8 ppm): 0.92 - 0.97 (1H, m), 1.33 - 1.36 (1H, m), 1.43 (9H, s), 1.55 - 1.60 (2H, m), 3.32 -3.37 (2H, m), 3.43 - 3.48 (1H, m), 3.53 - 3.58 (2H, m), 3.61 - 3.64 (1H, m); Mass (m/z): 158.1 (M+H)+. Step (Hi): Preparation of tert-butyl 6-methanesulfonyloxymethyI-3-aza bicyclo[3.1.0]hexane-3-carboxyiate A solution of methanesulfonylchloride (4.42 grams, 0.038 mole) in dichloromethane (25 mL) was added to a solution of tert-butyl 6-hydroxymethyl-3-azabicyclo[3.1.0]hexane-3-carboxylate (7.80 grams, 0.036 mole, obtained in above step) and triethylamine (5.58 grams, 0.055 mole) in dichloromethane (100 mL) at 0 °C. The reaction mass was stirred over night at RT, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was washed with chilled water (50 mL), brine solution (50 mL) and dried over sodium sulphate. The organic phase was concentrated under vacuum to afford the title compound. Yield: 9.30 grams (87 %). 'H - NMR (5 ppm): 1.11 - 1.15 (1H, m), 1.40 -1.42 (1H, m), 1.45 (9H, s), 3.05 (3H, s), 3.17 - 3.19 (1H, m), 3.37 - 3.41 (2H, m), 3.58 - 3.68 (2H, m), 4.09 - 4.18 (2H, m); Mass (m/z): 236.2 (M-56)+. Step (iv): Preparation of tert-butyl 6-Azidomethyl-3-azabicyclo[3.1.0]hexane-3-carboxylate Sodium azide (7.30 grams, 0.112 mole) was added to a solution of tert-butyl 6-methanesulfonyloxymethyl-3-azabicyclo[3.1.0]hexane-3-carboxylate (9.30 grams, 0.039 mole, obtained in above step) and potassium carbonate (11.00 grams, 0.079 mole) in dimethylformamide (100 mL) at 10 °C. Then the reaction mass was stirred over night at RT, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was poured onto chilled water (200 mL). The product was extracted with ethylacetate (3 x 150 mL) and the combined organic phase was washed with chilled water (150 mL), brine solution (150 mL) and dried over sodium sulphate. The organic phase was concentrated under vacuum to afford the title compound. Yield: 7 grams (90%). *H - NMR (5 ppm): 0.97 - 1.00 (1H, m), 1.45 (9H, s), 1.50 - 1.53 (2H, m), 3.10 - 3.15 (1H, m), 3.22 -3.27 (1H, m), 3.35 - 3.39 (2H, m), 3.57 - 3.67 (2H, m); Mass (m/z): 183.3 (M-56)+. Step (v): Preparation of tert-butyl 6-aminomethyl-3-azabicyclo[3.1.0]hexane-3-carboxylate A solution of tert-butyl 6-azidomethyl-3-azabicyclo[3.1.0]hexane-3-carboxylate (1.50 grams, 0.006 mole, obtained in above step) in THF (30 mL) and water (3 mL) mixture was treated with -28- triphenylphosphine (2.1 grams, 0.008 mole). The reaction mass was stirred for 36 hours at RT, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was concentrated under vacuum to obtain a crude residue, which was further purified by flash chromatography using triethylamine: methanol: dichloromethane (2:8:90) to afford the title compound. Yield: 1.20 grams (90%). 'H - NMR (8 ppm): 0.66 - 0.70 (1H, m), 0.95 - 0.99 (1H, t), 1.17 - 1.19 (1H, m), 1.33 (9H, s), 1.53 -1.55 (2H, m), 2.67 - 2.69 (2H, m), 3.36 - 3.41 (2H, m), 7.73 (2H, bs); Mass (m/z): 213.3. (M+H)+. Step (vi): Preparation of 6-Chlo'ro-5-nitro-yV-{[l-(tert-butoxycarbonyI)-3-azabicyclo[3.1.0]hex-6- y I] methyl} quinoline-8-carboxamide A solution of 6-chloro-5-nitro quinoline-8-carboxylic acid (1.90 grams, 0.019 mole, obtained from preparation 1) and CDI (1.34 grams, 0.008 mole) in dichloromethane (15 mL) was stirred for 3 hours at RT. Then a solution of tert-butyl 6-aminomethyl-3-aza bicyclo[3.1.0]hexane-3-carboxylate (1.34 grams, 0.006 mole, obtained in the above step) in dichloromethane (10 mL) was added at RT. The reaction mass was stirred over night (12 hours) at RT under nitrogen atmosphere, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was washed with chilled water (15 mL), brine solution (15 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using (ethyl acetate: n-hexane (30: 70) to afford the title compound Yield: 2.7 grams (80%). lH - NMR (8 ppm): 1.07 - 1.09 (1H, in), 1.25 - 1.31 (1H, m), 1.46 (9H, s), 1.60 - 1.63 (2H, m), 3.36 -3.49 (2H, m), 3.56 - 3.70 (2H, m), 4.12 - 4.16 (1H, m), 7.73 - 7.76 (1H, m), 8.19 - 8.21 (1H, dd, J = 8.72, 1.16 Hz), 8.97 (1H, s), 9.10 - 9.11 (1H, m), 11.05 - 11.08(1H, t); Mass (m/z): 447.4 (M+H)+, 449.3 (M+H)+. Step (vii): Preparation of 5-Amino-6-chloro-Ar-{[l-(tert-butoxycarbonyI)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide Iron powder (0.80 gram, 0.014 mole) and ammonium chloride (0.75 gram, 0.014 mole) were added to a solution of 5-nitro-6-chloro-A'-{[l-(tert-butoxycarbonyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide (1.30 grams, 0.003 mole, obtained in above step) in ethanol (26 mL), THF(13 mL) and water (6.5 mL) mixture. The reaction mass was stirred for 6 hours at 75 °C, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was cooled to RT and filtered through celite bed. The filtrate was concentrated and the slurry, thus obtained, was partitioned between ethyl acetate (20 mL) and water (15 mL) by stirring for 30 minutes. Then separated the both the layers and the aqueous phase was extracted with ethylacetate (3 x 10 mL). The combined organic phase was washed with water (15 mL), brine solution (15 mL) and dried over sodium sulphate. The organic phase was concentrated under vacuum to obtain a crude residue, which was further purified by flash chromatography using ethyl acetate:n-hexane (80:20) to afford the title compound. Yield: 1 gram (83 %). 'H - NMR (8 ppm): 0.78 - 0.82 (1H, m), 1.09 - 1.12 (IH, m), 1.32 (9H, s), 1.47 - 1.51 (2H, m), 3.20 -3.26 (2H, m), 3.36 - 3.40 (3H, m), 6.89 (2H, bs), 7.53 - 7.56 (IH, m), 8.35 (IH, s), 8.80 - 8.83 (IH, dd, J = 8.44, 1.00 Hz), 8.92 - 8.93 (IH, m), 10.85 -10.88 (IH, t); Mass (m/z): 417.3 (M+H)+, 419.1 (M+H)+. Step (viii): Preparation of 5-Amino-6-chloro-/V-{[3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide Ethanolic hydrogen chloride (23 % w/w, 3.03 gram, 0.019 mole) was added to a stirred solution of S-amino^-chloro-A^-ifl^tert-butoxycarbonyl^-azabicyclop. 1.0]hex-6-yl]methyl} quinoline-8-carboxamide (0.85 gram, 0.002 mole, obtained in above step) in ethanol (15 mL) at 10 °C. The reaction mass was stirred over night at RT, while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was concentrated and the slurry, thus obtained, was dissolved in water (15 mL). The pH was adjusted to ~ 9.5 using aqueous ammonia solution and the product was extracted with dichloromethane (3x10 mL). The combined organic phase was washed with water (10 mL), brine solution (10 mL) and dried over sodium sulphate. The organic phase was concentrated under vacuum to afford the title compound. Yield: 0.58 gram (90%). 'H - NMR (5 ppm): 0.98 - 1.01 (IH, m), 1.12 - 1.17 (IH, m), 1.35 - 1.36 (2H, m), 1.75 - 1.77 (IH, m), 1.96 - L99 (IH, m), 2.61-2.64 (2H, m), 2.81 - 2.84 (2H, m), 6.93 (2H, bs), 7.56 - 7.60 (IH, dd, J = 8.60 Hz, 4.20 Hz), 8.39 (IH, s), 8.84 - 8.86 (IH, m), 8.95 - 8.96 (IH, m), 10.87 -10.90 (IH, t); Mass (m/z): 317.2 (M+H)+, 319.4 (M+H)+. Preparation 5: Preparation of 5-Amino-6-chloro-jV-[4-fluoro-(4-piperidinyl)methyll quinoline-8- carboxamide Step (i): Preparation of tert-butyl l-Oxa-6-aza spiro[2.5|octane-6-carboxy!ate Trimethylsulfoxonium iodide (13.3 grams, 0.06 mole) was added to a stirred solution of sodium hydride (60 % dispersion in oil, 3.0 grams, 0.126 mole) in THF (150 mL) at 10 °C. Reaction mass temperature was slowly raised to RT and stirred further for 2 hours at the same temperature. Reaction mass was then cooled to 10 °C and added N-boc-piperidine-4-one (10 grams, 0.05 mole) solution in THF (50 mL) at the same temperature. Then reaction mass temperature was slowly raised to RT and stirred for 3 hours at same temperature. The progress of the reaction was monitored by. TLC. After completion of the reaction (TLC), the mass was quenched in chilled water (300 mL), the compound was extracted with dichloromethane (3 x 150 mL). The combined organic phase was washed with water (100 mL), brine solution (100 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using ethyl acetate: n-hexane (15:85) to afford the title compound. Yield: 7.1 grams (66%). 'H - NMR (5 ppm): 1.47 (9H, s), 1.59 - 1.62 (2H, m), 1.76 -1.83 (2H, m), 2.69 (2H, s), 3.39 - 3.45 (2H, m), 3.70 -3.73 (2H, m); Mass (m/z): 158.2 (M-56)+. Step (ii): Preparation of 4-[(Dibenzylamino) methyl|-4-hydroxy piperidine-1-carboxylic acid tert-butyl ester Dibenzylamine (7.98 grams, 0.04 mole) was added to a stirred solution of tert-butyl l-oxa-6-aza-spiro[2.5]octane-6-carboxylate (7.86 grams, 0.036 mole, obtained in above step) and triethylamine (11.19 grams, 0.118 mole) in methanol (100 mL) at RT. Then reaction mass temperature was slowly raised to 75 °C and stirred for 38 hours at same temperature. The progress of the reaction was monitored by TLC. After completion of the reaction (TLC), the reaction mass was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using ethyl acetate: n-hexane (15:85) to afford the title compound. Yield: 7.1 grams (46%). 'H - NMR (S ppm): 1.43 (9H, s), 1.89 - 1.94 (2H, m), 2.14 - 2.19 (1H, m), 2.55 - 2.60 (2H, m), 2.92 (1H, s), 3.03 -3.09 (2H, m), 3.43 - 3.45 (1H, m), 3.64 (4H, bs), 3.69 - 3.84 (2H, m), 7.16 - 7.35 (10H, m); Mass(m/z):411.3(M+H)+ Step (iii): Preparation of tert-Butyl 4-[(Dibenzylamino)-methyl|-4-fluoro piperidine-1-carboxylate Diethylaminosulfur trifluoride (DAST) (3.3 grams, 0.02 mole) was added to a stirred solution of tert-butyl 4-[(diben2ylamino) methyl]-4-hydroxy piperidine-l-carboxylate (7 grams, 0.017 mole, obtained in the above step) in DCM (70 mL) at - 40 °C. Then reaction mass temperature was slowly raised to RT and stirred over night at the same temperature. The progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the mass was quenched in chilled water (100 mL). The pH of the mass was adjusted to ~ 9.5 using aqueous ammonia, the compound was extracted with DCM (3 x 50 mL). The combined organic phase was washed with water (75 mL), brine solution (75 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using ethyl acetate:n-hexane (5:95) to afford the title compound. Yield: 4.35 grams (61%). 'H - NMR (5 ppm): 1.45 (9H, s), 1.89 - 1.94 (2H, m), 2.14 - 2.19 (1H, m), 2.55 - 2.60 (2H, m), 3.03 -3.09 (2H, m), 3.43 - 3.45 (1H, m), 3.64 (4H, bs), 3.69 - 3.84 (2H, m), 7.16 - 7.35 (10H, m); Mass (m/z): 413.3 (M+H)+. Step (iv): Preparation of tert-Butyl 4-aminomethyl-4-fluoro piperidine-1-carboxylate Hydrogen gas was passed into a stirred solution of tert-butyl 4-[(dibenzylamino)-methyl]-4-fluoro-piperidine-1-carboxylate (4.12 grams, 10 mmole, obtained in the above step) and palladium hydroxide (2 grams, 50 % w/w) in methanol (50 mL) over a period of 8 hours. The progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the reaction mass was filtered through celite bed and the filtrate was concentrated on rotavacuum to afford the title compound. Yield: 1.97 grams (85%). 'H - NMR (8 ppm): 1.38 (9H, s), 1.44 -1.71 (6H, m), 2.60 - 2.64 (2H, m), 2.95 (2H, bs), 3.73 - 3.76 (2H, m); Mass (m/z): 233.2 (M+H)+. Step (v): Preparation of 6-ChIoro-5-nitro-Ar-{[4-fluoro-l-(tert-butoxycarbonyl)-4-piperidinyll methyl}quinoline-8-carboxamide A solution of 6-chloro-5-nitro quinoline-8-carboxylic acid (1.3 grams, 5.14 mmole) and carbonyldiimidazole (1 gram, 6.17 mmole) in DCM (25 mL) was stirred for 3 hours at RT. Then added a solution of with 4-aminomethyl-4-fluoro piperidine-1-carboxylic acid tert-butyl ester (1.2 grams, 5.17 mmole, obtained in above step) in DCM (10 mL). The reaction mass was stirred over night (12 hours) at RT under nitrogen atmosphere, while monitoring the the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was washed with chilled water (10 mL), brine solution (10 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using (ethyl acetate: n-hexane (30: 70) to afford the title compound. Yield: 1.46 grams (61 %). 'H - NMR (5 ppm): 1.45 (9H, s), 1.61 - 1.72 (2H, m), 1.85 - 1.93 (2H, m), 3.11 - 3.16 (2H, m), 3.81 -4.13 (4H, m), 7.69 - 7.72 (1H, m), 8.15 - 8.18 (1H, m), 8.92 (1H, s), 9.07 - 9.08 (1H, tn), 11.23 - 11.25 (1H, t); Mass (m/z): 467.2 (M+H)\ 469.2 (M+H)+. Step (vi): Preparation of 5-Amino-6-chioro-A'-{[4-fluoro-l-{t-butoxycarbonyl)-4-piperidinyl] methyI}quinoline-8-carboxamide O i Added iron powder (0.41 grams, 7.50 mmole) and ammonium chloride (0.4 grams, 7.50 mmole) to a solution of 6-chloro-5-nitro-A'-{[4-fluoro-l-4-piperidinyl]methyl} quinoline-8-carboxamide (0.2 grams, 0.462 mmole, obtained from the step (i) of Example 23) in DCM (10 mL) at -30 °C. Then reaction mass temperature was slowly raised to room temperature and stirred for over night at same temperature. The progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the mass was quenched in chilled water (10 mL). The mass pH was adjusted to pH ~ 9.5 using aqueous ammonia, the compound was extracted with DCM (3x5 mL). The combined organic phase was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. Yield: 0.052 grams (52 %). 'H - NMR(5 ppm): 1.39 - 1.48 (2H, m), 1.64-1.71 (2H, m), 1.78 - 1.85 (6H, m), 2.16 - 2.21 (2H, m), 2.94 - 2.97 (2H, m), 3.47 - 3.51 (2H, m), 3.71 - 3.81 (3H, m), 4.97 (2H, bs), 7.47 - 7.50 (1H, m), 8.24 -8.27 (1H, dd, J = 8.56, 1.48 Hz), 8.80 (1H, s), 8.91 - 8.92 (1H, m), 11.08 -11.11 (1H, t); Mass (m/z): 435.2 (M+H)+, 437.4 (M+H)+. Step (ii): Preparation of 5-Amino-6-chloro-yv"-{[l-(4-fluorotetrahydro-2//-pyran-4-ylniethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate A clear solution of L(+)-tartaric acid (0.010 gram, 0.069 mole) in 1 mL methanol was added to a stirred solution of of S-amino^-chloro-A^ltl^-fluorotetrahydro^H-pyran^-ylmemyl)^-piperidinyl]methyl} quinoline-8-carboxamide (0.03 gram, 0.069 mmole, obtained in above step) in methanol (1 mL). The clear mass was stirred further for 2 hours at RT. The solvent was evaporated to afford solid mass. The solid mass was further triturated with diethyl ether (2 x 2 mL) and dried under reduced pressure to obtain the title compound. Yield: 0.036 gram (88 %). 'H - NMR (5 ppm): 1.27 - 1.34 (2H, m), 1.48 - 1.58 (1H, m), 1.60 - 1.73 (6H, m), 2.10 - 2.16 (2H, m), 2.90 - 2.93 (2H, m), 3.15 - 3.20 (4H, m), 3.49 - 3.55 (2H, m), 3.63 - 3.66 (2H, m), 4.25 (2H, s), 6.90 (2H, bs), 7.55 - 7.58 (1H, m), 8.37 (1H, s), 8.83 - 8.85 (1H, m), 8.93 - 8.94 (1H, m), 10.88 - 10.91 (1H, t); Mass (m/z): 435.2 (M+H)+; 437.2 (M+H)+. Example 31: Preparation of 5-Amino-6-chloro-Ar-{(l-(2-methoxy carbonyI-2-methyl propan-1-yl)-4-piperidinyl] methyl} quinoline-8-carboxamide A solution of 5-amino-6-chloro-Ar-[(4-piperidinyl)methyl] quinoline-8-carboxamide (0.35 grams, 1.09 mmole, obtained from preparation 2) and methyl 2,2-dimethyl-3-oxo propionate (0.3 grams, 2.3 mmole) in dichloroethane (20 mL) was cooled to 10 °C and treated with sodium triacetoxyborohydride (0.58 grams, 2.73 mmole). The reaction mass was stirred overnight at RT, the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (TLC), the reaction mass was concentrated and the obtained slurry was quenched in water (30 mL). The mass pH was adjusted to ~ 9.5 using aqueous ammonia, the compound was extracted with DCM (3x10 mL). The combined organic phase was washed with water (15 mL), brine solution (15 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.25:0.75:99) to afford the title compound. Yield: 0.3 grams (43 %). 'H - NMR (8 ppm): 1.05 (6H, s), 1.21 - 1.28 (3H, m), 1.58 - 1.61 (2H, m), 2.04 - 2.10 (2H, m), 2.39 -2.47 (2H, m), 2.67 - 2.70 (2H, m), 3.25 - 3.28 (2H, m), 3.55 (3H, s), 6.91 (2H, bs), 7.54 - 7.57 (1H, dd, J = 8.56,4.20 Hz), 8.37 (1H, s), 8.83 - 8.85 (1H, m), 8.92 - 8.93 (1H, m), 10.87 - 10.90 (1H, t); Mass (m/z): 433.4 (M+H)+; 435.3 (M+H)+. Example 32: Preparation of 5-Amino-6-chloro-/V-{[l-(2,2-dimethyl proponic acid-3-yl)-4-piperidinyljmethyl} quinoline-8-carboxamide L(+)-tartarate Step (i): Preparation of 5-Amino-6-chIoro-iV-{[l-(2^-dimethyl proponic acid-3-yI)-4-piperidinyl]methyl} quinoIine-8-carboxamide A solution of of 5-amino-6-chloro-./v"-{[l-(2-methoxy carbonyl-2-methyl propan-l-yl)-4-piperidinyljmethyl} quinoline-8-carboxamide (0.092 grams, 0.212 mmole obtained from Example 31) and lithium hydroxide mbnohydrate (0.044 grams, 1.04 mmole) in methanol (6 mL) and water (2 mL) was stirred overnight at RT, the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the reaction mass was concentrated and the obtained slurry was dissolved in DCM (25 mL). The undissolved inorganic solids were separated by filteration. The filterate was concentrated on rotavacuum to obtain the crude residue, which was further triturated with n-hexane (10 mL) and dried on rotavacuum to afford the title compound. Yield: 0.059 grams (67 %). *H - NMR (8 ppm): 0.96 (6H, s), 1.21 -1.26 (3H, m), 1.61-1.66 (2H, m), 2.02 - 2.09 (2H, m), 2.35 (2H, s), 2.81 - 3.85 (2H, m), 3.26 - 3.30 (3H, m), 6.93 (2H, s) 7.54 - 7.57 (1H, dd, J = 8.62, 4.21 Hz), 8.37 (1H, s), 8.84 - 8.94 (2H, m), 10.88 -10.91 (1H, t); Mass (m/z): 419.3 (M+H)+; 421.3 (M+H)+. Step (ii): Preparation of S-Amino-e-chloro-A^l-^jZ-dimethyl proponic acid-3-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate A clear solution of L(+)-tartaric acid (0.019 gram, 0.126 mole) in 2 mL methanol was added to a stirred solution of of 5-amino-6-chloro-AT-{[l-(2,2-dirnethyl proponic acid-3-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.058 gram, 0.138 mmole, obtainted in above step) in methanol (2 mL) at RT. The clear mass was stirred further for 2 hours at RT. The solvent was evaporated to afford solid mass. The solid mass was further triturated with diethyl ether (2x3 mL) and dried under reduced pressure to obtain the title compound. Yield: 0.05 gram (65%). 'H - NMR (8 ppm): 0.99 (6H, s), 1.20 -1.25 (3H, m), 1.61 - 1.64 (2H, m), 2.09 - 2.14 (2H, m), 2.35 (2H, s), 2.83 - 3.86 (2H, m), 3.26 - 3.30 (3H, m), 4.18 (2H, s), 6.91 (2H, s) 7.54 - 7.57 (1H, dd, J = 8.62, 4.21 Hz), 8.37 (1H, s), 8.84 - 8.94 (2H, m), 10.88 - 10.91 (lH,t); Mass (m/z): 419.3 (M+H)+; 421.3 (M+H)+. Example 33: Preparation of S-Amino-e-chloro-A^lfl^-hydroxy-l^-dimethyl propyl)-4-piperidinyl] methyl} quinoline-8-carboxamide L(+)-tartarate i\n2 Step (i): Preparation of 5-Amino-6-chloro-A'-{[l-(3-hydroxy-2,2-dimethyi propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide - —^ 1M solution of Lithium aluminum hydride (0.38 mL) was added to a stirred solution of 5-amino-6-chloro-iV-{[l-(2-methoxy carbonyl-2-methyl propan-l-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.11 grams, 0.254 mmole, obtained from Example 31) in THF (5 mL) at 0 °C. Then reaction mass temperature was slowly raised to RT and stirred for 4 hours at same temperature. The progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the mass was cooled to 0 °C and added water (0.2 mL), followed by ethyl acetate (10 mL). The resulting solution was filtered through celite pad and was washed with ethyl acetate (10 ml). The filterate was dried over sodium sulphate. The organic phase was filtered and concentrated under vacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.5:5:94.5) to afford the title compound. Yield: 0.051 grams (49 %). 'H - NMR (5 ppm): 0.75 (6H, s), 1.21 - 1.29 (2H, m), 1.33 - 1.36 (1H, m), 1.61 - 1.46 (2H, m), 2.08 -2.15 (4H, m), 2.77 - 2.80 (2H, m), 3.12 - 3.17 (2H, m), 3.30 - 3.36 (2H, m), 4.59 - 4.63 (1H, m), 6.89 (2H, bs), 7.54 - 7.58 (1H, dd, J = 8.60,4.24 Hz), 8.37 (1H, s), 8.83 - 8.93 (2H, m), 10.87 - 10.90 (1H, t); Mass (m/z): 405.1 (M+H)+; 407.3 (M+H)+. Step (ii): Preparation of 5-Amino-6-chIoro-Ar-{[l-(3-hydroxy-2,2-dimethyI propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate A clear solution of L(+)-tartaric acid (0.015 gram, 0.1 mmole) in 2 mL methanol was added to a stirred solution of 5-amino-6-chloro-A^-{[l-(3-hydroxy-2,2-dimethyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.04 gram, 0.098 mmole, obtainted in above step), in methanol (2 mL) at RT. The clear mass was stirred further for 2 hours at RT. The solvent was evaporated to afford solid mass. The solid mass was further triturated with diethyl ether (2x3 mL) and dried under vacuum to obtain the title compound. Yield: 0.045 gram (82 %). 'H - NMR (5 ppm): 0.80 (6H, s), 1.35 - 1.40 (2H, m), 1.58 - 1.60 (1H, m), 1.67 - 1.70 (2H, m), 2.35 - 2.41 (4H, m), 2.95 - 2.97 (3H, m), 3.12 - 3.17 (2H, m), 3.30 - 3.36 (2H, m), 4.14 (2H, s), 6.91 (2H, bs), 7.55 - 7.58 (1H, dd, J = 8.60, 4.24 Hz), 8.37 (1H, s), 8.83 - 8.94 (2H, m), 10.88 - 10.91 (1H, t); Mass (m/z): 405.1 (M+H)+; 407.3 (M+H)+. Example 34: The compound of Example 34 was prepared by following the experimental procedure as described in the Example 33 given above, with some noncritical variations. Example 35: Preparation of 5-Amino-6-chloro-A'-{[l-{2-hydroxy-2-methyI propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate Step (i): Preparation of 5-Amino-6-chIoro-Ar-{[l-(2-hydroxy-2-methyl propyl)-4-piperidinyljmethyl} quinoline-8-carboxamide A solution of 5-amino-6-chloro-A'-[(4-piperidinyl)methyl] quinoIine-8-carboxamide (0.85 grams, 2.66 mmole, obtained from preparation 2), isobutyleneoxide (0.38 grams, 5.33 mmole) and triethylamine (0.54 grams, 5.33 mmole) in methanol (15 mL) was stirred overnight at 75 °C. The progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the reaction mass was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.25:0.75:99) to afford the title compound. Yield: 0.69 grams (67 %). 'H - NMR (8 ppm): 1.25 (6H, s), 1.27 - 1.30 (2H, m), 1.81-1.92 (2H, m), 1.97 - 2.08 (2H, m), 2.38 - 2.54 (4H, m), 3.05 - 3.07 (2H, m), 3.47 - 3.50 (2H, m), 4.93 - 4.96 (2H, m), 7.45 - 7.48 (1H, dd, J = 8.60, 4.24 Hz), 8.22 - 8.24 (1H, m), 8.77 (1H, s), 8.89 - 8.90 (1H, m), 11.08 - 11.12 (1H, t); Mass (m/z): 391.3 (M+H)+; 393.2 (M+H)+. Step (ii): Preparation of 5-Amino-6-chloro-Af-{[l-(2-hydroxy-2-inethyl propyI)-4- piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate A clear solution of L(+)-tartaric acid (0.155 gram, 1.03 mole) in 2 mL methanol was added to a stirred solution of 5-amino-6^hloro-N-{[l-(2-hydroxy-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.42 gram, 1.07 mmole, obtainted in above step) in methanol (2 mL) at RT. The clear mass was stirred further for 2 hours at RT. The solvent was evaporated to afford solid mass. The solid mass was further triturated with diethyl ether (2x3 mL) and dried under vacuum to obtain the title compound. Yield: 0.524 gram (89 %). lH - NMR (6 ppm): 1.12 (6H, s), 1.43 - 1.46 (2H, m), 1.69 - 1.73 (2H, m), 2.48 - 2.65 (4H, m), 3.15 -3.34 (6H, m), 4.09 (2H, s), 6.91 (2H, s), 7.55 - 7.59 (1H, dd, J = 8.60, 4.24 Hz), 8.38 (1H, s), 8.83 - 8.86 (1H, m), 8.93 - 8.94 (1H, m), 10.88 -10.91 (1H, t); Mass (m/z): 391.3 (M+H)+; 393.2 (M+H)+. Examples 36 to 45: The compounds of Examples 36 to 45 were prepared by following the experimental procedure as described in the Example 35 given above, with some noncritical variations. Example 46: Preparation of 5-Amino-6-chloro-A'-{[l-(2-fluoro-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide DAST (0.03 grams, 0.186 mmole) was added to a stirred solution of 5-amino-6-chloro-JV-{[l-(2-hydroxy-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.03 grams, 0.076 mmole, obtainted from the step (i) of example 35) in DCM (5 mL) at - 30 °C. Then reaction mass temperature was slowly raised to RT and stirred for overnight at same temperature. The progress of the reaction was monitored by TLC. After completion of the reaction (TLC), the mass was quenched in chilled water (10 mL). The pH of the mass was adjusted to ~ 9.5 using aqueous ammonia, the compound was extracted with DCM (3x5 mL). The combined organic phase was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (1:5:94) to afford the title compound. Yield: 0.013 grams (43%). 'H - NMR (5 ppm): 1.24 (6H, s), 1.30 - 1.38 (3H, m), 1.48 - 1.52 (2H, m), 1.63 - 1.66 (2H, m), 2.01 -2.06 (2H, m), 2.35 - 2.41 (2H, m), 2.86 - 2.89 (2H, m), 6.90 (2H, bs), 7.55 - 7.58 (1H, dd, J = 8.56, 4.16 Hz), 8.37 (1H, s), 8.83 - 8.85 (1H, m), 8.93 - 8.94 (1H, m), 10.88 - 10.90 (1H, t); Mass (m/z): 393.2 (M+H)+; 395.2 (M+H)+. Examples 47 to 48: The compounds of Examples 47 to 48 were prepared by following the experimental procedure as described in the Example 46 given above, with some noncritical variations. Example 49: Preparation of S-Amino-e-chloro-A^dl^-hydroxy ethyl)-4-piperidinylJ methyl} quinoline-8-carboxamide A solution of 5-amino-6-chloro-7/-[(4-piperidinyl)methyl] quinoline-8-carboxamide (0.1 grams, 0.313 mmole, obtained from preparation 2), bromoethanol (0.047 grams, 0.376 mmole) and potassium carbonate (0.086 grams, 0.623 mmole) in acetonitrile (15 mL) was stirred overnight at 85 °C, the progress of the reaction was monitored by TLC. After completion of the reaction (TLC), the reaction mass was concentrated and the obtained slurry was quenched in water (30 mL). The mass pH was adjusted to ~ 9.5 using aqueous ammonia, the compound was extracted with DCM (3 x 15 mL). The combined organic phase was washed with water (15 mL), brine solution (15 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (1:3:96) to afford the title compound. Yield: 0.07 grams (62%). 'H - NMR (5 ppm): 1.36 - 1.45 (3H, m), 1.72 - 1.85 (3H, m), 2.05 - 2.17 (2H, m), 2.50 - 2.53 (2H, m), 2.92 - 2.94 (2H, m), 3.47 - 3.50 (2H, m), 3.58 - 3.60 (2H, m), 4.97 (2H, s), 7.45 - 7.48 (1H, dd, J = 8.56; 4.20 Hz), 8.23 - 8.25 (1H, m), 8.78 (1H, s), 8.89 - 8.90 (1H, m), 11.07 - 11.12 (1H, t); Mass (m/z): 363.2 (M+H)+; 365.2 (M+H)+. Examples 50 to 51: The compounds of Examples 50 to 51 were prepared by following the experimental procedure as described in the Example 49 given above, with some noncritical variations. Example 52: Preparation of 5-Amino-6-chloro-/V-{[l-(2-fluoro ethyl)-4-piperidinylJmethyl} quinoline-8-carboxamide Nrt2 DAST (0.072 grams, 0.448 mmole) was added to a stirred solution of 5-amino-6-chloro-A^-{[l-(2-hydroxy ethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.07 grams, 0.179 mmole, obtained from Example 49) in DCM (5 mL) at - 30 °C. Then reaction mass temperature was slowly raised to RT and stirred overnight at same temperature. The progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the mass was quenched in chilled water (10 mL). The mass pH was adjusted to ~ 9.5 using aqueous ammonia, the compound was extracted with DCM (3x5 mL). The combined organic phase was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. Yield: 0.014 grams (20%). 'H - NMR (5 ppm): 1.22 - 1.34 (4H, m), 1.49 - 1.53 (1H, m), 1.66 - 1.69 (2H, m), 1.93 - 1.99 (2H, m), 2.51 - 2.53 (1H, m), 2.58 - 2.60 (1H, m), 2.86 - 2.88 (2H, m), 4.42 - 4.44 (1H, m), 4.54 - 4.56 (1H, m), 6.90 (2H, bs), 7.55 - 7.58 (1H, dd, J = 8.64,4.28 Hz), 8.37 (1H, s), 8.83 - 8.85 (1H, m), 8.93 - 8.94 (1H, m), 10.88 -10.91 (lH,t); Mass (m/z): 365.2 (M+H)+; 367.2 (M+H)+. Example 53: The compound of Example 53 was prepared by following the experimental procedure as described in the Example 52 given above, with some noncritical variations. Example 54: Preparation of 5-Amino-6-chloro-iV-{[3-(3-methoxy propyl)-3-azabicyclo[3.1.0]hex-6-yI]methyl} quinoline-8-carboxamide L(+)-tartarate Step (i): Preparation of 5-Amino-6-chtoro-Ar-{[3-(3-methoxy propyl)-3-azabicyclo[3.1.Gjhex-6-yljmethyl} quinoIine-8-carboxamide A solution of 5-Amino-6-chIoro-A^-{[3-azabicyclo[3.l.0]hex-6-yl]methyl} quinoline-8-carboxamide (0.05 grams, 0.141 mmole, obtained from preparation 4), 3-methoxy bromo propane (0.03 grams, 196 mmole) and potassium carbonate (0.065 grams, 0.471 mmole) in acetonitrile (5 mL) was stirred for 6 hours at 85 °C, the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (thin layer chromatography), the reaction mass was quenched into chilled water (5 mL). The compound was extracted with ethyl acetate (3x5 mL), the extract was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. Yield: 0.03 grams (55%). Step (ii): Preparation of 5-Amiito-6-chloro-A'-{l3-(3-methoxy propyl)-3-azabicyclo[3.1.0|hex-6-yI]methyl} quinoline-8-carboxamide L(+)-tartarate A solution of L(+)-tartaric acid (0.011 grams, 0.073 mole) in 2 mL methanol was added to a stirred solution of 5-Amino-6-chloro-A'-{[3-(3-methoxy propyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide (0.03 grams, 0.077 mole, obtainted from above step) in methanol (5 mL). The obtained clear mass was further stirred for 2 hrs at room temperature. The solvent was evaporated to afford solid mass. The solid mass was further triturated with diethyl ether (5 mL) and dried under reduced pressure to obtain title compound. Yield: 0.039 grams (95 %). 'H - NMR (8 ppm): 1.31 - 1.35 (1H, m), 1.42 - 1.50 (1H, m), 1.86 - 1.94 (4H, m), 3.10 - 3.11 (1H, m), 3.18 - 3.21 (3H, m), 3.41 - 3.49 (6H, m), 3.61 - 3.69 (2H, m), 4.41 (2H, s), 7.50 - 7.53 (1H, m), 8.49 (1H, s), 8.66 - 8.68 (1H, dd, J = 8.41, 1.42 Hz), 8.90 - 8.91 (1H, m); Mass (m/z): 389.3 (M+H)+, 391.4 (M+H)+. Example 55: Preparation of 5-Amino-6-chloro-yV-{[l-(3-inethoxy-2,2-dirnethyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate Step (i): Preparation of 5-Amino-6-chloro-A'-{[l-(3-methoxy-2,2-dimethyl-propyl)-4-piperidinyllmethyl} quinoline-8-carboxamide A solution of 5-amino-6-chIoro-A'-[(4-piperidinyl)methyl] quinoline-8-carboxamide (0.2 grams, 0.627 mmole, obtained from preparation 2), '3-methoxy-2,2-dimethyl propyl toluene-4-sulfonate (0.34 grams, 1.255 mmole, obtained from preparation 7), cesium carbonate (0.41 grams, 1.255 mmole) and potassium iodide (0.21 grams, 1.255 mmole) in dimethylformamide (5 mL) was stirred for 24 hours at 120 °C while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the reaction mass was cooled to room temperature and quenched onto chilled water (10 mL). The product was extracted with ethyl acetate (3x5 mL), the organic extracts were washed with water (5 mL), brine solution (5 mL) and dried over sodium sulfate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. Yield: 0.033 grams (12.5 %). 'H - NMR (8 ppm): 0.77 (6H, s), 1.22 - 1.30 (3H, m), 1.47 (1H, m), 1.61 - 1.63 (2H, m), 2.07 - 2.16 (5H, m), 2.69 - 2.72 (2H, m), 3.01 - 3.02 (2H, d), 3.19 (3H, s), 6.91 (2H, s), 7.55 - 7.58 (1H, dd, J = 8.52,4.20 Hz), 8.37 (1H, s), 8.83 - 8.85 (1H, m), 8.93 - 8.94 (1H, m), 10.88 - 10.91 (1H, t); Mass (m/z): 419.2 (M+H)+, 421.3 (M+H)+. Step (ii): Preparation of S-Amino-e-chloro-A^fl-^-methoxy-ljl-dimethyl propyl)-4-piperidinyI]methyl} quinoline-8-carboxamide L(+)-tartarate A solution of L(+)-tartaric acid (0.011 grams, 0.073 mole) in 2 mL methanol was added to a stirred solution of 5-amino-6-chloro-N-{[l-(3-methoxy-2,2-dirnethyl propyI)-4-piperidinyl]methyl} quinoline-8-carboxamide (0.033 grams, 0.078 mole, obtainted from above step) in methanol (5 mL). The clear mass was further stirred for 2 hrs at room temperature. The solvent was evaporated, the residual solid mass was triturated with diethyl ether (5 mL) and dried under reduced pressure to obtain title compound. Yield: 0.042 grams (95 %). lH - NMR (6 ppm): 1.06 (6H, s), L67 - 1.70 (2H, m), 1.98 - 2.01 (3H, m), 2.98 - 3.02 (4H, m), 3.37 (3H, s), 3.41 - 3.50 (6H, m), 4.38 (2H, s), 7.51 - 7.55 (1H, d, J = 8.60,4.20 Hz), 8.50 (1H, s), 8.67 - 8.69 (1H, m), 8.91-8.92 (lH,m); Mass (m/z): 419.3 (M+H)+, 421.3 (M+H)+. Example 56: Preparation of 5-Amino-6-chloro-Ar-{[l-(2-methoxy-2-methyI propyl)-4-piperidinyljmethyl} quinoline-8-carboxamide A solution of 5-amino-6-chloro-iV-[(4-piperidinyl)rnethyl] quinoline-8-carboxamide (0.15 grams, 0.471 mmole, obtained from preparation 2), toluene-4-sulfonic acid 2-methoxy-2-methyl-propyl ester (0.25 grams, 0.968 mmole, obtained from preparation 8), cesium carbonate (0.31 grams, 0.968 mmole) and potassium iodide (0.156 grams, 0.968 mmole) in dimethylformamide (5 mL) was stirred for 24 hours at 120 °C, the progress of the reaction was monitored by TLC. After completion of the reaction (TLC), the reaction mass was cooled to room temperature and quenched into chilled water (10 mL). The compound was extracted with ethyl acetate (3x5 mL), the extract was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulphate. The organic phase was concentrated on rotavacuum to obtain the crude residue, which was further purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. 'H - NMR (5 ppm): 1.06 (6H, s), 1.23 -1.27 (4H, m), 1.35 -1.42 (1H, m), 1.61 -1.64 (2H, m), 2.01 -2.07 (2H, m), 2.49 (2H, s), 2.88 -2.94 (2H, m), 3.02 (3H, s), 6.89 (2H, s), 7.54 -7.58 (1H, dd, J = 8.56, 4.20 Hz), 8.37 (1H, s), 8.83 -8.85 (1H, d, J = 8.6 Hz), 8.93 -8.94 (1H, d, J = 3.64 Hz), 10.87 -10.90 (1H, t); Mass (m/z): 405.3 (M+H)+; 407.2 (M+H)+. Example 57 to 58: The compounds of Examples 57 to 58 were prepared by following the experimental procedure as described in the Example 56 given above, with some noncritical variations. Example 59: Preparation of 5-Amino-6-chloro-A'-{[4-fluoro-l-(3-methoxy-2,2-dimethyl propyI)-4-piperidinyl]methyl} quinoline-8-carboxamide A solution of 5-amino-6-chloro-A44-fluoro-(4-piperidinyl)methyl] quinoline-8-carboxamide (0.2 grams, 0.529 mmole, obtained from preparation 5), 3-methoxy-2,2-dimethyl propyl toluene-4-sulfonate (0.32 grams, 1.19 mmole, obtained from preparation 7), cesium carbonate (0.39 grams, 1.19 mmole) and potassium iodide (0.2 grams, 1.20 mmole) in dimethylformamide (5 mL) was stirred for 24 hours at 120 °C and the progress of the reaction was monitored by TLC. After completion of the reaction (TLC), the reaction mass was cooled to room temperature and quenched onto chilled water (10 mL). The product was extracted with ethyl acetate (3x5 mL) and the combined organic extract was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulfate. The organic phase was concentrated on rotavacuum and the residual mass was purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. Yield: 0.032 grams (12.5 %). 'H - NMR (8 ppm): 0.79 (6H, s), 1.24 - 1.30 (3H, m), 1.63 - 1.65 (2H, m), 2.09 - 2.15 (5H, m), 2.70 -2.74 (2H, m), 3.03 - 3.04 (2H, m), 3.18 (3H, s), 6.92 (2H, s), 7.54 - 7.57 (IH, dd, J = 8.62,4.24 Hz), 8.39 (1H, s), 8.84 - 8.86 (lH,m), 8.94-8.95 (lFLm), 10.98-11.00 (lH,t); Mass (m/z): 437.2 (M+H)+, 439.3 (M+H)+. Example 60: Preparation of 5-Amino-6-chIoro-A'-{[4-fIuoro-l-(2-methoxy-2-methyl propyl)-4-piperidinyljmethyl} quinoline-8-carboxantide A solution of 5-amino-6-chloro-A^-[4-fluoro-(4-piperidinyl)methyl] quinoline-8-carboxamide (0.15 grams, 0.446 mmole, obtained from preparation 5), 2-methoxy-2-methyl-propyl toluene-4-sulfonate (0.23 grams, 0.892 mmole, obtained from preparation 8), cesium carbonate (0.29 grams, 0.892 mmole) and potassium iodide (0.148 grams, 0.892 mmole) in dimethylformamide (5 mL) was stirred for 24 hours at 120 °C while monitoring the progress of the reaction by TLC. After completion of the reaction (TLC), the mass was cooled to room temperature and quenched onto chilled water (10 mL). The product was extracted with ethyl acetate (3x5 mL), the combined organic extract was washed with water (5 mL), brine solution (5 mL) and dried over sodium sulfate. The organic phase was concentrated on rotavacuum and the residual mass was purified by flash chromatography using TEA: methanol: chloroform (0.5:2:97.5) to afford the title compound. Yield: 0.024 grams (12.76 %). lH - NMR (5 ppm): 1.10 (6H, s), 1.25 - 1.31 (2H, m), 1.63 - 1.66 (2H, m), 1.82 - 1.92 (2H, m), 2.10 -2.16 (2H, m), 2.68 - 2.72 (2H, m), 3.03 - 3.04 (2H, m), 3.23 (3H, s), 6.90 (2H, s), 7.55 - 7.59 (1H, dd, J = 8.60,4.20 Hz), 8.40 (1H, s), 8.86 - 8.88 (1H, m), 8.94 - 8.95 (1H, m), 10.91 - 10.94 (1H, t); Mass (m/z): 423.3 (M+H)+, 425.3 (M+H)+. Example 61 to 62: The compounds of Examples 61 to 62 were prepared by following the experimental procedure as described in the Example 60 given above, with some noncritical variations. Biological Assays Example 63: Determination of EC50 values for 5-HT4 receptor: A stable CHO cell line expressing recombinant human 5-HT4 receptor and pCRE-Luc reporter system was used for cell-based assay. The assay offers a non-radioactive based approach to determine binding of a compound to GPCRs. In this specific assay, the level of intracellular cyclic AMP, which is modulated by activation, or inhibition of the receptor is measured. The recombinant cells harbor luciferase reporter gene under the control of cAMP response element. The above cells were grown in 96 well clear bottom white plates in Hams F12 medium containing 10 % fetal bovine serum (FBS). Prior to the addition of compounds or standard agonist, cells were serum starved overnight Increasing concentrations of test compounds were added in OptiMEM medium to the cells. The incubation was continued at 37 °C in C02 incubator for 4 hours. Medium was removed and cells were washed with phosphate buffered saline. The cells were lysed and luciferase activity was measured in a Luminometer. Luminescence units were plotted against the compound concentrations using Graphpad software. EC50 values of the compounds were defined as the concentration required in stimulating the luciferase activity by 50 %. Example 64: Rodent Pharmacokinetic Study Male wistar rats (225 ± 25 grams) were used as experimental animals. Three to five animals were housed in each cage. Two days prior to dosing day, male wistar rats (225 - 250 grams) were anesthetized with isoflurane for surgical placement of jugular vein catheter. Animals were fasted over night before oral dosing (p.o) and food pellets were allowed 2 hours post dosing, whereas during intravenous dosing food and water were provided as ad libitum. Three rats were dosed with compounds of formula (I) (3 mg/kg) orally and intravenously (1 mg/kg). At each time point blood was collected through jugular vein and immediately replenish with an equivalent volume of normal saline from freely moving rats. Collected blood was transferred into a labeled eppendr off containing 10 uL of heparin as anticoagulant. Typically blood samples were collected as following time points: Pre dose, 0.08 (only i.v.), 0.25, 0.5, 1, 2, 4, 6, 8, and 24 hours post dose (n=3). Blood was centrifuged at 4000 rpm for 10 minutes. Plasma was prepared and stored frozen at -20 °C until analysis. The concentrations of the compounds of formula (I) were quantified in plasma by qualified LC-MS/MS method using suitable extraction technique. The compounds of formula (I) were quantified in the calibration range around 2-2000 ng/mL in plasma Study samples were analyzed using calibration samples in the batch and quality control samples spread across the batch. Pharmacokinetic parameters Cmax, Tmax, AUQ, Tm and Bioavailability were calculated by non-compartmental model using standard non-compartmental model by using WinNonLin 5.0.1 or Phoenix WinNonlin 6.2 version Software package. Example 65: Rodent Brain Penetration Study Male Wistar rats (225 ± 25 grams) were used as experimental animals. Three animals were housed in each cage. Animals were given water and food ad libitum throughout the experiment and maintained on a 12 hours light/dark cycle. Brain penetration was determined in discrete manner in rats. One day prior to dosing day, male wistar rats (225 - 250 grams) were acclimatized. After acclimatization the rats were grouped according to their weight. In each group, 3 animals were kept in individual cage and allowed free access to food and water. At each time point (0.50,1, and 2 hours) n = 3 animals were used. The compounds of formula (I) were suitably preformulated and administered orally at (free base equivalent) 3 mg/kg. Blood samples were removed via, cardiac puncture by using isoflurane anesthesia. The animals were sacrificed to collect brain tissue. Plasma was separated and brain samples were homogenized and stored frozen at -20 °C until analysis. The concentrations of the compounds of formula (I) in plasma and brain were determined using LC-MS/MS method. The compounds of formula (I) were quantified in plasma and brain homogenate by qualified LC-MS/MS method using suitable extraction technique. The compounds of formula (I) were quantified in the calibration range of 1-500 ng/mL in plasma and brain homogenate. Study samples were analyzed using calibration samples in the batch and quality control samples spread across the batch. Extent of brain-plasma ratio was calculated (CyCp). Example 66: Estimation of mice brain cortical sAPPa levels Experimental Procedure: The control group of mice received sterile water for injection subcutaneously (s.c.). The treated groups (9 mice per group) received a single s.c. injection of test compound (different doses) in a volume of 5.0 mL/kg) or prucalopride (10.0 mg/kg in a volume of 5.0 mL/kg) dissolved in sterile water for injection. Mice were sacrificed 60 minutes after the drug injection by cervical dislocation, the brains were quickly isolated and the cortex was dissected at -20 °C. The cortex was immediately kept on a dry ice and weighed before being stored at -80 °C until Emyme-linked immunosorbent assay (ELISA) was performed. Sample Preparation: 1. Brain tissues were thawed and Tris Buffer Saline containing protease inhibitors (TBS, 4 times by volume) added (0.8 mL/200 mg tissues). 2. Brain tissue samples were homogenized using glass-Teflon homogenizer at 10 strokes. The resulting homogenates were centrifuged at 15,000 rpm at 4 °C for 60 minutes. 3. The supernatant was discarded and to the precipitate, 4 times volume (0.8 mL/200 mg tissues) of TBS was added. Again homogenized followed by centrifugation at 15,000 rpm 4 °C for 30 minutes. 4. From the above centrifuged mixture the supernatant was discarded and 10 times volume of 6M Guanidine-HCl in 50 mM Tris buffer pH:7.6 (500 uL/50 mg tissues) was added. The resulting solution was sonicated for 5 seconds, 4 times. 5. Resulting mixture was incubated at the RT for 30 minutes, followed by centrifugation at 15,000 rpm, 4 °°C for 30 minutes. From this 5 uL of supernatant solution was taken and diluted with 155 uL of EIA buffer (dilution factor 32). Measurement of sAPPa by ELISA Kit-To investigate the role of an acute treatment of test compound on sAPPa levels, we measured the expression of this protein in homogenates from the cortex of treated and untreated mice by ELISA assay. The entire procedure was followed as described in the ELISA kit manual (Mouse/Rat sAPPa ELISA, Catalog Number: JP27415, Innovation Beyond Limits International, Hamburg, Germany). Statistical analysis: Statistical analyses were performed using the Graph Pad Prism (Version 4). Data are Mean ± SD of sAPPa levels expressed as percentage of control values (mice which received water for injection). Values were compared between the different groups by using unpaired t test. The significance level was set at */K0.05; **p<0.0V, ***p<0.00l. Result for Example 13 (Figure 1) At 60 minutes post treatment, the compound of Example 13 showed significant increase in the mice brain cortical sAPPa levels i.e. 39 %, 41 %, 46 % and 66 % when tested at doses 0.3, 1.0,3.0, and 10.0 mg/kg, s.c. respectively. The positive control, 5-HT4 receptor agonist, prucalopride significantly increased the level of sAPPa in adult mice cortex at 10.0 mg/kg s.c. (These results are in line with results of reported literature, reference: British Journal of Pharmacology, 2007,150,883 - 892). Other references: Journal of Pharmacology and Experimental Therapeutics, 2003, 305, 864 - 871; Current Pharmaceutical Design 2006, 12, 671 - 676 and Journal of Pharmacology and Experimental Therapeutics 2006, 317, 786 - 790. Result for Example 23 (Figure 2) At 60 minutes post treatment, the compound of Example 23 showed significant increase in the mice brain cortical sAPPa levels i.e. 42 % and 33 % at 0.3 and 1.0 mg/kg, s.c. dose respectively. The positive control, 5-HT4 receptor agonist, prucalopride significantly increased the level of sAPPa in adult mice cortex at 10.0 mg/kg s.c. (These results are in line with results of reported literature, reference: British Journal of Pharmacology, 2007,150, 883 - 892). Example 67: To evaluate the effect of compounds of present invention on modulation of acetylcholine from the ventral hippocampus of male Wistar rats. Experimental Procedure: Male Wistar rats (240 - 300 gram body weights) were stereotaxically implanted with a microdialysis guide cannula in the ventral hippocampus (AP: -5.2 mm, ML: +5.0 mm, DV: -3.8 mm). Co-ordinates were taken according to Paxinos and Watson (2007) with reference points taken from bregma and vertical from the skull. The rats were allowed to recover individually for five days in a round bottom Plexiglas bowl with free access to feed and water. One day prior to the microdialysis experiment, rats were connected to a dual quartz lined two-channel liquid swivel (Instech, UK) on a counter balance lever arm, which allowed unrestricted movements of the animal. Sixteen hour before start of the study, a pre-equilibrated microdialysis probe (4 mm dialysis membrane) was inserted into the ventral hippocampus through the guide cannula. On the day of study, probe was perfused at a constant flow rate of 1.5 uL/min with artificial cerebrospinal fluid (aCSF; NaCl 147 mM, KC1 3.0 mM, MgCl2 1.0 mM, CaCi2. 2H20 1.3 mM, NaH2P04.2H20 0.2 mM and Na2HP04.7H20 1.0 mM, pH 7.2). A stabilization period of 2 h was maintained and five basal samples were collected at 20 min intervals. Compound or vehicle was administered and dialysate samples were collected at 20 min interval for an additional period of 4 h. Dialysates were stored below -70 °C until quantitation of acetylcholine. Quantitation of acetylcholine: Acetylcholine in dialysate was quantified in the calibration range of 0.103 nmol - 103.497 nmol using LC-MS/MS method. Statistical analysis: All microdialysis data were plotted as percent change from mean dialysate basal concentrations with 100% defined as the average of five predose values. The AUC was calculated by trapezoidal rule using WinNonlin (5.0.1 version, Pharsight Corp. CA). The statistical significance between the mean AUC values of treatment groups with vehicle was calculated using one-way ANOVA followed by Dunnett's test. For each treatment group, the percent increase in acetylcholine levels was compared to the vehicle group using two-way analysis of variance (time and treatment), followed by Bonferroni's multiple comparison test Statistical significance was considered at ap value less than 0.05. Incorrect probe placement was considered as criteria to reject the data from animal. References: Neuropharmacology, 2007, 53, 563 - 573; Paxinos G and Watson C (2007) Rat brain in stereotaxic coordinates. Academic Press, New York. Result of Example 13 (Figures 3 and 4): The compound of Example 13 produced dose dependent increase in acetylcholine levels from the ventral hippocampus of male Wistar rats (Figure 3, Effect of compound of Example 13 (3.0 and 10.0 mg/kg, p.o.) on acetylcholine levels in ventral hippocampus of male Wistar rats. Values are expressed as mean ± SEM. */K0.05, ***p <0.001). Area under the curve values calculated to evaluate the overall effect of treatment was significant after treatment with compound of Example 13 (10.0 mg/kg, p.o.) (Figure 4, Cumulative changes in acetylcholine levels expressed as mean area under the curve (AUC) ± S.E.M. of % change from mean basal value for each treatment group. **p <0.01) Example 68: To evaluate the effect of compounds of present invention on modulation of acetylcholine from the frontal cortex of male Wis tar rats. Experimental Procedure: Male Wistar rats (240 - 300 gram body weights) were stereotaxically implanted with a microdialysis guide cannula in the frontal cortex (AP: +3.2 mm, ML: -3.2 mm,' DV: -1.5 mm). Co¬ordinates were taken according to Paxinos and Watson (2007) with reference points taken from bregma and vertical from the skull. The rats were allowed to recover individually for five days in a round bottom Plexiglas bowl with free access to feed and water. One day prior to the microdialysis experiment, rats were connected to a dual quartz lined two-channel liquid swivel (Instech, UK) on a counter balance lever arm, which allowed unrestricted movements of the animal. Sixteen hour before start of the study, a pre-equilibrated microdialysis probe (3 mm dialysis membrane) was inserted into the frontal cortex through the guide cannula. On the day of study, probe was perfused at a constant flow rate of 1.5 uL/min with artificial cerebrospinal fluid (aCSF; NaCl 147 mM, KC1 3.0 mM, MgCl2 1.0 raM, CaCl2. 2H20 1.3 mM, NaH2P04.2H20 0.2 mM and Na2HP0„.7H20 1.0 mM, pH 7.2). A stabilization period of 2 h was maintained and five basal samples were collected at 20 minutes intervals. The compound of Example 18 or vehicle was administered and dialysate samples were collected at 20 minutes interval for an additional period of 4 hours. Dialysates were stored below -70 °C until quantitation of acetylcholine. Quantitation of acetylcholine: Acetylcholine in dialysate was quantified in the calibration range of 0.103 nmol - 103.497 nmol using LC-MS/MS method. Statistical analysis: All microdialysis data were plotted as percent change from mean dialysate basal concentrations with 100% defined as the average of five predose values. The AUC was calculated by trapezoidal rule using WinNonlin (5.0.1 version, Pharsight Corp. CA). The statistical significance between the mean AUC values of treatment groups with vehicle was calculated using one-way ANOVA followed by Dunnett's test. For each treatment group, the percent increase in acetylcholine levels was compared to the Vehicle group using two-way analysis of variance (time and treatment), followed by Bonferroni's multiple comparison test Statistical significance was considered at &p value less than 0.05. Incorrect probe placement was considered as criteria to reject the data from animal. References: Current Drug Targets - CNS & Neurological Disorders, 2004, 3, 39-51; Paxinos G and Watson C (2007) Rat brain in stereotaxic coordinates. Academic Press, New York Result of Example 13 (Figure 5 and 6): The compound of Example 13 produced dose dependent increase in acetylcholine levels from the frontal cortex of male Wistar rats (Figure 5, effect of compound of Example 13 (3.0 and 10.0 mg/kg, p.o.) on acetylcholine levels in the frontal cortex of male Wistar rats. Values are expressed as mean ± SEM. */X0.05, **p <0.01, ***p O.001). Area under the curve values calculated to evaluate the overall effect of treatment was significant after treatment with compound of Example 13 (10.0 mg/kg, p.o.) (Figure 6, cumulative changes in acetylcholine levels expressed as mean area under the curve (AUC) ± S.E.M. of % change from mean basal value for each treatment group. *p <0.05). Example 69: To evaluate the effect of compounds of present invention on CSF Ap i^o level in male Sprague Dawley rat. Experimental Procedure: The control group of male rats received a vehicle (reagent grade water) per orally by gavage at a dose volume of 10 mL/kg. The treated groups (6 rat per group) received a single dose of test compound (different doses) or DAPT (50.0 mg/kg). Two hour post dose of vehicle or test compounds, rats were anesthetized with isoflurane and CSF was collected from Cisterna magna using 0.5 mL syringes by utilizing stereotaxic frame. The CSF samples were frozen in liquid nitrogen and stored at -80 °C until ELISA was performed. Sample Preparation: 1. CSF samples were thawed to RT and diluted with Tris Buffer Saline containing protease inhibitors at 1:10 ratio [15:150 uL (15 uL CSF + 135 uL TBS]. 2. To this diluted CSF samples 0.15 mL of EIA buffer (1:1 ratio) was added. These diluted samples were subjected for ApMo level measurement by ELISA. Measurement of Ap^ by ELISA Kit: To investigate the role of an acute treatment of test compound on ApMo levels, expression of this protein in CSF was measured in treated and untreated rat by ELISA assay. The entire procedure was followed as per ELISA kit manual (Mouse/Rat Amyloid-pM0 ELISA, Cat No: 27721, IBL International, Hamburg, Germany): Statistical analysis: Statistical analysis was performed using the Graph Pad Prism (Version 4). Data are Mean ± SD of A01.4O levels expressed as percentage of control values (rat which received regent grade water). Values were compared between the different groups by using unpaired t test. The significance level was set at *p<0.05; **p<0.01; ***/?<0.001. References: Current Pharmaceutical Design 12, 671 - 676, 2006; Journal of Pharmacology and Experimental Therapeutics, 305, 864 - 871, 2003 and Journal of Pharmacology, and Experimental Therapeutics, 317,786 - 790,2006. Results for Example 1 (Figures 7 and 8) The compound of Example 1 shown significant decrease in the rat CSF A0MO levels at hso hour i.e. 27, 24,40,22, and 29 % when tested at doses 0.03,0.1,0.3, 1.0, and 3.0 mg/kg, p.o. respectively. The positive control DAPT significantly decreased the level of ApM0 in rat CSF at 50.0 rug/kg p.o. (In line with literature). Example 70: To evaluate the effect of compounds of present invention on CSF AfJ M2 level in male Sprague Dawley rat. Experimental Procedure: The control group of male rats received a vehicle (reagent grade water) per oraiiy by gavage at a dose volume of 10 mL/kg. The treated groups (6 rat per group) received a single dose of test compound (different doses) or DAPT (50.0 mg/kg). Two hour post dose of vehicle or test compounds, rats were anesthetized with isoflurane and CSF was collected by puncturing Cisterna magna using 0.5 mL syringes by utilizing stereotaxic frame. CSF samples were frozen in liquid nitrogen and stored at -80 °C until ELISA was performed. Sample Preparation: 1. CSF samples were thawed to RT and diluted with Tris Buffer Saline containing protease inhibitors at 1:10 ratio [15:150 uL (15 uL CSF + 135 uL TBS]. 2. To this diluted CSF samples 0.15 mL of EIA buffer (1:1 ratio) was added. These diluted samples were subjected for Ap^ level measurement by ELISA. Measurement of ApM2 by ELISA Kit: To investigate the role of an acute treatment of test compound on ApM2 levels, expression of this protein was measured in CSF of treated and untreated rat by ELISA assay. The entire procedure was followed as described in ELISA kit manual (Mouse/Rat Amyloid-pM0 ELISA, Cat No: 27720, IBL International, Hamburg, Germany). Statistical analysis: Statistical analyses were performed using the Graph Pad Prism (Version 4). Data are Mean ± SD of APi.42 levels expressed as percentage of control values (rat which received regent grade water). Values were compared between the different groups by unpaired t test. The significance level was set at *p<0.05; **pO.0l; ***p<0.00l. References: Current Pharmaceutical Design 12, 671 - 676, 2006; Journal of Pharmacology and Experimental Therapeutics, 305, 864 - 871, 2003 and Journal of Pharmacology and Experimental Therapeutics, 317, 786 - 790,2006. Results for Example 1 (Figures 9 and 10) At two hour post treatment, the compound of Example 1 showed significant decrease in the rat CSF AP,^ levels i.e. 25, 21,35, 22, and 26 % when tested at doses 0.03, 0.1, 0.3, 1.0, and 3.0 mg/kg, p.o. dose respectively. The positive control DAPT significantly decreased the levels of APi^2 in rat CSF at 50.0 mg/kg p.o. (In line with the literature). Example 71: Object Recognition Task Model The cognition enhancing properties of compounds of this invention were estimated by using this model. Male Wistar rats (230 - 280 grams) were used as experimental animals. Four animals were housed in each cage. Animals were kept on 20 % food deprivation before one day and given water ad libitum throughout the experiment and maintained on a 12 hours light/dark cycle. Also the rats were habituated to individual arenas for 1 hour in the absence of any objects. One group of 12 rats received vehicle (1 mL/Kg) orally and another set of animals received compound of the formula (I> either orally or i.p., before one hour of the familiar (Tl) and choice trial (T2). The experiment was carried out in a 50 x 50 x 50 cm open field made up of acrylic. In the familiarization phase, (Tl), the rats were placed individually in the open field for 3 minutes, in which two identical objects (plastic bottles, 12.5 cm height x 5.5 cm diameter) covered in yellow masking tape alone (al and a2) were positioned in two adjacent comers, 10 cms from the walls. After 24 hours of the (Tl) trial for long-term memory test, the same rats were placed in the same arena as they were placed in Tl trial. Choice phase (T2) rats were allowed to explore the open field for 3 minutes in presence of one familiar object (a3) and one novel object (b) (Amber color glass bottle, 12 cm high and 5 cm in diameter). Familiar objects presented similar textures, colors and sizes. During the Tl and T2 trial, explorations of each object (defined as sniffing, licking, chewing or having moving vibrissae whilst directing the nose towards the object at a distance of less than 1 cm) were recorded separately by stopwatch. Sitting on an object was not regarded as exploratory activity, however, it was rarely observed. Tl is the total time spent exploring the familiar objects (al + a2). T2 is the total time spent exploring the familiar object and novel object (a3 + b). The object recognition test was performed as described by Behaviour Brain Research, (1988), 31, 47-59. Example 72: Radial arm maze The cognition enhancing properties of compounds of formula (I) of this invention were estimated by using this model. Radial arm maze consists of a central hub of 45 cm diameter. Each arm was of dimension 42.5 x 15 x 24 cm. The maze was elevated to a height of 1 m above the ground. The animals were placed on a restricted diet until they reached approximately 85 % of their free feeding weight. During this diet restriction period animals were habituated to the novel feed (pellets). Once the rats reached approximately 85 % of their free feeding weight rats were habituated to the maze on the 1st and 2nd day. The animals that did not eat the pellets were rejected from the study. Animals were randomized on day 2. On the subsequent days the treatment was given as per the allotment. Each animal was introduced into the maze individually for a period of 10 minutes. The arms were baited only once and the animal had to leam the rule that repeated arm entries would not be rewarded. The trial ended once the rat had visited 16 arms or 10 minutes were over or all the pellets were eaten. The arm entries were recorded using the software. Once the trial was over the rat was removed and the maze was cleaned using soap water. We claim: 1. A compound of the general formula (I): or a pharmaceutically acceptable salt thereof, wherein, "X" is hydrogen or halogen; "vn/w" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; R2 is hydrogen, hydroxy or fluoro; R» is alkyl, cycloalkyl, cycloalkylalkyl, / N or n ; R5 is halo, hydroxy, alkoxy, "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 3, both inclusive. 2. A compound selected from: (a) a compound of formula ([a): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "v/vwr" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; R[ is hydrogen, hydroxy or halogen; R« is alkyl, cycloalkyl or cycloalkylalkyl; "m" is an integer ranging from 0 to 1, both inclusive; (b) a compound of formula (Ib-1): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; <\/V\A/>" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (c) a compound of formula (Ib-2): 11117 or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; '\A/wr" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (d) a compound of formula (Ic-1): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "««w" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; R( is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (e) a compound of formula (Ic-2): O or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; ">AAA^" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; R, is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (f) a compound of formula (Ic-3): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "v/wv>" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; R, is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (g) a.compound of formula (Ic-4): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "vA/wr" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (h) a compound of formula (Id-1): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "i/vwo" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (i) a compound of formula (Id-2): or a pharmaceutical^ acceptable salt thereof, wherein, "X" is halogen; '\zwvr" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Rt is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; (j) a compound of formula (Ie-1): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; 'WvAr«" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; R[ is hydrogen, hydroxy or halogen; "tn" is an integer ranging from 0 to I, both inclusive; "n" is an integer ranging from 0 to 2, both inclusive; (k) a compound of formula (Ie-2): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "v/vn/vo" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Rt is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 2, both inclusive; (1) a compound of formula (Ie-3): or a pharmaceutically acceptable salt thereof, wherein, "X" is halogen; "v/w\r" is a bond represents racemic mixture, R-enantiomer, S-enantiomer, exo isomer, endo isomer or achiral; Ri is hydrogen, hydroxy or halogen; "m" is an integer ranging from 0 to 1, both inclusive; "n" is an integer ranging from 0 to 2, both inclusive. 3. The compound according to claim 1, which is selected from the group consisting of: 5-Amino-6-chloro-Ar- {[ 1 -(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide hemifumarate; 5-Amino-6-chloro-//-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamideL(+)-tartarate; 5-Amino-6-chloro-JV-[ 1 -(tetrahydro-2//-pyran-4-ylmethyl)-4-piperidinyl] quinoline-8-carboxamide; (R,S) 5-Amino-6-chloro-A/-{[l-(tetrahydro-3-furanylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; (R,S)5-Amino-6-chloro-A'-{[l-(tetrahydro-2-furanylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-A'-{[ 1 -(tetrahydro-2i/-pyran-4-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[3-(tetrahydro-3-furanylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-AT-{[3-isobutyl-3-azabicyclo[3.1.0]hex-6-yl]methyl}quinoline-8-carboxamideL(+)- tartarate; 5-Amino-6-chloro-A^-{[3-cyclopropylmethyl-3-azabicyclo[3.1.0]hex-6-yI]methyl} quinoline-8- carboxamide L(+)-tartarate; S-Amino^-chloro-A^P-isopropyW-azabicyclop. 1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)- tartarate; 5-Amino-6-fluoro-N- {[ 1 -(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl] methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chioro-A'-{[l-{tetrahydro-2H-pyran-4-ylmethyl)-3-pyrrolidinyI] methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'- {[ 1 -(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; (Exo) 5-Amino-6-chloro-A'-{ [3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide; 5-Amino-6-chloro-Ar-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide (exo/endo mixture); 5-Amino-6-bromo-Af- {[ I -(tetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl] methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-bromo-A^{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A^-{[l-(tetrahydro-2-ruranylmethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino^-fluoro-Ar-{[3-(tetrahydro-2H-pyran-4-ylmethyl)-3-a2abicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-Ar- {[4-fluoro-1 -(tetrahydro-2H-pyran-4-yImethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; (R,S) 5-Amino-6-chloro-iV-{[4-fluoro-1 -(tetrahydro-3-furanylmethyl)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[4-hydroxy-l-(tetrahydro-2H-pyran-4-yl methyl)-4-piperidinyl] methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Ammo^^hloro-A^-{[H4-hydroxytetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl]methyl} quinoline- 8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-[ 1 -(4-hydroxytetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl] quinoline-8- carboxamide; 5-Amino-6-chloro-A'- {[3 -(4-hydroxytetrahydro-2H-pyran-4-ylmethyl)-3-azabicyclo[3.1.0]hex-6- yljmethyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino^^;hloro-iV-{[l-(4-hydroxytetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl]metiiyl} quinoline- 8-carboxamide; 5-Ammo^-chloro-JV^{[4-fluoro-l-(4-hydroxytetrahydro-2H-pyran^-ylmemylH-P>peridmyl]me%^ quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-fluoro-A^-{[l-(4-hydroxytetrahydro-2H-pyran-4-ylmethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[4-hydroxy-l-(4-hydroxy tetrahydro-2H-pyran-4-yl methyl)-4-piperidinyl] methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-Af-{[ 1 -(4-fluorotetrahydro-2//-pyran-4-ylmethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[l-(2-methoxy carbonyl-2-methyl propan-l-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide; S-Amino^-chloro-iV-ffl-^^-dimethyl proponic acid-3-yl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-iV-{[l-(3-hydroxy-2,2-dimethyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[3-(3-hydroxy-2,2-dimethyl propyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-iV-{[l-(2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-iV-{[4-fluoro-l-(2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide; 5-Amino-6-chloro-A'-{[4-fluoro-l-(2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'-{[4-£luoro-l-(2-hydroxy-2-methylpropyI)-4-piperidinyl]methyl}quinoline-8-carboxamide hydrochloride; 5-Amino-6-chloro-A'-{[4-fluoro-l-(2-hydroxy-2-methylpropyl)-4-piperidinyl]methyI}quinoline-8-carboxamide fumarate; 5-Amino-6-chloro-A/-{[3-(2-hydroxy-2-methyl propyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-fluoro-A'-{[l-(2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-fluoro-iV:-{[4-fluoro-l-(2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide; 5-Amino-6-fluoro-AT-{[4-fluoro-l-<2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Amino-6-bromo-A'-{[l-(2-hydroxy-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide L(+)-tartarate; 5-Ammo^-bromo-A^{[4-fluoro-H2-hydroxy-2-methylpropyl)-4-piperidinyl]methyl}quinoline-8-carboxamide L(+>tartarate; S-Amino^-chloro-A^-ffl^-fluoro^-methylpropylH-piperidinyymethyl} quinoline-8-carboxamide; 5-Ammo-6-chloro-JV-{[3-(2-fluoro-2-methyl propyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-A^-{[4-fluoro-l-(2-fluoro-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8- carboxamide; 5-Ammo-6-chloro-A^[l-(2-hydroxyethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide; 5-Amino-6-chloro-A'-{[3-(2-hydroxyethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-A/-{[3-(3-hydroxy propyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-A'-{[l-(2-fluoroethyl)-4-piperidinyl]methyl} quinoline-8-carboxamide; 5-Amino-6-chloro-Ar-{[3-(2-hydroxyethyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-AL{[3-(3-methoxy propyl)-3-azabicyclo[3.1.0]hex-6-yl]methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-A'- {[ 1 -(3-methoxy-2,2-dimethyl propyl)-4-piperidinyl]methyl} quinoline-8- carboxamide L(+)-tartarate; 5-Amino-6-chloro-Af-{[ 1 -(2-methoxy-2-methyl propyl)-4-piperidinyI]methyl} quinoline-8-carboxamide; 5-Ammo-6-fluoro-Af-{[l-(2-methoxy-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8-carboxamide; 5-Amino-6-bromo-Ar-{[l-(2-methoxy-2-methylpropyl)-4-piperidinyl]methyl} quinoline-8-carboxamide; 5-Amino-6-chloro-iV-{[4-fluoro-l-(3-methoxy-2,2-dimethylpropyl)-4-piperidinyl]methyl} quinoline-8- carboxamide; 5-Amino-6-chloro-Af- {[4-fluoro-1 -(2-methoxy-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8- carboxamide; 5-Amino-6-fluoro-Af-{[4-fluoro-1 -(2-methoxy-2-methyl propyl)-4-piperidinyl]methyl} quinoline-8- carboxamide; and 5-Amino-6-bromo-AT-{[4-fluoro-l-(2-methoxy-2-methylpropyl)-4-piperidinyI]methyl} quinoline-8- carboxamide; or pharmaceutically acceptable salt thereof. 4. A pharmaceutical composition comprising a compound according to any of claims 1 to 2 and pharmaceutically acceptable excipients. 5. The pharmaceutical composition according to claim 5, for the treatment of clinical conditions mediated through 5-HT4 receptor agonists such as alzheimer's disease, schizptierenia, attention deficit hyperactivity disorder, huntington's disease, parkinson's disease, depression, psychiatric disorders, pain or gastrointestinal disorders. 6. A method of treating alzheimer's disease, schizpherenia, attention deficit hyperactivity disorder, huntington's disease, parkinson's disease, depression, psychiatric disorders, pain or gastrointestinal disorders, comprising administering to a patient in need thereof an effective amount of a compound or pharmaceutically acceptable salt thereof according to any one of claims 1 to 3. 7. Use of a compound according to any one of the claims 1 to 3 in the manufacture of medicament for the treatment of diseases related to 5-HT4 receptor agonists. 8. The use of compound according to' the claim 7, for the treatment of clinical conditions such as alzheimer's disease, schizpherenia, attention deficit hyperactivity disorder, huntington's disease, parkinson's disease, depression, psychiatric disorders, pain or gastrointestinal disorders.