NOVEL SUBSTITUTED INDOLYL COMPOUNDS AND THEIR USE AS 5-HT6 LIGANDS
FIELD OF INVENTION
The present invention relates to novel substituted indolyl compounds of the formula (I), their derivatives, their stereoisomers, their pharmaceutically acceptable salts and pharmaceutically acceptable compositions containing them.

The present invention also relates to a process for the preparation of above said novel compounds, their derivatives, their stereoisomers, their pharmaceutically acceptable salts and pharmaceutically acceptable compositions containing them. This invention also relates to the novel intermediates involved therein and process of their preparation.
These compounds are useful in the treatment of various disorders that are related to 5-HT6 receptor functions. Specifically, the compounds of this invention are also useful in the treatment of various CNS disorders, hematological disorders, eating disorders, obesity, anxiety, depression, diseases associated with pain, respiratory diseases, gastrointestinal, cardiovascular diseases and cancer.
BACKGROUND OF THE INVENTION
Various central nervous system disorders such as anxiety, depression, motor disorders etc., are believed to involve a disturbance of the neurotransmitter 5-hydroxytryptamine (5-HT) or serotonin. Serotonin is localized in the central and peripheral nervous systems and is known to affect many types of conditions including psychiatric disorders, motor activity, feeding behavior, sexual activity and neuroendocrine regulation among others. 5-HT receptor subtypes regulate the various effects of serotonin. Known 5-HT receptor family includes the 5-HT family (e.g. 5-HT,.), the 5-HT-
family (e.g.5-HT2A & 5-HT2C), 5-HT3, 5-HT4, 5-HT5, 5-HT6 and 5-HT? subtypes.

The 5-HT6 receptor subtype was first cloned from rat tissue in 1993 (Monsma, F. J.; Shen, Y.; Ward, R. P.; Hamblin, M. W., Sibley, D.R., Molecular Pharmacology, 1993, 43, 320-327) and subsequently from human tissue (Kohen, R.; Metcalf, M. A.; Khan, N.; Druck, T.; Huebner, K.; Sibley, D. R., Journal of Neurochemistry, 1996, 66, 47-56). The receptor is a G-protein coupled receptor (GPCR) positively coupled to adenylate cyclase (Ruat, M.; Traiffort, E.; Arrang, J-M.; Tardivel-Lacombe, L.; Diaz, L.; Leurs, R.; Schwartz, J-C, Biochemical Biophysical Research Communications, 1993, 193, 268-276). The receptor is found almost exclusively in the central nervous system (CNS) areas both in rats as well as in humans.
In situ hybridization studies of 5-HT6 receptor in rat brain using mRNA indicate principal localization in the areas of 5-HT projection including striatum, nucleus accumbens, olfactory tubercle and hippocampal formation (Ward, R. P.; Hamblin, M. W.; Lachowicz, J. E.; Hoffman, B. J.; Sibley, D. R.; Dorsa, D. M., Neuroscience, 1995, 64, 1105-1111). Highest levels of 5-HT6 receptor mRNA
has been observed in the olfactory tubercle, the striatum, nucleus accumbens, dentate gyrus as well as CA|, CA2 and CA3 regions of the hippocampus. Lower levels of 5-HT6 receptor mRNA were seen
in the granular layer of the cerebellum, several diencephalic nuclei, amygdala and in the cortex. Northern blots have revealed that 5-HT6 receptor mRNA appears to be exclusively present in the brain, with little evidence for its presence in peripheral tissues.
The high affinity of number of antipsychotic agents towards 5-HT6 receptor, the localization of its mRNA in striatum, olfactory tubercle and nucleus accumbens suggests that some of the clinical actions of these compounds may be mediated through this receptor. Its ability to bind a wide range of therapeutic compounds used in psychiatry, coupled with its intriguing distribution in the brain has stimulated significant interest in new compounds which are capable of interacting with the said receptor (Ref: Sleight, A.J. et al. (1997) 5-HT6 and 5-HT7 receptors: molecular biology, functional correlates and possible therapeutic indications, Drug News Perspect. 10, 214-224). Significant efforts are being made to understand the possible role of the 5-HT6 receptor in psychiatry, cognitive dysfunction, motor function and control, memory, mood and the like. The compounds which demonstrate a binding affinity for the 5-HTe receptor are earnestly sought both as an aid in the study of the 5-HT6 receptor and as potential therapeutic agents in the treatment of central nervous system disorders, for example see Reavill C. and Rogers D. C, Current Opinion in Investigational Drugs, 2001, 2(1): 104-109, Pharma Press Ltd.
Monsma F.J. et al. (1993) and Kohen, R. et al. (2001) have shown that several tricyclic antidepressant compounds, such as amitriptyline and atypical antidepressant compounds, such as mianserin have high affinity for the 5-HT6 receptor. These findings have led to the hypothesis that the 5-HT6 receptor is involved in the pathogenesis and/or treatment of affective disorders. Rodent models of anxiety-related behavior yield conflicting results about the role of the 5-HT6 receptor in anxiety. Treatment with 5-HT6 receptor antagonists increases seizure threshold in a rat maximal

electroconvulsive-shock test [Stean, T. et al. (1999) Anticonvulsant properties of the selective 5-HT6 receptor antagonist SB-271046 in the rat maximal electroshock seizure threshold test. Br. J. Pharmacol. 127, 131P; Routledge, C. et al. (2000) Characterization of SB-271046: a potent, selective and orally active 5-HT6 ) receptor antagonist. Br. J. Pharmacol. 130, 1606-1612]. Although this indicates that 5-HT6 receptors might regulate seizure threshold, the effect is not as pronounced as that of known anticonvulsant drugs.
Our understanding of the roles of 5-HT6 receptor ligands is most advanced in two therapeutic indications in which this receptor is likely to have a major role: learning and memory deficits and abnormal feeding behaviour. The exact role of the 5-HT6 receptor is yet to be established in other CNS indications such as anxiety; although one 5-HT6 agonist has reached Phase I clinical trials recently, the exact role of the receptor is still to be established and is the focus of significant investigation. There are many potential therapeutic uses for 5-HT6 receptor ligands in humans based on direct effects and on indications from available scientific studies. These studies include the localization of the receptor, the affinity of ligands with known in-vivo activity and various animal studies conducted so far. Preferably, antagonist compounds of 5-HT6 receptors are sought after as therapeutic agents.
One potential therapeutic use of modulators of 5-HT6 receptor functions is in the enhancement of cognition and memory in human diseases such as Alzheimer's. The high levels of receptor found in structures such as the forebrain, including the caudate/putamen, hippocampus, nucleus accumbens and cortex suggests a role for the receptor in memory and cognition since these areas are known to play a vital role in memory (Gerard, C; Martres, M.P.; Lefevre, K.; Miquel, M. C; Verge, D.; Lanfumey, R.; Doucet, E.; Hamon, M; EI Mestikawy, S., Brain Research, 1997, 746, 207-219). The ability of known 5-HT6 receptor ligands to enhance cholinergic transmission also supports the potential cognition use (Bentey, J. C; Boursson, A.; Boess, F. G.; Kone, F. C; Marsden, C. A.; Petit, N.; Sleight, A. J., British Journal of Pharmacology, 1999, 126 (7), 1537-1542).
Studies have found that a known 5-HT6 selective antagonist significantly increased glutamate and aspartate levels in the frontal cortex without elevating levels of noradrenaline, dopamine or 5-HT. This selective elevation of certain neurochemicals is noted during memory and cognition, strongly suggests a role for 5-HT6 ligands in cognition (Dawson, L. A.; Nguyen, H. Q.; Li, P. British Journal of Pharmacology, 2000, 130 (1), 23-26). Animal studies of memory and learning with a known selective 5-HT6 antagonist has some positive effects (Rogers, D. C; Hatcher, P. D.; Hagan, J. J. Society of Neuroscience, Abstracts, 2000, 26, 680).
A related potential therapeutic use for 5-HT6 ligands is in the treatment of attention deficit disorders (ADD, also known as Attention Deficit Hyperactivity Disorder or ADHD) in children as well as adults. As 5-HT6 antagonists appear to enhance the activity of the nigrostriatal dopamine pathway and ADHD has been linked to abnormalities in the caudate (Ernst, M; Zametkin, A. J.;

%fatochik, J. H.; Jons, P. A.; Cohen, R, M., Journal ofNeuroscience, 1998,18(15), 5901-5907), 5-HT6
antagonists may attenuate attention deficit disorders.
At present, a few fully selective agonists are available. The Wyeth agonist WAY-181187 is currently in Phase I trials to target anxiety [Cole, D.C. et al. (2005) Discovery of a potent, selective and orally active 5-HT6 receptor agonist, WAY-181187. 230th ACS Natl. Meet. (Aug 28-Sept 1, Washington DC), Abstract MEDI 17.]
International Patent Publication WO 03/066056 Al reports that antagonism of 5-HT6 receptor could promote neuronal growth within the central nervous system of a mammal. Another International Patent Publication WO 03/065046 A2 discloses new variant of human 5-HT6 receptor and proposes that 5-HT6 receptor is associated with numerous other disorders.
Early studies examining the affinity of various CNS ligands with known therapeutic utility or a strong structural resemblance to known drugs suggests a role for 5-HT6 ligands in the treatment of schizophrenia and depression. For example, clozapine (an effective clinical antipsychotic) has high affinity for the 5-HTe receptor subtype. Also, several clinical antidepressants have high affinity for the receptor as well and act as antagonists at this site (Branchek, T. A.; Blackburn, T. P., Annual Reviews in Pharmacology and Toxicology, 2000, 40,319-334).
Further, recent in-vivo studies in rats indicate that 5-HT6 modulators may be useful in the treatment of movement disorders including epilepsy (Stean, T.; Routledge, C; Upton, N., British Journal of Pharmacology, 1999, 127 Proc. Supplement-131P; and Routledge, C; Bromidge, S. M.; Moss, S. F.; Price, G. W.; Hirst, W.; Newman, H.; Riley, G.; Gager, T.; Stean, T.; Upton, N.; Clarke, S. E.; Brown, A. M., British Journal of Pharmacology, 2000, 30 (7), 1606-1612).
Taken together, the above studies strongly suggest that compounds which are 5-HT6 receptor modulators, i.e. ligands, may be useful for therapeutic indications including, the treatment of diseases associated with a deficit in memory, cognition and learning such as Alzheimer's and attention deficit disorder; the treatment of personality disorders such as schizophrenia; the treatment of behavioral disorders, e.g. anxiety, depression and obsessive compulsive disorders; the treatment of motion or motor disorders such as Parkinson's disease and epilepsy; the treatment of diseases associated with neurodegeneration such as stroke or head trauma; or withdrawal from drug addiction including addiction to nicotine, alcohol and other substances of abuse.
Such compounds are also expected to be of use in the treatment of certain gastrointestinal (GI) disorders such as functional bowel disorder. See for example, Roth, B. L.; et al., Journal of Pharmacology and Experimental Therapeutics, 1994, 268, pages 1403-1412; Sibley, D. R.; et al., Molecular Pharmacology, 1993, 43, 320-327, Sleight, A. J.; et al., Neurotransmission, 1995, 11,1-5; and Sleight, A. J.; et al., Serotonin ID Research Alert, 1997, 2(3), 115-118.
Furthermore, the effect of 5-HT6 antagonist and 5-HT6 antisense oligonucleotides to reduce food intake in rats has been reported, thus potentially in treatment of obesity. See for example,

Bentley, J. C; Boursson, A.; Boess, F. G.; Kone, F. C; Marsden, C. A.; Petit, N.; Sleight, A. J., British Journal of Pharmacology, 1999, 126 (7), 1537-1542); Wooley et al., Neuropharmacology, 2001, 41: 210-129; and WO 02/098878.
Recently a review by Holenz, Jo"rg et.al., Drug Discovery Today, 11, 7/8, April 2006, Medicinal chemistry strategies to 5-HT6 receptor ligands as potential cognitive enhancers and antiobesity agents, gives elaborate discussion on evolution of 5-HT6 ligands. It had summarized pharmacological tools and preclinical candidates used in evaluation of 5-HT6 receptor in illnesses such as schizophrenia, other dopamine-related disorders and depression and to profile the neurochemical and electrophysiological effects of either blockade or activation of 5-HT6 receptors. Furthermore, they huve been used lo characterize the 5-1 IT$ receptor and to Investigate its distribution. So far several clinical candidates form the part of indole-type structures and are closely related structurally to the endogenous ligand 5-HT, for example compounds by Glennon, R.A. et.al., 2-Substituted tryptamines: agents with selectivity for 5-HT6 serotonin receptors, J. Med. Chem. 43, 1011-1018, 2000; Tsai, Y. et.al., Nl-(Benzenesulfonyl)tryptamines as novel 5-HT6 antagonists, Bioorg. Med. Chem. Lett. 10, 2295-2299, 2000; Demchyshyn L. et al., ALX-1161: pharmacological properties of a potent and selective 5-HT6 receptor antagonist, 31st Annu. Meet. Soc. Neurosci. (Nov 10-15), Abstract 266.6, 2001; Slassi, A.et.al., Preparation of 1 -(arylsulfonyl)-3-(tetrahydropyridinyl)indoles as 5-HT6 receptor inhibitors, WO 200063203, 2000; Mattsson, C. etal., Novel, potent and selective 2-alkyl-3-(l,2,3,6-tetrahydropyridin-4-yl)-lH-indole as 5-HT6 receptor agonists, XVIIth International Symposium on Medicinal Chemistry, 2002; Mattsson, C. et.al., 2-Alkyl-3-(l,2,3,6-tetrahydropyridin-4-yl)-lH-indoles as novel 5-HT6 receptor agonists, Bioorg. Med. Chem. Lett. 15, 4230-4234, 2005]
Structure functionality relationships are described in the section on indole-like structures and in a receptor-modeling study in which Pullagurla et.al., claim different binding sites for agonists and antagonists [Pullagurla, M.R. et al. (2004) Possible differences in modes of agonist and antagonist binding at human 5-HT6 receptors. Bioorg. Med. Chem. Lett. 14, 4569- 4573]. Most antagonists that are reported form part of the monocyclic, bicyclic and tricyclic aryl-piperazine classes [Bromidge, S.M.etal.,(1999)5-Chloro-N-(4-methoxy-3-piperazin-l-ylphenyl)-3-methyl-2-benzothiophenesulfonamide (SB-271046): A potent, selective and orally bioavailable 5-HT6 receptor antagonist. J. Med. Chem. 42, 202-205; Bromidge, S.M. et al. (2001) Phenyl benzenesulfonamides are novel and selective 5-HT6 antagonists: Identification of N-(2,5-dibromo-3-fIuorophenyl)-4-methoxy-3-piperazin-l-ylbenzenesuIfonamide (SB-357I34). Bioorg. Med. Chem. Lett. 11, 55- 58; Hirst, W.D. et al. (2003) Characterisation of SB-399885, a potent and selective 5-HT6 receptor antagonist. 33rd Annu. Meet. Soc. Neurosci. (Nov. 8-12, New Orleans), Abstract 576.7; Stadler, H. et al. (1999) 5-HT6 antagonists: A novel approach for the symptomatic treatment of Alzheimer's disease. 37th IUPAC Cong. Berlin, Abstract MM-7; Bonhaus, D.W. et al. (2002) Ro-4368554, a high affinity,

^Selective, CNS penetrating 5-HT6 receptor antagonist. 32nd Annu. Meet. Soc. Neurosci., Abstract 884.5.; Beard, C.C. et al. (2002) Preparation of new indole derivatives with 5-HT6 receptor affinity. WO patent 2002098857].
Ro 63-0563: Potent and selective antagonists at human and rat 5-HT6 receptors. Br. J. Pharmacol. 124, (556-562). Phase II antagonist candidate from GlaxoSmithKline, SB-742457 for the therapeutic indication of cognitive dysfunction associated with Alzheimer's disease [Ahmed, M. et al. (2003) Novel compounds. WO patent 2003080580], and the Lilly compound LY-4815518 |HMa, S.A. et al. (2002) Preparation of benzenesulfonic acid indol-5-yl esters as antagonists of the 5-HT6 receptor. WO 2002060871], SB-271046, the first 5-HT6 receptor antagonist to enter Phase 1 clinical development, has been discontinued (probably because of low penetration of the blood-brain barrier). In addition, the selective 5-HT6 receptor antagonist SB-271046 is inactive in animal tests related to either positive or negative symptoms of schizophrenia [Pouzet, B. et al. (2002) Effects of the 5-HT6 receptor antagonist, SB-271046, in animal models for schizophrenia. Pharmacol. Biochem. Behav. 71, 635-643].
International Patent Publications WO 2004/055026 Al, WO 2004/048331 Al, WO 2004/048330 Al and WO 2004/048328 A2 (all assigned to Suven Life Sciences Limited) describe the related prior art. Further WO 98/27081, WO 99/02502, WO 99/37623, WO 99/42465 and WO 01/32646 (all assigned to Glaxo SmithKline Beecham PLC) disclose a series of aryl sulfonamide and sulfoxide compounds as 5-HT6 receptor antagonists and are claimed to be useful in the treatment of various CNS disorders. While some 5-HT6 modulators have been disclosed, there continues to be a need for compounds that are useful for modulating 5-HT6. Surprisingly, it has been found that substituted indolyl compounds of formula (I) demonstrate very high 5-HT6 receptor affinity. Therefore, it is an object of this invention to provide compounds, which are useful as therapeutic agents in the treatment of a variety of central nervous system disorders or disorders affected by the 5-HT6 receptor.
OBJECTS OF THE INVENTION
Primary object of the present invention is to provide a novel substituted indolyl compounds of the formula (I) for the treatment of various disorders that are related to 5-HT6 receptor functions.
Another object of the present invention is to provide the process for the preparation of the novel substituted indolyl compounds of the formula (I).
Yet another object of the present invention is to provide a pharmaceutical composition comprising the compound of formula (I).

till another object of the present invention is to provide a method for the treatment of a disorder of the central nervous system related to or affected by the 5-HT6 receptor, in a patient which comprises providing the patient a therapeutically effective amount of a compound of formula (I).
SUMMARY OF THE INVENTION
The present invention relates to novel substituted indolyl compounds of the formula (I), their derivatives, their stereoisomers, their pharmaceutical^ acceptable salts and pharmaceutical^ acceptable compositions containing them.

Wherein R represents hydrogen, (CrC3) alkyl or (C3-C6) cycloalkyl;
Rj, R2 and R3 may be same or different and each independently represent hydrogen, halogen, (CrC3)alkyl, (C3-C6) cycloalkyl, halo(CrC3)alkyl, (C,-C3)alkoxy or halo (CrC3)alkoxy;
R4 represents hydrogen, (Ci-C3)alkyl, halo(CrC3)alkyl, aryl, aralkyl, (C3-C6) cycloalkyl or t-butyloxy carbonyl;
"m" represents 0 to 4;
"n" represents 0 to 5;
"p" represents 0 to 5;
The present invention also relates to use of a therapeutically effective amount of compound of formula (I), to manufacture a medicament, in the treatment or prevention of a disorder involving selective affinity for the 5-HT6 receptor.
Specifically, the compounds of this invention are also useful in the treatment of various CNS disorders, hematological disorders, eating disorders, obesity, anxiety, depression, diseases associated with pain, respiratory diseases, gastrointestinal, cardiovascular diseases and cancer.
fn another aspect, the invention relates to pharmaceutical compositions containing a therapeutically effective amount of at least one compound of formula (1) or individual stereoisomers,

r
racemic or non-racemic mixture of stereoisomers or pharmaceutically acceptable salts or solvates
thereof, in admixture with at least one suitable carrier, diluents, adjuvants or excipients.
In another aspect, the invention relates to compositions comprising and methods for using
compounds of Formula (I).
In another aspect, the invention relates to novel intermediates and process of their preparation
of general formula (II) and (III), which are useful in the preparation of compounds of formula (I).
In still another aspect, the invention relates to the use of a therapeutically effective amount of
compound of formula (I), to manufacture a medicament, in the treatment or prevention of a disorder
involving selective affinity for the 5-HT6 receptor.
In yet another aspect, the invention further relates to the process for preparing compounds of
formula (I).
Following is the partial list of the compounds belonging to general formula (I):
l-(2'-Bromo benzenesu!fonyl)-4-[N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-(piperidin-4-yl)] amino-lH-indole dihydrochloride;
l-(2'-Bromo benzenesulfonyl)-4-[N-methyi-N-(piperidin-4-yl)] amino-IH-indole dihydrochloride;
l-(2*-Bromo benzenesulfonyl)-4-[N-ethyl-N-(l-methyl piperidin-4-yI)] amino-lH-indole; 4-[N-Ethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methyl benzenesulfonyl)-lH-indole;
l-(2'-Chloro benzenesuIfonyI)-4-[N-ethyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(3'-Chloro benzenesulfonyl)-4-[N-(l-t-butyloxycarbonyI piperidin-4-yl)-N-methyI] amino-1H-indole;
4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-l-(4'-isopropyl benzenesulfonyi)-IH-indole;
4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-l-(4'-fluoro benzenesulfonyi)-! H-indole;
4-[N-(l-t-ButyIoxycarbonyl piperidin-4-yl)-N-methyl] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indole;
4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)] amino-1-(3'-chloro benzenesulfonyl)-lH-indole; l-(3'-Chloro benzenesulfonyI)-4-[N-methy!-N-(piperidin-4-yI)] amino-IH-indole dihydrochloride; l-(3'-Chloro benzenesulfonyl)-4-[N-(piperidin-4-yl)] amino-lH-indole dihydrochloride; l-(3'-Chloro benzenesulfonyl)-4-[N-(l-methyl piperidin-4-yI)] amino-lH-indole; l-(4'-Fluoro benzenesulfonyI)-4-[N-methyI-N-(piperidin-4-yl)] amino-1 H-indole dihydrochloride; i-(4'-Isopropyl benzenesulfonyl)-4-[N-methyl-N-(piperidin-4-yl)] amino-IH-indole dihydrochloride; 4-[N-( 1 -Benzyl piperidin-4-yI) amino-1-(4'-fIuoro benzenesulfonyl)-l H-indole; l-(2\ 5'-Dimethoxy benzenesulfonyl)-4-[N-methyl~N-(l-methyl piperidin-4-yl)] amino-1 H-indole; l-(4'-Methyl benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole; !-(2'-Ch!oro benzenesulfonyi)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;

l-(4'-Fluoro benzenesulfonyl)-4-[N-methyI-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(3'-Chloro benzenesulfonyl)-4-[N-methyl-N-(l-methyI piperidin-4-yl)] amino-lH-indole;
4-[N-Methyl-N-(l-methyl piperidin-4-yl)] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indole;
l-(4'-Isopropyl benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole;
l-(4'-Methoxy benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
4-[N-Cyclopropylmethyl-N-( 1 -methyl piperidin-4-yl)] amino-1 -(4' -methyl benzenesulfonyl)-1H-
indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-1H-
indole;
l-(2'-Chloro benzenesu!fonyl)-4-[N-cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-lH-
indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-fluoro benzenesulfonyI)-lH-
indole;
l-(3'-Chloro benzenesulfonyl)-4-[N-cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino- 1H-
indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(3'-trifluoromethyl benzenesulfonyl)-
lH-indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methoxy benzenesulfonyl)-lH-
indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino- l-(4'-isopropyl benzenesulfonyI)-lH-
indole;
4-[N-IsopropyI-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methyl benzenesulfonyl)-lH-indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole;
l-(2'-Ch!oro benzenesulfonyl)-4-[N-isopropyI-N-(Nmethy! piperidin-4-yI)] amino-IH-indole;
]-(4'-Fluoro benzenesuIfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(3'-Chloro benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
4-[N-Isopropyl-N-(l-methyl piperidin-4-yI)] amino-I-^'-trifluoromethyl benzenesu!fonyl)-lH-
indole;
4-[N-Isopropyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methoxy benzenesulfonyI)-lH-indole;
l-(4'-IsopropyI benzenesu!fonyI)-4-[N-isopropyI-N-(l-methyl piperidin-4-yl)] amino-IH-indole;
4-[N-(l-Ethyl piperidin-4-yl)] amino-l-(4'-methyl benzenesu!fonyl)-lH-indole;
l-(2'-Bromo benzenesulfonyI)-4-[N-(l-ethyl piperidin-4-yl)] amino-IH-indole;
l-(2'-Chloro benzenesu!fonyl)-4-[N-(l-ethyl piperidin-4-yl)] amino-IH-indole;
l-(4'-Fluoro benzenesu!fonyl)-4-[N-(l-ethyl piperidin-4-yl)] amino—lH-indole;
l-(3'-Chloro benzenesulfonyI)-4-[N-(l-ethyl piperidin-4-yI)] amino-lH-indole;

4-[N-(l-Ethyl piperidin-4-yl)] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indo!e; 4-[N-(l-Ethyl piperidin-4-yl)] amino-l-(4'-methoxy benzenesulfonyl)-lH-indole; 4-[N-(l-Ethyl piperidin-4-yl)] amino-l-(4'-isopropyl benzenesulfonyl)-lH-indole; 1-(4'-Methyl benzenesulfonyl)-4-[N-(l-propyl piperidin-4-yl)] amino-lH-indole; l-(2'-Bromo benzenesulfonyl)-4-[N-(l-Propyl piperidin-4-yl)] amino-lH-indole; l-(2*-Chloro benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole; l-(4'-Fluoro benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole; l-(3'-Chloro benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole; 4-[N-(l- Propyl piperidin-4-yl)] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indole; l-(4'-Methoxy benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole and l-(4'-Isopropyl benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole; the stereoisomer thereof; and the pharmaceutically acceptable salts thereof.;
DETAILED DESCRIPTION OF THE INVENTION
Unless otherwise stated, the following terms used in the specification and claims have the meanings given below:
"Halogen" means fluorine, chlorine, bromine or iodine;
"(CrC3)alkyl" means straight or branched chain alkyl radicals containing one to three carbon atoms and includes methyl, ethyl, n-propyl and iso-propyl;
"(CrC3)alkoxy" means straight or branched chain alkyl radicals containing one to three carbon atoms and includes methoxy, ethoxy, propyloxy and iso-propyloxy;
"Halo(Cl-C3)alkyr' means straight or branched chain alkyl radicals containing one to three carbon atoms and includes fluoromethyl, difluoromethyl, trifluoromethyl, trifluoroethyl, fluoroethyl, difluoroethyl and the like;
"Halo(Ci-C3)alkoxy" means straight or branched chain alkyl radicals containing one to three carbon atoms and includes fluoromethoxy, difluoromethoxy, trifluoromethoxy, trifluoroethoxy, fluoroethoxy, difluoroethoxy and the like;
"Cyclo(C3-C6)alkyr means cyclic or branched cyclic alkyl radicals containing three to six carbon atoms and includes cyclopropyl, cyclobutyl, cyclopentyl, cyclopropylmethyl, cyclo(C3-C6>alkyl methyl or cyclohexyl, which may be substituted or unsubstituted and optionally the substituents may be selected from halogen, (Ci-C3)alkyl or (CrC3)alkoxy;
"Aryl " means monocyclic aromatic ring system, which can optionally be substituted with hydrogen, halogen, (CrC3)alkyl, haIo(CrC3)alkyl, (CrC3)alkoxy or halo (Ci-C3)alkoxy;
"Aralkyl" means benzyl or heterocyclylmethyl and the like;
The term "schizophrenia" means schizophrenia, schizophreniform, disorder, schizoaffective disorder and psychotic disorder wherein the term "psychotic" refers to delusions, prominent

r
hallucinations, disorganized speech or disorganized or catatonic behavior. See Diagnostic and Statistical Manual of Mental Disorder, fourth edition, American Psychiatric Association, Washington, D.C.
The phrase "pharmaceutically acceptable" indicates that the substance or composition must be compatible chemically and/or toxicologically, with the other ingredients comprising a formulation, the mammal being treated therewith.
"Therapeutically effective amount" is defined as can amount of a compound of the present invention that (i) treats or prevents the particular disease, condition or disorder (ii) attenuates, ameliorates or eliminates one or more symptoms of the particular disease, condition or disorder (iii) prevents or delays the onset of one or more symptoms of the particular disease, condition or disorder described herein'.
The terms "treating", "treat" or "treatment" embrace all the meanings such as preventative, prophylactic and palliative.
The term "stereoisomers" is a general term for all isomers of the individual molecules that differ only in the orientation of their atoms in space. It includes mirror image isomers (enantiomers), geometric (cis-trans) isomers and isomers of compounds with more than one chiral centre that are not mirror images of one another (diastereomers).
Certain compounds of formula (I) are capable of existing in stereoisomeric forms (e. g. diastereomers and enantiomers) and the invention extends to each of these stereoisomeric forms and to mixtures thereof including racemates. The different stereoisomeric forms may be separated from one another by the usual methods or any given isomer may be obtained by stereospecific or asymmetric synthesis. The invention also extends to tautomeric forms and mixtures thereof.
The stereoisomers as a rule are generally obtained as racemates that can be separated into the optically active isomers in a manner known per se. In the case of the compounds of general formula (I) having an asymmetric carbon atom the present invention relates to the D-form, the L-form and D,L - mixtures and in the case of a number of asymmetric carbon atoms, the diastereomeric forms and the invention extends to each of these stereo isomeric forms and to mixtures thereof including racemates. Those compounds of general formula (I) which have an asymmetric carbon and as a rule are obtained as racemates can be separated one from the other by the usual methods, or any given isomer may be obtained by stereo specific or asymmetric synthesis. However, it is also possible to employ an optically active compound from the start, a correspondingly optically active enantiomeric or diastereomeric compound then being obtained as the final compound.
The stereoisomers of compounds of general formula (I) may be prepared by one or more ways
presented below:
i) One or more of the reagents may be used in their optically active form.

ii) Optically pure catalyst or chiral ligands along with metal catalyst may be employed in the
reduction process. The metal catalyst may be Rhodium, Ruthenium, Indium and the like. The chiral ligands may preferably be chiral phosphines (Principles of Asymmetric synthesis, J. E. Baldwin Ed., Tetrahedron series, 14,311-316). iii) The mixture of stereoisomers may be resolved by conventional methods such as forming diastereomeric salts with chiral acids or chiral amines or chiral amino alcohols, chiral amino acids. The resulting mixture of diastereomers may then be separated by methods such as fractional crystallization, chromatography and the like, which is followed by an additional step of isolating the optically active product by hydrolyzing the derivative (Jacques et. al.s "Enantiomers, Racemates and Resolution", Wiley Interscience, 1981). iv) The mixture of stereoisomers may be resolved by conventional methods such as microbial resolution, resolving the diastereomeric salts formed with chiral acids or chiral bases. Chiral acids that can be employed may be tartaric acid, mandelic acid, lactic acid, camphorsulfonic acid, amino acids and the like. Chiral bases that can be employed may be cinchona alkaloids, brucine or a basic amino acid such as lysine, arginine and the like. In the case of the compounds of general formula (I) containing geometric isomerism the present invention relates to all of these geometric isomers.
Suitable pharmaceutically acceptable salts will be apparent to those skilled in the art and include those described in J. Pharm. Sci., 1977, 66, 1-19, such as acid addition salts formed with inorganic acids e. g. hydrochloric, hydrobromic, sulfuric, nitric or phosphoric acid and organic acids e. g. succinic, maleic, acetic, fumaric, citric, tartaric, benzoic, p-toluenesulfonic, methanesulfonic or naphthalenesulfonic acid. The present invention includes, within its scope, all possible stoichiometric and non-stoichiometric forms.
The pharmaceutically acceptable salts forming a part of this invention may be prepared by treating the compound of formula (I) with 1-6 equivalents of a base such as sodium hydride, sodium methoxide, sodium ethoxide, sodium hydroxide, potassium t-butoxide, calcium hydroxide, calcium acetate, calcium chloride, magnesium hydroxide, magnesium chloride and the like. Solvents such as water, acetone, ether, THF, methanol, ethanol, t-butanol, dioxane, isopropanol, isopropyl ether or mixtures thereof may be used.
In addition to pharmaceutically acceptable salts, other salts are included in the invention. They may serve as intermediates in the purification of the compounds, in the preparation of other salts, or in the identification and characterization of the compounds or intermediates.
The compounds of formula (I) may be prepared in crystalline or non-crystalline form and if crystalline, may optionally be solvated, eg. as the hydrate. This invention includes within its scope stoichiometric solvates (eg. hydrates) as well as compounds containing variable amounts of solvent (eg. water).

The following Schemes and Examples describe procedures for making representative compounds of the present invention. Moreover, by utilizing the procedures described in details, one of ordinary skill in the art can readily prepare additional compounds of the present invention claimed herein; Scheme-1:
The compounds of general formula (I), wherein R represents (C1-C3) alkyl group or Cyclo(C3-C6)alkyl group, and all other symbols are as defined earlier, may be prepared by the process as shown in Scheme-1 below:

with arylsulfonyl chloride derivatives, using a suitable base in presence of inert solvent and inert gases at ambient temperature to obtain a compound of formula (I), wherein all substitutions are described as earlier.
The above reaction is preferably carried out in a solvent such as tetrahydrofuran (THF), toluene, ethyl acetate, dimethylformamide (DMF), dimethyl sulfoxide (DMSO), dimethyl ether (DME) and the like or a mixture thereof and preferably using THF. The inert atmosphere may be

maintained by using inert gases such as N2, Ar or He. The reaction may be affected in the presence of a base such as potassium carbonate, sodium bicarbonate, sodium hydride or mixtures thereof and preferably using sodium hydride. The reaction temperature may range from 20 °C to 50 °C based on the choice of solvent and preferably at a temperature in the range from 25 °C to 35 °C. The duration of the reaction may range from 1 to 6 hours, preferably from a period of 1 to 3 hours.
The key intermediate (a) is synthesized as described in preparations 4. This key intermediate (a) may be commercially available or they may be prepared by conventional methods or by modification, using known process. Scheme-2;
The compounds of general formula (I), wherein R represents hydrogen, and all other symbols are as defined earlier, may be prepared by the process as shown in Scheme-2 below:


with piperidine-4-one derivatives, using a suitable reducing agent and base in presence of suitable solvent at ambient temperature to obtain a compound of formula (I), wherein all substitutions are described as earlier.
The above reaction is preferably carried out in a solvent such as ethanol, tetrahydrofiiran (THF), toluene, ethyl acetate, water, titanium isopropoxide, dimethylformamide (DMF), dimethyl sulfoxide (DMSO), dimethyl ether (DME) and the like or a mixture thereof and preferably using titanium isopropoxide and ethanol. The reaction is carried by using reducing agents like sodium, sodium borohydride, sodium cyanoborohydride and the like or a mixture thereof and preferably using sodium cyanoborohydride. The reaction may be affected in the presence of a base such as potassium carbonate, sodium hydroxide, sodium bicarbonate, sodium hydride or mixtures thereof and preferably using sodium hydroxide. The reaction temperature may range from 20 °C to 45 °C based on the choice of solvent and preferably at a temperature in the range from 25 °C to 35 °C. The duration of the reaction may range from 4 to 10 hours, preferably from a period of 5 to 7 hours.
The key intermediate (b) is synthesized as described in preparations 10. This key intermediate (b) may be commercially available or they may be prepared by conventional methods or by modification, using known process. Scheme-3:
The compounds of general formula (I), wherein R and R4 represents hydrogen and all other
symbols are as defined earlier, may be prepared by the process as shown in Scheme-3 below:
p.

The compound of formula (II) is converted into formula (I) by convenient derivatization.

The above reaction is preferably carried out by using methanolic hydrochloric acid. The inert atmosphere may be maintained by using inert gases such as N2, Ar or He. The reaction temperature may range from 20 °C to 40 °C and preferably at a temperature in the range from 25 °C to 35 °C. The duration of the reaction may range from 1 to 4 hours, preferably from a period of 0.5 to 3 hours. The product, thus obtained, can be further derivatized to compounds (I) by methods described within.
The novel intermediate compounds represented by the general formula (II) are prepared by process as described in the specification. Scheme-4:
The compounds of general formula (I), wherein R4 represents hydrogen and all other symbols are as defined earlier, may be prepared by the process as shown in Scheme-4 below:

The compound of formula (III) is converted into formula (I) by convenient derivatization.
The above reaction is preferably carried out by using methanolic hydrochloric acid. The inert atmosphere may be maintained by using inert gases such as N2, Ar or He. The reaction temperature may range from 20 °C to 40 °C and preferably at a temperature in the range from 25 °C to 35 °C. The duration of the reaction may range from 1 to 4 hours, preferably from a period of 0.5 to 3 hours.
The novel intermediate compound represented by the general formula (III) is prepared by the process as described in the specification.
According to a feature of the present invention, there are novel intermediates of general formula (II) and (III), which are useful in the preparation of compounds of formula (I).
Novel intermediates of general formula (II) are represented as given below, wherein all symbols are as defined earlier:

The above reaction is preferably carried out in a solvent such as ethanol, tetrahydrofuran (THF), toluene, ethyl acetate, titanium isopropoxide, dimethylformamide (DMF), dimethyl sulfoxide (DMSO), dimethyl elher (DME) and the like or a mixture thereof and preferably using titanium isopropoxide and ethanol. The reaction is carried by using reducing agents like sodium borohydride, sodium cyanoborohydride and the like or a mixture thereof and preferably using sodium cyanoborohydride. The reaction may be affected in the presence of a base such as potassium carbonate, sodium hydroxide, sodium bicarbonate, sodium hydride or mixtures thereof and preferably using sodium hydroxide. The reaction temperature may range from 20 °C to 45 °C based on the choice of solvent and preferably at a temperature in the range from 25 °C to 35 °C. The duration of the reaction may range from 4 to 10 hours, preferably from a period of 5 to 7 hours.
The key intermediate (b) is synthesized as described in preparations 10. This key intermediate (b) may be commercial available or they may be prepared by conventional methods or by modification, using known process.
Another novel intermediate of general formula (III) are represented as given below, wherein all symbols are as defined earlier:
The present invention also provides a process for the preparation of a novel intermediate of formula (111), which comprises of the following route:


Converting the compound of formula (II) by reductive amination, using a suitable base in presence of inert solvent and inert gases at ambient temperature to obtain compound of formula (III), wherein all substitutions are described as earlier.
The above reaction is preferably carried out in a solvent such as ethanol, tetrahydrofuran (THF), toluene, ethyl acetate, formaldehyde, acetic acid, dimethylformamide (DMF), dimethyl sulfoxide (DMSO), dimethyl ether (DME) and the like or a mixture thereof and preferably using acetic acid, formaldehyde and methanol. The reaction is carried by using reductive amination agents like sodium triacetoxy borohydride and sodium cyanoborohydride. The reaction may be affected in the presence of a base such as potassium carbonate, sodium hydroxide, sodium bicarbonate and sodium hydride. The reaction temperature may range from 20 °C to 45 °C based on the choice of solvent and preferably at a temperature in the range from 25 °C to 35 °C. The duration of the reaction may range from 2 to 6 hours, preferably from a period of 3 to 5 hours, wherein the key intermediate (II) is synthesized as described as earlier in specification
Compounds obtained by the above method of preparation of the present invention can be transformed into another compound of this invention by further chemical modifications using well-known reactions such as oxidation, reduction, protection, deprotection, rearrangement reaction, halogenation, hydroxylation, alkylation, alkylthiolation, demethylation, O-alkylation, O-acylation, N-alkylation, N-alkenylation, N-acylation, N-cyanation, N-sulfonylation, coupling reaction using transition metals and the like.
If necessary, any one or more than one of the following steps can be carried out,
i) Converting a compound of the formula (I) into another compound of the formula (I)
ii) Removing any protecting groups; or
iii) Forming a pharmaceutical^ acceptable salt, solvate or a prodrug thereof.

Process (i) may be performed using conventional interconversion procedures such as epimerisation, oxidation, reduction, alkylation, nucleophilic or electrophilic aromatic substitution and ester hydrolysis or amide bond formation.
In process (ii) examples of protecting groups and the means for their removal can be found in T. W. Greene 'Protective Groups in Organic Synthesis' (J. Wiley and Sons, 1991). Suitable amine protecting groups include sulphonyl (e.g. tosyl), acyl (e.g. acetyl, 2\ 2\ ^-trichloroethoxycarbonyl, benzyloxycarbonyl or t-butoxycarbonyl) and arylalkyl (eg. benzyl), which may be removed by hydrolysis (e. g. using an acid such as hydrochloric or trifluoroacetic acid) or reductively (e. g. hydrogenolysis of a benzyl group or reductive removal of a 2', 2\ 2'-trichloroethoxycarbonyl group using zinc in acetic acid) as appropriate. Other suitable amine protecting groups include trifluoroacetyl, which may be removed by base catalysed hydrolysis or a solid phase resin bound benzyl group, such as a Merrifield resin bound 2,6-dimelhoxybenzyl group (Ellman linker), which may be removed by acid catalyzed hydrolysis, for example with trifluoroacetic acid.
In process (iii) halogenation, hydroxylation, alkylation and/or pharmaceutically acceptable salts may be prepared conventionally by reaction with the appropriate acid or acid derivative as described earlier in detail.
In order to use the compounds of formula (I) in therapy, they will normally be formulated into a pharmaceutical composition in accordance with standard pharmaceutical practice.
The pharmaceutical compositions of the present invention may be formulated in a conventional manner using one or more pharmaceutically acceptable carriers. Thus, the active compounds of the invention may be formulated for oral, buccal, intranasal, parenteral (e.g., intravenous, intramuscular or subcutaneous) or rectal administration or a form suitable for administration by inhalation or insufflation.
For oral administration, the pharmaceutical compositions may take the form of, for example, tablets or capsules prepared by conventional means with pharmaceutically acceptable excipients such as binding agents (e.g., pregelatinised maize starch, polyvinylpyrrolidone or hydroxypropyl methylcellulose); fillers (e.g., lactose, microcrystalline cellulose or calcium phosphate); lubricants (e.g., magnesium stearate, talc or silica); disintegrants (e.g., potato starch or sodium starch glycolate); or wetting agents (e.g., sodium lauryl sulphate). The tablets may be coated by methods well known in the art. Liquid preparations for oral administration may take the form of, for example, solutions, syrups or suspensions or they may be presented as a dry product for constitution with water or other suitable vehicle before use. Such liquid preparations may be prepared by conventional means with pharmaceutically acceptable additives such as suspending agents (e.g., sorbitol syrup, methyl cellulose or hydrogenated edible fats); emulsifying agents (e.g., lecithin or acacia); non-aqueous vehicles (e.g., almond oil, oily esters or ethyl alcohol) and preservatives (e.g., methyl or propyl p-hydroxybenzoates or sorbic acid).

For buccal administration, the composition may take the form of tablets or lozenges formulated in conventional manner.
The active compounds of the invention may be formulated for parenteral administration by injection, including using conventional catheterization techniques or infusion. Formulations for injection may be presented in unit dosage form, e.g., in ampoules or in multi-dose containers, with an added preservative. The compositions may take such forms as suspensions, solutions or emulsions in oily or aqueous vehicles and may contain formulating agents such as suspending, stabilizing and/or dispersing agents. Alternatively, the active ingredient may be in powder form for reconstitution with a suitable vehicle, e.g., sterile pyrogen-free water, before use.
The active compounds of the invention may also be formulated in rectal compositions such as suppositories or retention enemas, e.g., containing conventional suppository bases such as cocoa butter or other glycerides.
For intranasal administration or administration by inhalation, the active compounds of the invention are conveniently delivered in the form of an aerosol spray from a pressurized container or a nebulizer or from a capsule using a inhaler or insufflator. In the case of a pressurized aerosol, a suitable propel lant, e.g., dichlorodifluoromethane, trichlorofluoromethane, dichlorotetrafluoroethane, carbon dioxide or other suitable gas and the dosage unit may be determined by providing a valve to deliver a metered amount. The medicament for pressurized container or nebulizer may contain a solution or suspension of the active compound while for a capsule, it preferably should be in the form of powder. Capsules and cartridges (made, for example, from gelatin) for use in an inhaler or insufflator may be formulated containing a powder mix of a compound of the invention and a suitable powder base such as lactose or starch.
Aerosol formulations for treatment of the conditions referred to above (e.g., migraine) in the average adult human are preferably arranged so that each metered dose or "puff of aerosol contains 20 ng to 1000 fig of the compound of the invention. The overall daily dose with an aerosol will be within the range 100 (ig to 10 mg. Administration may be several times daily, for example 2, 3, 4 or 8 times, giving for example, I, 2 or 3 doses each time.
An effective amount of a compound of general formula (1) or their derivatives as defined above can be used to produce a medicament, along with conventional pharmaceutical auxiliaries, carriers and additives.
Such therapy includes multiple choices: for example, administering two compatible compounds simultaneously in a single dose form or administering each compound individually in a separate dosage; or if required at same time interval or separately in order to maximize the beneficial effect or minimize the potential side-effects of the drugs according to the known principles of pharmacology.

The dose of the active compounds can vary depending on factors such as the route of administration, age and weight of patient, nature and severity of the disease to be treated and similar factors. Therefore, any reference herein to a pharmacologically effective amount of the compounds of general formula (I) refers to the aforementioned factors. A proposed dose of the active compounds of this invention, for either oral, parenteral, nasal or buccal administration, to an average adult human, for the treatment of the conditions referred lo above, is 0.1 to 200 mg of the active ingredient per unit dose which could be administered, for example, 1 to 4 times per day.
Commercial reagents were utilized without further purification. Room temperature refers to 25 - 30 °C. IR were taken using KBr and in solid state. Unless otherwise stated, all mass spectra were carried out using ESI conditions. *H-NMR spectra were recorded at 400 MHz on a Bruker instrument. Deuterated chloroform (99.8 % D) was used as solvent. TMS was used as internal reference standard. Chemical shift values are expressed in parts per million (8) values. The following abbreviations are used for the multiplicity for the NMR signals: s^singlet, bs=broad singlet, d=doublet, t=triplet, q=quartet, qui=quintet, h=heptet, dd=double doublet, dt=double triplet, tt=triplet of triplets, m=multipiet. Chromatography refers to column chromatography performed using 100 -200 mesh silica-gel and executed under nitrogen pressure (flash chromatography) conditions.
The present invention is illustrated and supported by the following experiments and examples. These are merely representative examples and optimization details and are not intended to restrict the scope of the present invention in any way. Examples
The novel compounds of the present invention were prepared according to the following procedures, using appropriate materials and are further exemplified by the following specific examples. The most preferred compounds of the invention are any or all of those specifically set forth in these examples. These compounds are not, however, to be construed as forming the only genus that is considered as the invention and any combination of the compounds or their moieties may itself form a genus. The following examples further illustrate details for the preparation of the compounds of the present invention. Those skilled in the art will readily understand that known variations of the conditions and process of the following preparative procedures can be used to prepare these compounds. Preparation 1: 4-amino indole.
A mixture of 4-nitroindole (15 grams, 92.5 mmol), iron powder (25.92 grams, 462.9 mmol), concentrated hydrochloric acid (5 mL) and water (50 mL) in ethanol (150 rnL) was refluxed at 90 °C and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (2 hours), the reaction mixture was filtered through hy-flow bed and the filtrate was concentrated under reduced pressure. The residual mass was diluted with ice water (500 mL), basified with aqueous sodium hydroxide solution to pH 9 - 10 and extracted with ethyl acetate (2 x

250 mL). The combined organic layer was washed with brine, dried over anhydrous sodium sulphate
and concentrated under reduced pressure. The crude product (13.2 grams), thus obtained, was
purified by column chromatography using silica-gel (100 - 200 mesh), the eluent system being ethyl
acetate and n-hexane (1:9) to obtain 12.13 grams of title product.
Melting Range: 101.7 - 106.8 °C;
I.R(cm_1): 1109, 1519,2931,3325,3394,3440;
lH-NMR (ppm): 3.92 (2H, bs), 6.40 - 6.42 (1H, m), 6.46 - 6.47 (1H, m), 6.86 - 6.88 (1H, d, J = 8.14
Hz), 6.99 - 7.03 (1H, t, J * 7.8 Hz), 7.11 - 7.12 (1H, t, 2.8 Hz), 8.11 (1H, bs);
Mass(m/z): 133.15 (M+H)+.
Preparation 2: 4-[N~(l-Methy! piperidin-4-yI)) amino-lH-indole.
A mixture of 4-aminoindole (5 grams, 37.8 mmol) (obtained from preparation 1), 1-methyl piperidine-4-one (5.5 mL5 45.4 mmol), sodium triacetoxyborohydride (16.02 grams, 75.6 mmol) and acetic acid (2.15 mL, 37.8 mmol) in ethylene dichloride (100 mL) was stirred at room temperature and the progress of the reaction was monitored by thin layer chromatography. After completion of reaction (5 hours), the reaction mixture was diluted with ice water (500 mL), basified with 10% aqueous sodium hydroxide solution and extracted the mass with ethyl acetate (2 x 250 mL). The combined organic layer was washed with brine, dried over anhydrous sodium sulphate and concentrated under reduced pressure. The obtained crude product (11.32 grams) was purified by column chromatography using silica-gel (100 - 200 mesh), the eluent system being ethyl acetate and triethyl amine (99:1) to obtain 7.6 grams of the title product. Melting Range: 128.3 - 131°C; LR(cm_l): 1109,1373,1519,2931,3417;
!H-NMR (ppm): 1.55 - 1.64 (2H, m), 2.14 - 2.20 (4H, m), 2.32 (3H, s), 2.83 - 2.86 (2H, m), 3.48 (1H, m), 3.82 (1H, bs), 6.28 - 6.30 (1H, d, J = 7.6), 6.43 - 6.44 (1H, t), 6.79 - 6.81 (1H, d, J = 8.08 Hz), 7.03 - 7.09 (2H, m), 8.19 (1H, bs); Mass(m/z): 230.4 (M+H)+. Preparation 3: 4-{N-(l-BenzyI piperidin-4-yl)] amino-lH-indole*
Using a similar procedure as given in the preparation 2 and using 1-benzyl piperidine-4-one the above derivative was prepared. I.R (cm'1): 1150,2770, 2937,2977;
'H-NMR (ppm): 1.53 - 1.62 (211, m), 2.13 - 2.22 (4H, m), 2.87 - 2.90 (2H, m), 3.48 - 3,52 (1H, m), 3.54 (2H, s), 3.81 (111, bs), 6.28 - 6.30 (1H, d, J - 7.64 Hz), 6.42 - 6.43 (1H, t), 6.78 - 7.80 (1H, d, J -8.12 Hz), 7.03 - 7.07 (1H, t), 7.08 7.09 (1H, t), 7.32 - 7.33 (511, m), 8.11 (111, bs); Moas(m/a): 306.4.1 (Mill)'.

f reparation 4: 4-[N-EthyI-N-(l-methyl piperidin-4-yI)} amino-1 H-indole.
A mixture of 4-[N-(l-methyl piperidin-4-yl)] amino-1 H-indole (1.5 grams, 6.5 mmol), (obtained from preparation 2), acetaldehyde (1.1 mL, 19.6 mmol), sodium cyanoborohydride (0.0819 grams, 13 mmol) and acetic acid (1.1 mL, 19.5 mmol) in methanol (15 mL) was stirred at room temperature and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (4 hours), the reaction mass was diluted with ice water (500 mL), and basified with aqueous sodium hydroxide solution and the product was extracted with ethyl acetate (2 x 250 mL). The combined organic layer was washed with brine, dried over anhydrous sodium sulphate and concentrated the mass under reduced pressure. The obtained technical product (2.37 grams), was purified by column chromatography using silica-gel (100 - 200 mesh), the eluent system being ethyl acetate and triethyl amine (99:01) to obtain 1.28 grams of the title product. Melting Range: 140.7 -143.7 °C; I.R (cm-1): 1275, 1509,2783,2919, 3082;
'H-NMR (ppm): 0.93 - 0.96 (3H, t), 1.72 - 1.82 (4H, m), 1.99 - 2.04 (2H, m), 2.23 (3H, s), 2.86 - 2.89 (2H, m), 3.23 - 3.29 (2H, q) 3.40 - 3.47 (1H, m), 6.45 - 6.46 (1H, dd, J = 0.72, 3.16 Hz), 6.67 - 6.69 (1H, dd J = 0.52, 3.16 Hz), 6.96 - 7.00 (1H, t), 7.06 - 7.08 (1H, d, J = 8.08 Hz), 7.12 - 7.13 (1H, d, J = 3.16 Hz), 8.19 (lH,bs); Mass (m/z): 258.3 (M+H)+ Preparation 5: 4-[N-MethyI-N-(l-methyl piperidin-4-y!)| amino-lH-Indole.
Using a similar procedure as given in the preparation 4 and using aqueous formaldehyde solution the above derivative was prepared. Melting Range: 156.3 - 158.7 °C; I.R (cm1): 1033, 1270, 1514,2791;
'H-NMR (ppm): 1.76 - 1.80 (2H, m), 1.90 - 2.04 (4H, m), 2.27 (3H, s), 2.86 (3H, s), 2.91 (2H, m), 3.69 - 3.72 (1H, m), 6.51 - 6.52 (1H, t), 6.56 - 6.58 (1H, d, J = 7.56 Hz), 6.98 - 7.00 (1H, d, J = 8.08 Hz), 7.06 - 7.10 (1H, t), 7.12 - 7.13 (1H, t), 8.16 (1H, bs); Mass (m/z): 244.2 (M+H)+ Preparation 6: 4-[N-Methyl-N-(l-t-butyloxycarbonyl piperidin-4-yl)] amino-1 H-indole,
Using a similar procedure as given in the preparation 4, with some non-critical variations the above derivative was prepared. I.R (cm1): 1161, 2788, 2937, 3300;
'H-NMR (ppm): 1.46 (9H, s), 1.73 - 1.77 (4H, m), 2.61 (2H, m), 2.82 (3H, s), 3.77 - 3.83 (1H, m), 4.10 - 4.17 (2H, m), 6.50 - 6.51 (1H, d, J = 3.0 Hz), 6.58 - 6.59 (1H, d, J = 7.44 Hz), 7.00 - 7.02 (1H, d, J = 8.04 Hz), 7.07 - 7.11 (1H, t), 7.13 - 7.14 (1H, t), 8.16 (1H, bs); Mass (m/z): 330.2 (M+H)+.

Preparation 7: 4-[N-MethyI-N-(piperidin-4-yl)] amino-lH-indoIe.
A mixture of 4-[N-Methyl-N-(l-t-butyloxycarbonyl piperidin-4-yl)] amino-IH-indole (0.329 grams, 1.0 mmol) (obtained from preparation 6) and mcthanolic hydrochloric acid (2.0 mL, 18 % w/v, 10 mmol) was refluxed for a period of 1 hour under nitrogen atmosphere and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (1 hour), the reaction mixture was cooled to room temperature and the reaction mass was concentrated under reduced pressure, diluted with ice cold water (25 mL) and pH is adjusted to 9.0 with aqueous sodium hydroxide solution and extracted the product with (2 x 25 mL) ethyl acetate. The combined organic layer was washed with brine solution, dried over anhydrous sodium sulfate and concentrated the mass under reduced pressure to obtain 0.18 grams of the title product. I.R (cm-1): 1150,2783,2937,3300;
'H-NMR (ppm): 2.13 - 2.17 (4H, m), 2.61 - 2.69 (2H, m), 2.99 (3H, s), 3.20 - 3,23 (2H, m), 3.78 -3.82 (1H, m), 6.50 - 6.51 (1H, d, J = 2.32), 6.57 - 6.59 (1H, d, J = 7.52 Hz), 6.99 - 7.01 (1H, d, J » 8.08 Hz), 7.07 - 7.13 (2H, m), 8.19 (1H, bs); Mass(m/z): 230.1 (M+H)+. Preparation 8: l-(4'-Fluoro benzenesulfonyl)-4-nitro-lH-indole.
4-Nitro indole (1 grams, 6.1 mmol) was dissolved in tetrahydrofuran (5 mL) in two necked round bottom flask (50 mL), equipped with guard tube and thermometer socket. Potassium hydroxide powder (1.22 grams, 85 %, 18.5 mmol) was added to the above reaction mass, followed by the addition of 4-fluorobenzene sulfonyl chloride (1.84 grams, 9.2 mmol) dissolved in tetrahydrofuran (5 mL) at room temperature and the progress of the reaction was monitored by thin layer chromatography. After completion of reaction, the reaction mass was poured onto ice-cold water (20 mL) and extracted with ethyl acetate (3 x 20 mL). The combined organic layer was washed with brine solution, dried over anhydrous sodium sulfate and concentrated the mass under reduced pressure to get 1.9 grams (96.44 %) of the title product, which can be used for the next step without further purification.
Melting Range: 140.5 - 145.1 °C; LR(cm"'): 1159,1347,1506;
lH-NMR (ppm): 7,14 - 7.18 (2H, t), 7.44 - 7.48 (2H, m), 7.80 - 7.81 (1H, d, J - 3.67 Hz), 7.91 - 7.94 (2H, m), 8.21 - 8.23 (1H, m), 8.32 - 8.34 (IH, m); Mass(m/z): 321.1 (M+H)+. Preparation 9: 4-Amino-l-(4'-FHioro benzenesulfonyl)-lH-lndole.
l-(4-Fluoro benzenesulfonyl)-4-nitro-lH~indole (1.9 grams, 5.9 mmol) (obtained from preparation 8) dissolved in ethanol (30 mL) was taken in three neck round bottom flask (100 mL), equipped with condenser and thermometer socket. Add water (2 mL) at room temperature, and slowly heat the reaction mass to 40 °C. Iron powder, (1.66 grams, 29.6 mmol) was added pinch wise

to the above reaction mass, followed by the addition of concentrated hydrochloric acid (1 mL). The above reaction mass was refluxed for a period of one hour and the progress of the reaction was monitored by thin layer chromatography. The above reaction mass was cooled to room temperature and filtered through hy-flow bed. The filtrate was concentrated under reduced pressure and the residue was poured onto water (100 mL) and basified with 40% aqueous sodium hydroxide solution, and the product was extracted with ethyl ucelulu (2 x 50 mL). The combined organic layer was washed with brine solution, dried over anhydrous sodium sulfate and concentrated under reduced pressure. The obtained technical product (1.6 grams) was purified by flash chromatography using silica-gel (100 - 200 mesh), the eluent system being ethyl acetate and n-Hexane (15: 85) to obtain 1.4 grams of pure compound. Melting Range: 94.4 -100.7 °C; LR^m"1): 1159, 1347, 1506;
'H-NMR (ppm): 3.9 (2H, bs), 6.5 - 6.52 (1H, d, J = 7.72 Hz), 6.59 - 6.60 (1H, d, 3.76 Hz), 7.09 - 7.13 (3H, m), 7.38 - 7.40 (1H, d, J = 8.32 Hz), 7.45 - 7.46 (1H, d, 3.76 Hz), 7.87 - 7.90 (2H, m); Mass(m/z): 291.3 (M+H)+. Preparation 10: 4-Amino-l-(2,-bromobenzenesuIfonyl)-lH-indoIe.
Using a similar procedure as given in the preparation 9, with some non-critical variations the above derivative was prepared. I.R(cm"'): 1159, 1268, 1347, 1506,2933;
'H-NMR (ppm): 3.94 (2H, bs), 6.49 - 6.51 (1H, dd, J = 7.36, 0.92 Hz), 6.59 - 6.60 (1H, d, 3.76 Hz), 7.0 - 7.07 (2H, m), 7.36 - 7.40 (1H, dt, J = 7.6, 1.64 Hz), 7.43 - 7.47 (1H, dt, 7.84, 1.32 Hz), 7.65 -7.67 (1H, dd, J - 7.84, 1.24 Hz), 7.69 - 7.7 (1H, d, J = 3.84 Hz), 8.04 - 8.07 (1H, dd, J = 7.96, 1.76 Hz);
Mass (m/z): 351.1, 353.1 (M+H)+.
Preparation 11: l-(2'-Bromo benzenesulfonyl)-4-[N-(l-t-butyloxycarbonyl piperidin-4-yI)] amino-lH-indole.
A mixture of 4-amino-l-(2'-bromobenzenesulfonyl)-lH-indole (1.9 grams, 5.4 mmol), (obtained from preparation 10), 1-Boc piperidine-4-one (1.29 grams, 6.5 mmol) and titanium isopropoxide (10 mL, 33.6 mmol) was stirred at room temperature for a period of 5 hours under nitrogen atmosphere. Absolute ethanol (50 mL) was added to the above reaction mass, followed by the addition of sodium cyanoborohydride (0.68 grams, 10.8 mmol) and stirred this reaction mass at room temperature and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (6 hours), the reaction mixture was diluted with ice water (200 mL) and filtered through hy-flow bed. The bed was washed with ethyl acetate (50 mL) and the combined filtrate was basified with 10 % aqueous sodium hydroxide solution and extracted with (2 x 50 mL) ethyl acetate (2 x 50 mL). The combined organic layer was washed with brine, dried over anhydrous

y—
sodium sulphate and concentrated under reduced pressure. The obtained technical product (3.60
grains) was purified by column chromatography using silica-gel (100 - 200 mesh), the eluent system
being ethyl acetate and n-hexane (3:7), to obtain 0.49 grams of the title compound.
I.R(cm*1): 1133,1367, 1676,3340;
!H-NMR (ppm): 1.36 - 1.44 (2H, m), 1.46 (9H, s), 2.04 - 2.10 (2H, m), 2.91 - 2.97 (2H, t), 3.54 (IH,
bs), 4.07 - 4,13 (2H, bs), 6.40 - 6.42 (1H, d, J = 7.65 Hz), 6.54 - 6.55 (1H, d, J - 3.88 Hz), 6.99 - 7.08
(2H, m), 737 - 7.41 (1H, m), 7.44 - 7.52 (1H, m), 7.65 - 7.69 (2H, m), 8.08 - 8.10 (1H, dd, J = 1.69,
7.93 Hz);
Mass (m/z): 534.5,536.2 (M+H)+.
Preparation 12: l-(24-Bromobenzencsulfonyl)-4-[N*(l-t-butyloxycarboflyl piperidin-4-yl)-N-
methyl] amino-IH-indole.
A mixture of l-(2*-Bromo benzenesulfonyl)-4-[N-(l-t-butyloxycarbonyl piperidin-4-yl)] amino-lH-indole (0.39 grams, 0.7 mmol) (obtained from preparation 11), formaldehyde solution (0.2 mL, 30%, 2.1 mmol), sodium triacetoxy borohydride (0.44 grams, 2.1 mmol) and acetic acid (0.04 mL, 0.7 mmol) in methanol (8 mL) was stirred at room temperature and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (4 hours), the reaction mass was diluted with ice water (100 mL) and pH was made basified with aqueous sodium hydroxide solution. The above product was extracted with ethyl acetate (2 x 50 mL), and the combined organic layer was washed with brine solution, dried over anhydrous sodium sulphate and concentrated under reduced pressure. The obtained crude compound (0.28 grams) was purified by column chromatography using silica-gel (100 - 200 mesh), the eluent system being ethyl acetate and n-hexane (2:8) to obtain (0.075 grams) of the title product. Melting Range: 179.4 - 180.7 °C; I.Rfcnf1): 1142, 1363, 1682,2951;
'H-NMR (ppm): 1.45 (9H, s), 1.70 - 1.72 (4H, m), 2.69 - (2H, bs), 2.78 (3H, s), 3.54 - 3.59 (1H, m), 4.16 (2H, bs), 6.63 - 6.64 (1H, d, J = 3.74 Hz), 6.70 - 6.72 (1H, d, J = 7.78 Hz), 7.07 - 7.11 (IH, t), 7.21 - 7.23 (IH, d, J - 8.34 Hz), 7.37 - 7.41 (IH, m), 7.45 - 7.51 (IH, m), 7.66 - 7.67 (IH, d, J = 7.34 Hz), 7.71 - 7.72 (IH, d, J - 4,0 Hz), 8.09 - 8.11 (IH, dd, J = 1.43,7.9 Hz); Mass (m/z): 548.4, 550.1 (M+H)+. Example 1: l-(2'-Broiiiobenzenesulfonyl)-4«|N-(l-methylpiperidin-4-yI)J amino-lH-indoIe.
A mixture of 4-Amino-l-(2'-bromo benzenesulfonyI)-lH-indole (0.1 grams, 0.2 mmol), (obtained from preparation 10), 1-methyl piperidin-4-one (0.04 mL, 0.3 mmol) and titanium isopropoxide (5 mL, 16.8 mmol) was stirred at room temperature for a period of 5 hours under nitrogen atmosphere. Absolute ethanol (50 mL) and sodium cyanoborohydride (0.025 grams, 0.4 mmol) was added to the above reaction mass and further stirred at room temperature and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (6

hours), the reaction mass was diluted with ice water (200 mL) and filtered through hy-flow bed. The
bed was washed with ethyl acetate (50 mL) and the filtrate was basified with 10 % aqueous sodium
hydroxide solution and extracted the product with ethyl acetate (2 x 50 mL). The combined organic
layer was washed with brine solution, dried over anhydrous sodium sulphate and concentrated under
reduced pressure. The obtained crude product (0.61 grams) was purified by column chromatography
using silica-gel (100-200 mesh), the eluent system being ethyl acetate and triethyl amine (99:01), to
obtain 0.093 grams of the title product.
Melting Range: 156.4 -159.0 °C;
I.R(cm*!): 1138, 1393,2776,2940;
'H-NMR(ppm): 1.56-1.61 (2H, m), 2.04 -2.17 (4H, m), 2.31 (3H, s), 2.81 - 2.84 (2H, m), 3.40 (1H,
s), 6.38 - 6.40 (1H, d, J - 7.7 Hz), 6.56 - 6.57 (1H, d, J = 3.8 Hz), 6.97 - 6.99 (1H, d, J = 8.14 Hz),
7.04 - 7.08 (1H, t), 7.36 - 7.40 (1H, m), 7.43 - 7.47 (1H, m), 7.64 - 7.68 (2H, m), 8.05 - 8.08 (1H, dd);
Mass (m/z): 448.2,450.3 (M+H)+.
Example 2: l-^'-Bromo benzenesulfonyl)-4-fN-(piperidin-4-yl)] amino- 1H-indole
dihydrochloride.
A mixture of l-(2'-Bromo benzenesulfonyl)-4-[N-(l-t-butyloxycarbonyI piperidin-4-yl)] amino-lH-indole (0.103 grams, 0.2 mmol) (obtained from preparation 11) and methanolic hydrochloric acid (4 mL, 18 % w/v, 20 mmol) was refluxed for a period of 1 hour under nitrogen atmosphere and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (1 hour), the reaction mixture was cooled to room temperature. The obtained separated solids were filtered and washed with diethyl ether (3 x 10 mL) to obtain 0.084 grams of the title product. Melting Range: 228.6 - 231.0 °C; I.R^m-1): 1174, 1464,2413,2923;
'H-NMR (ppm): 1.63 - 1.71 (2H, m), 2.04 - 2.07 (2H, m), 2.94 - 3.03 (2H, m), 3.29 - 3.32 (2H, m), 3.6 - 3.7 (3H, m), 6.40 - 6.42 (1H, d, J = 8.00 Hz), 7.78 - 7.80 (IH, d, J = 8.2 Hz), 7.00 (1H, t), 7.13 -7.14 (IH, d, J = 3.7 Hz), 7.58 - 7,67 (3H, m), 7.83 - 7.86 (IH, m), 8.02 - 8.04 (IH, dd), 8.71 - 8.82 (2H, bs);
Mass (m/z): 434.2,436.3 (M+H)+. Example 3: l-(2'-Bromo benzenesuIfonyI)-4-[N-methyI-N-(piperidin-4-yl)| amino-lH-indole
dihydrochloride.
A mixture of l-(2'-Bromo benzenesulfonyl>4-[N-(l-t-butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-lH-indole (0.075 grams, 0.1 mmol) (obtained from preparation 12) and methanolic hydrochloric acid (0.13 mL, 18 % w/v, 6 mmol) was refluxed for a period of 1 hour under nitrogen atmosphere and the progress of the reaction was monitored by thin layer chromatography. After completion of the reaction (1 hour), the reaction mixture was cooled to room temperature. The

obtained separated solids were filtered and washed with diethyl ether (3 x 10 mL) to obtain 0.059
grams of the title product.
Melting Range: 200.4 - 201.6 °C;
LRCcm"1): 1149, 1366,1472, 3445;
!H-NMR (ppm): 1.84 - 2.01 (4H, m), 2.82 - 2.94 (4H, m), 3.27 - 3.30 (3H, m), 3.71 - 3.75 (2H, bs),
6.95 (2H, bs), 7.17 - 7.23 (2H, m), 7.63 - 7.70 (2H, m), 7.85 - 7.88 (2H, m), 8.16 - 8.18 (1H, dd);
Mass (m/z): 448.2,450.3 (M+H)+.
Example 4: 1-(2'-Bromo benzenesulfonyI)-4-[N-ethyI-N-(l-methyl piperidin-4-yI)] amino-lH-
indole.
A mixture of 4-[N-Ethyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole (0.2 grams, 0.7
mmol) (obtained from preparation 4) and sodium hydride (0.046 grams, 1.1 mmol) in tetrahydrofuran
(10 mL) was stirred at room temperature for a period of 30 minutes under nitrogen atmosphere. 2-
Bromobenzenesulfonyl chloride (0.2133 grams, 0.8 mmol), dissolved in tetrahydrofuran (10 mL) was
added drop wise to the above reaction mass at temperature of 0 - 5 °C. The above reaction mass was
further stirred at room temperature and the progress of the reaction was monitored by thin layer
chromatography. After completion of the reaction (2 hours), the reaction mixture was diluted with ice
water (100 mL) and extracted with ethyl acetate (2 x 150 mL). The combined organic layer was
washed with brine solution, dried over anhydrous sodium sulphate and concentrated under reduced
pressure. The technical material (0.44 grams), thus obtained, was purified by column chromatography
using silica-gel (100 - 200 mesh), the eluent system being ethyl acetate and triethyl amine (99:01), to
obtain 0.144 grams of the title product.
Melting Range: 118.7-119.5 °C;
LR(cm"'): 1146, 1380, 1483,2777,2935;
'H-NMR (ppm): 0.90 - 0.94 (3H, t), 1.70 - 1.83 (4H, m), 2.02 - 2.07 (2H, t), 2.24 (3H, s), 2.86 - 2.89
(2H, m), 3.21 - 3.26 (3H, m), 6.73 - 6.74 (1H, d, J = 3.56 Hz), 6.89 - 6.91 (1H, d, J = 7.77 Hz), 7.09 -
7.13 (1H, t), 7.26 - 7.28 (1H, d, J = 8.22 Hz), 7.49 - 7.60 (2H, m), 7.73 - 7.77 (2H, m), 8.17 - 8.19
(lH,d,J = 7.l8Hz);
Mass (m/z): 476.2, 478.1 (M+H)+.
Example 5: 4-[N-EthyI-N-(l-methyl piperidin-4-yl)) amino-l-(4'-methyl benzenesu!fonyl)-lH-
indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. Melting Range: 134.4 - 135.2 °C; LRCcm-1): 1137, 1367, 1482,2279,2938;
'H-NMR (ppm): 0.86 - 0.90 (3H, t), 1.66 - 1.79 (4H, m), 1.98 - 2.04 (2H, t), 2.22 (3H, s), 2.33 (3H, s), 2.83 - 2.86 (2H, m), 3.17 - 3.25 (3H, m), 6.71 (1H, d, J = 3.5 Hz), 6.88 - 6.90 (1H, d, J = 7.79 Hz),

7.16 - 7.20 (1H, t), 7.29 - 7.31 (2H, m), 7.55 - 7.56 (1H, d, J = 3.65 Hz), 7.60 - 7.62 (1H, d, J = 8.24
Hz), 7.77 - 7.80 (2H, m);
Mass (m/z): 412.3 (M+H) +
Example 6: 1-(2'-Chloro benzenciulfuiiyl)-4-[N-ethyl-N-(1-meithyI pipcridin-4-yl)| amino-111-
indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. Melting Range: 128.4 - 128.9 °C; LRCcm-1): 1146, 1367, 1484, 2782;
'H-NMR (ppm): 0.90 - 0.94 (3H, t), 1.67 - 1.83 (4H, m), 2.01 - 2.07 (2H, t), 2.24 (3H, s), 2.86 - 2.88 (2H, m), 3.20 - 3.26 (3H, m), 6.73 - 6.74 (1H, d, J = 3.56 Hz), 6.89 - 6.91 (1H, d, J = 7.77 Hz), 7.09 -7.13 (1H, t), 7.28 - 7.30 (1H, d, J = 8.22 Hz), 7.53 - 7.63 (3H, m), 7.69 - 7.70 (1H, d, J = 3.66 Hz), 8.21-8.23(lH,d,J = 7.65Hz); Mass (m/z): 432.3,434.1 (M+H)+
Example 7: l-(3'-Chloro benzenesulfonyl)-4-|N-(l-t-buty!oxycarbonyl piperidin-4-yl)-N-methyl| amino-lH-indole.
Using a similar procedure as given in the preparation 12, with some non-critical variations the above derivative was prepared. Melting Range: 170.8 - 175 °C; I.R(cm''): 1173, 1373, 1689,2956;
'H-NMR (ppm): 1.45 (9H, s), 1.68 - 1.71 (4H, m), 2.67 (2H, bs), 2.76 (3H, s), 3.49 - 3.53 (1H, m), 4.16 (2H, bs), 6.66 - 6.67 (1H, d, J = 3.76 Hz), 6.72 - 6.74 (1H, d, J = 7.78 Hz), 7.19 - 7.23 (1H, t), 7.36 - 7.40 (1H, t), 7.48 - 7.56 (3H, m), 7.75 - 7.78 (1H, m), 7.86 - 7.87 (1H, m); Mass (m/z): 504.4, 506.1 (M+H)+
Example 8: 4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-l-(4'-isopropyI benzenesulfonyl)-lH-indole.
Using a similar procedure as given in the preparation 12, with some non-critical variations the above derivative was prepared. I.R(cm"'): 1170, 1375, 1683,2950;
'H-NMR (ppm): 1.18-1.20 (6H, d), 1.45 (9H, s), 1.71 - 1.76 (4H, bs), 2.66 (2H, bs), 2.81 (3H, s), 2.89 - 2.91 (1H, sept), 3.52 - 3.54 (1H, m), 4.13 (2H, bs), 6.62 (1H, d, J = 3.6 Hz), 6.70 - 6.72 (1H, d, J = 7.78 Hz), 7.17 - 7.21 (1H, t), 7.26 - 7.28 (2H, m), 7.51 - 7.52 (1H, d, J = 4.0 Hz), 7.56 - 7.58 (1H, d, J = 7.78 Hz), 7.80 - 7.82 (2H, m); Mass (m/z): 512.5 (M+H) +
Example 9: 4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)-N-methyl| amino-l-(4'-fluoro benzenesulfony I)-1 H-indole.

Using a similar procedure as given in the preparation 12, with some non-critical variations the above derivative was prepared. I.R (cm"1): 1129, 1370, 1688;
'H-NMR (ppm): 1.45 (9H, s), 1.71 (4H, bs), 2.66 (2H, bs), 2.76 (3H, s), 3.51 - 3.52 (1H, m), 4.16 (2H, bs), 6.64 - 6.65 (1H, d, J = 4 Hz), 6.71 - 6.73 (1H, d, J = 7.78 Hz), 7.08 - 7.13 (2H, m), 7.17 -7.21 (1H, t), 7.48 - 7.49 (IH, d, J = 4 Hz), 7.54 - 7.56 (1H, d, J = 7.78 Hz), 7.88 - 7.93 (2H, m); Mass(m/z): 488.3, (M+H) *
Example 10: 4-[N-(l-t-ButyloxycarbonyI piperidin-4-yl)-N-methyl] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indole.
Using a similar procedure as given in the preparation 12, with some non-critical variations the above derivative was prepared. I.R(cm-'): 1135,1363,1688;
'H-NMR (ppm): 1.45 (9H, s), 1.67 (4H, bs), 2.66 (2H, bs), 2.76 (3H, s), 3.49 - 3.52 (IH, m), 4.11-4.16 (2H, bs), 6.67 - 6.68 (IH, d, J = 4 Hz), 6.72 - 6.74 (IH, d, J = 7.78 Hz), 7.19 - 7.23 (IH, t), 7.49 -7.50 (IH, d J = 4 Hz), 7.55 - 7.61 (2H, m), 7.78 - 7.80 (IH, d, J = 7.78 Hz), 8.04 - 8.06 (IH, d, J = 7.78 Hz), 8.15 (lH,s); Mass (m/z): 538.4 (M+H)+
Example 11: 4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)] amino-l-(3'-ch!oro benzenesulfonyl)-lH-indoIe.
Using a similar procedure as given in the preparation 11, with some non-critical variations the above derivative was prepared. I.R (cm1): 1129, 1366, 1682, 3367;
!H-NMR (ppm): 1.37 - 1.39 (2H, m), 1.46 (9H, s), 2.04 - 2.09 (2H, m), 2.90 - 2.96 (2H, t), 3.52 (IH, bs), 4.06 (2H, bs), 6.42 - 6.44 (IH, d, J = 7.9 Hz), 6.57 - 6.58 (IH, d, J = 3.78 Hz), 7.15 - 7.19 (IH, t), 7.32 - 7.39 (2H, m), 7.43 - 7.44 (IH, d, J = 3.79 Hz), 7.48 - 7.50 (IH, m), 7.74 - 7.76 (IH, d, J = 7.92 Hz), 7.85- 7.86 (lH,t); Mass (m/z): 490.2, 492.3 (M+H)+
Example 12: l-(3'-Chloro benzenesuIfonyI)-4-[N-methyI-N-(piperidin-4-yl)l amino-lH-indole dihydrochloride.
Using a similar procedure as given in the example 3, with some non-critical variations the above derivative was prepared. Melting Range: 172.8 - 175.5 °C; I.R (cm1): 1177, 1383, 2935, 3419;
'H-NMR (ppm): 1.85 - 2.02 (4H, m), 2.84 - 2.90 (5H, bs), 3.32 - 3.34 (3H, m), 7.05 (2H, bs), 7.28 -7.32 (IH, t), 7.61 - 7.67 (2H, m), 7.78 - 7.79 (IH, dd), 7-88 (IH, bs), 7.98 - 8.00 (IH, d, J = 7.9 Hz), 8.10(lH,s);

Mass (m/z): 404.3,406.3 (M+H) +
Example 13: l-(3'-Chloro benzenesulfonyl)-4-[N-(piperidin-4-yl)] atnino-lH-indole
dihydrochloride.
Using a similar procedure as given in the example 2, with some non-critical variations the above derivative was prepared. Melting Range: 149.4 -151.5 °C; I.R (cm'1): 1134, 1380, 1573,3391;
'H-NMR (ppm): 1.68 - 1.74 (2H, m), 2.01 - 2.04 (2H, m), 2.93 - 2.96 (2H, m), 3.26 - 3.29 (2H, m), 3.60 - 3.65 (3H, m), 6.51 - 6.53 (1H, d, J = 7.8 Hz), 7.11 - 7.15 (1H, t), 7.18 - 7.19 (1H, d, J = 3.7 Hz), 7.23 - 7.25 (1H, d), 7.58 - 7.62 (1H, t, J - 8.0 Hz), 7.65 - 7.66 (1H, d, J = 3.76 Hz), 7.75 - 7.77 (1H, m), 7.89 - 7.91 (1H, m), 7.97 - 7.98 (1H, t), 8.90 - 9.02 (2H, bs); Mass (m/z): 390.2,392.3, (M+H)+ Example 14: l-(3'-Chloro benzenesulfonyl)-4-[N-(l-methyl piperidin-4-yl)] amino-lH-indole.
Using a similar procedure as given in the example 1, with some non-critical variations the above derivative was prepared. Melting Range: 135.1 -140.8 °C; I.R (cm'1): 1130, 1371, 1593,3418;
'H-NMR (ppm): 1.50 - 1.51 (2H, m), 2.04 - 2.16 (4H, m), 2.30 (3H, s), 2.81 - 2.84 (2H, m), 3.36 -3.41 (1H, m), 6.40 - 6.42 (1H, d, J = 7.9 Hz), 6.58 - 6.59 (1H, d, J = 3.7 Hz), 7.14 - 7.18 (1H, t), 7.30 -7.32 (1H, d, J = 8.2 Hz), 7.38 - 7.34 (1H, t), 7.42 - 7.43 (1H, d, J = 3.78 Hz), 7.46 - 7.49 (1H, m), 7.73 - 7.75 (1H, dd), 7.84 - 7.85 (1H, t); Mass (m/z): 404.2,406.3, (M+H)+.
Example 15: l-(4'-Fluoro benzenesulfonyl)-4-[N-methyl-N-(piperidin-4-yl)] amino-lH-indole dihydrochloride.
Using a similar procedure as given in the example 3, with some non-critical variations the above derivative was prepared. I.R (cm-1): 1140, 1390, 2774, 2941;
'H-NMR (ppm): 1.73 - 1.82 (2H, m), 1.99 - 2.02 (2H, m), 2.81 - 2.87 (2H, t), 3.12 (3H, s), 3.35 - 3.41 (3H, m), 3.85 - 3.91 (1H, m), 6.90 - 6.91 (1H, d, J = 3.8 Hz), 7.10 - 7.14 (2H, t), 7.23 - 7.25 (1H, d, J = 7.9 Hz), 7.33 - 7.37 (1H, t), 7.78 - 7.79 (1H, d. J - 3.8 Hz), 7.89 - 7.96 (3H, m); Mass (m/z): 388.4 (M+H)+
Example 16: l-(4'-Isopropyl benzenesulfonyl)-4-|N-methyI-N-(piperidin-4-yI)J amino-lH-indole dihydrochloride.
Using a similar procedure as given in the example 3, with some non-critical variations the above derivative was prepared. I.R (cm4): 1135, 1363, 2735, 2938;

'H-NMR (ppm): 1.09 - 1.19 (6H, d), 1.83 - 1.91 (2H, m), 2.00 - 2.03 (2H, m), 2.87 - 2.93 (3H, m),
3.05 (3H, s), 3.39 - 3.47 (2H, m), 3.82 - 3.85 (1H, m), 6.96 - 6.97 (1H, d, J = 3.8 Hz), 7.22 - 7.24 (1H,
d, J = 7.94 Hz), 7.41 - 7.47 (3H, m), 7.88 - 7.95 (4H, m);
Mass (m/z): 412.3 (M+H)+
Example 17: 4-[N-(l-Benzyl piperidin-4-yl) amino-l-(4'-fluoro benzenesulfonyl)-lH-indole.
Using a similar procedure as given in the preparation 11, with some non-critical variations the above derivative was prepared. I.R (cm"1): 1135, 1363,2735,2938;
'H-NMR (ppm): 1.48 - 1.57 (2H, m), 2.04 - 2.07 (2H, m), 2.12 - 2.18 (2H, m), 2.84 - 2.87 (2H, m), 3.39 - 3.45 (1H, m), 3.52 (2H, s), 3.72 (1H, bs), 6.38 - 6.40 (1H, d, J = 7.9 Hz), 6.55 - 6.56 (1H, d, J = 3.8 Hz), 7.06 - 7.16 (3H, m), 7.25 - 7.32 (6H, m), 7.42 - 7.43 (1H, d, J = 3.7 Hz), 7.86 - 7.90 (2H, m); Mass (m/z): 464.3 (M+H)+
Example 18: 1-(2% 5'-Dimethoxy benzenesuIfonyl)-4-[N-methyl N-(l-mcthyI pipcridin-4-yl)| amino-lll-indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. Melting Range: 168.5 -170.3 °C; I.R (cm1): 1142, 1364,2779,2936;
"H-NMR (ppm): 1.71 - 1.73 (2H, m), 1.89 - 1.95 (4H, m), 2.26 (3H, s), 2.79 (3H, s), 2,90 - 2.92 (2H, m), 3.45 - 3.49 (1H, m), 3.65 (3H, s), 3.82 (3H, s), 6.57 - 6.58 (1H, d, J = 3.7 Hz), 6.67 - 6.69 (1H, d, J = 7.7 Hz), 6.79 - 6.81 (1H, d, J = 9.0 Hz), 7.02 - 7.05 (1H, dd, J = 3.1, 9.0 Hz), 7.07 - 7.12 (1H, t, J = 8.0 Hz), 7.31 - 7.33 (1H, d, J = 8.5 Hz), 7.59 - 7.63 (2H, dd, J = 3.7,11.8 Hz); Mass (m/z): 444.3 (M+H)+
Example 19: l-(4'-Methyl benzenesulfonyI)-4-{N-methyl-N-(l-methyl piperldin-4-yl)] amino-lH-indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm-1): 1140, 1360, 2779, 2935;
'H-NMR (ppm): 1.70 - 1.73 (2H, m), 1.89 - 1.97 (4H, m), 2.27 (3H, s), 2.34 (3H, s), 2.77 (3H, s), 2.91 - 2.93 (2H, m), 3.42 (1H, m), 6.61 - 6.62 (1H, d, J = 3.6 Hz), 6.67 - 6.69 (1H, d, J = 7.7 Hz), 7.14 -7.18 (1H, t, J = 8.0 Hz), 7.21 - 7.23 (2H, m), 7.49 - 7.50 (IH, d, J = 3.7 Hz), 7.53 - 7.55 (1H, d, J = 8.2 Hz), 7.76 - 7.78 (2H, m); Mass (m/z): 398.3 (M+H)+
Example 20: l-(2'-ChIoro benzenesulfonyl)-4-|N-methyI-N-(l-methyl piperidin-4-yl)| amino-lH-indole.

Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm'1): 1145,1372,2780,2933;
'H-NMR (ppm): 1.72 - 1.75 (2H, m), 1.91 - 1.97 (4H, m), 2.27 (3H, s), 2.80 (3H, s), 2.90 - 2.92 (2H, m), 3.44 - 3.47 (1H, m), 6.63 - 6.64 (1H, d, J = 3.77 Hz), 6.67 - 6.69 (1H, d, J = 7.75 Hz), 7.07 - 7.11 (1H, t), 7.20 - 7.20 (1H, d, J = 8.2 Hz), 7.41 - 7.45 (2H, m), 7.47 - 7.52 (1H, m) 7.67 - 7.68 (1H, d, J = 3.8 Hz), 8.14- 8.16 (lH,m); Mass (m/z): 418.4,420.2 (M+H)+
Example 21: l-(4'-Fluoro bcnzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-111-indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm'1): 1126, 1374, 2776, 2929;
■H-NMR (ppm): 1.83 -1.88 (2H, m), 2.04 - 2.08 (2H, m), 2.71 (3H, s), 2.87 - 2.93 (2H, m), 3.12 (3H, s), 3.44 - 3.48 (2H, m), 3.92 (1H, m), 6.93 - 6.94 (1H, d, J = 3.8 Hz), 7.13 - 7.17 (2H, t), 7.25 - 7.27 (1H, d, J = 7.9 Hz), 7.36 - 7.40 (1H, t), 7.81 - 7.82 (1H, d, J = 3.8 Hz), 7.92 - 7.98 (3H, m); Mass (m/z): 402.3 (M+H)+
Example 22: l-(3'-Chloro benzenesulfonyl)-4-[N-methyI-N-(l-methyl piperidin-4-yl)] amino-lH-indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm1): 1129, 1372,2775,2941;
'H-NMR (ppm): 1.70 - 1.72 (2H, m), 1.89 - 1.95 (4H, m), 2.26 (3H, s), 2.79 (3H, s), 2.89 - 2.91 (2H, m), 3.39 - 3.42 (1H, m), 6.66 - 6.71 (2H, m), 7.18 - 7.2 (1H, t), 7.57 - 7.58 (1H, t), 7.49 - 7.53 (3H, m), 7.53 - 7.55 (1H, d, J = 8.0 Hz), 7.85 - 7.86 (1H, t); Mass (m/z): 418.4, 420.1(M+H)+.
Example 23: 4-lN-Methyl-N-(l-methyl piperidin-4-yl)] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm1): 1139, 1389, 2793, 2945;
'H-NMR (ppm): 1.69 - 1.71 (2H, m), 1.85 - 1.97 (4H, m), 2.26 (3H, s), 2.78 (3H, s), 2.89 - 2.91 (2H, m), 3.37 - 3.43 (1H, m), 6.67 - 6.68 (1H, d, J = 3.75 Hz), 6.70 - 6.72 (1H, d, J = 7.85 Hz), 7.18 - 7.22 (1H, t), 7.48 - 7.49 (1H, d, J = 3.70 Hz), 7.52 - 7.54 (1H, d, J = 8.29 Hz), 7.56 - 7.60 (1H, t), 7.77 -7.79 (1H, d, J = 7.86 Hz), 8.03 - 8.05 (1H, d, J = 8.0 Hz), 8.15 (1H, bs); Mass (m/z): 452.8 (M+H)+

Example 24: l-(4'-IsopropyI benzenesulfonyl)-4-|N-methyl-IN-(l-methyl piperidin-4-yl)] amino-IH-indoIe.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R(cm-'): 1134, 1371,2781,2938;
'H-NMR (ppm): 1.18-1.20 (6H, d), 1.70 - 1.72 (2H, m), 1.88 -1.94 (4H, m), 2.26 (3H, s), 2.78 (3H, s), 2.86 - 2.91 (3H, m), 3.43 (1H, m), 6.62 - 6.63 (1H, d, J = 3.6 Hz), 6.68 - 6.69 (1H, d, J = 7.84 Hz), 6.98 - 6.69 (1H, d. J = 7.81 Hz), 7.16 - 7.20 (1H, t, J = 8.12 Hz), 7.26 - 7.28 (2H, dd), 7.50 - 7.51 (1H, d, J = 3.76 Hz), 7.55 - 7.57 (1H, d, J = 8.29 Hz), 7.79 - 7.81 (1H, dd); Mass (m/z): 426.3 (M+H)+.
Example 25: l-(2'-Bromo benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-lH-indoie.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm"1): 1143, 1369,2779,2929;
'H-NMR (ppm): 1.72 - 1.75 (2H, m), 1.90 - 1.97 (4H, m), 2.27 (3H, s), 2.81 (3H, s), 2.90 - 2.92 (2H, m), 3.46 - 3.47 (1H, m), 6.64 - 6.65 (1H, d, J = 3.76 Hz), 6.68 - 6.70 (1H, d, J = 7.8 Hz), 7.09 - 7.11 (1H, t), 7.19 - 7.21 (1H, d, J = 8.24 Hz), 7.39 - 7.46 (2H, m), 7.66 - 7.71 (2H, m), 8.06 - 8.09 (1H, dd, J = 1.72, 7.96 Hz); Mass (m/z): 462.2,464.3 (M+H)+
Example 26: l-(4'-Methoxy benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole.
Using a similar procedure as given in the example 4, with some non-critical variations the above derivative was prepared. I.R (cm1): 1161, 1366,2788,2937;
"H-NMR (ppm): 1.69 - 1.75 (2H, m), 1.88 - 1.99 (4H, m), 2.27 (3H, s), 2.77 (3H, s), 2.89 - 2.91 (2H, m), 3.41 - 3.43 (1H, m), 3.79 (3H, s), 6.60 - 6.61 (1H, d, J = 3.76 Hz), 6.66 - 6.68 (1H, d, J = 7.83 Hz), 6.85 - 6.88 (2H, dd, J = 2.8, 9.9 Hz), 7.14 - 7.18 (1H, t), 7.48 - 7.49 (1H, d, J = 3.71 Hz), 7.52 -7.54 (1H, d, J = 8.27 Hz), 7.80 - 7.83 (2H, dd, J = 2.9,9.99 Hz); Mass (m/z): 414.4 (M+H)+. Examples 27-58:
The person skilled in the art can prepare the compounds of Examples 27-58 by following the procedures described above.

The ingredients were melted together and mixed on a steam bath and poured into molds containing 2.5 grams total weight Example 64: Topical Formulation

All of the ingredients, except water, were combined! and heated to about 60 °C with stirring. A sufficient quantity of water at about 60 °C was then addfed with vigorous stirring to emulsify the ingredients and then water added q.s about 100 grams. Example 65: Binding assay for human 5-HT6 receptor
Compounds can be tested according to the following the procedures. Materials and Methods:
Receptor source: Human recombinant expressed in H|EK293 cells
Radioligand : [3H]LSD (60-80 Ci/mmol)
Final ligand concentration - [1.5 nM]
Non-specific determinant: Methiothepin mesylate - [0.1 \xM]
Reference compound : Methiothepin mesylate
Positive control: Methiothepin mesylate Incubation conditions:
Reactions were carried out in 50 ^iM TRIS-HCI (pH 7.4) containing 10 \iM MgCl2, 0.5 mM EDTA for 60 minutes at 37 °C. The reaction was terminated by rapid vacuum filtration onto glass fiber filters. Radioactivity trapped onto the filters was determined (and compared to control values in order to ascertain any interactions of test compound(s) with the cloned serotonin 5-HT6 binding site.

Literature Reference: Monsma F. J. Jr., et al., Molecular Cloning and Expression of Novel Serotonin Receptor with High Affinity for Tricyclic Psychotropic Drugs. Mol. Pharmacol. (43); 320-327 (1993). Example 66: 5-HT6 functional assay cyclic AMP
The antagonist property of the compounds at the human 5-HT6 receptors was determined by testing their effect on cAMP accumulation in stably transfected HEK293 cells. Binding of an agonist to the human 5-HT6 receptor will lead to an increase in adenyl cyclase activity. A compound that is an agonist will show an increase in cAMP production and a compound that is an antagonist will block the agonist effect.
Human 5-HT6 receptors were cloned and stably expressed in HEK293 cells. These cells were plated in 6 well plates in DMEM/F12 media with 10% fetal calf serum (FCS) and 500 tig/mL G418 and incubated at 37 °C in a C02 incubator. The cells were allowed to grow to about 70 % confluence before initiation of the experiment. On the day of the experiment, the culture media was removed and the cells were washed once with serum free medium (SFM). Two mL of SFM+IBMX media was added and incubated at 37 °C for 10 minutes. The media were removed and fresh SFM+IBMX media containing various compounds and 1 jaM serotonin (as antagonist) were added to. the appropriate wells and incubated for 30 minutes. Following incubation, the media were removed and the cells were washed once with 1 mL of PBS (phosphate buffered saline). Each well was treated with 1 mL cold 95% ethanol and 5 \xM EDTA (2:1) at 4 °C for 1 hour. The cells were then scraped and transferred into Eppendorf tubes. The tubes were centrifuged for 5 minutes at 4 °C and the supernatants were stored at 4 °C until assayed.
cAMP content was determined by EIA (enzyme-immunoassay) using the Amersham Biotrak cAMP EIA kit (Amersham RPN 225). The procedure used is as described for the kit. Briefly, cAMP is determined by the competition between unlabeled cAMP and a fixed quantity of peroxidase-labelled cAMP for the binding sites on anti-cAMP antibody. The antibody is immobilized onto polystyrene microtitre wells precoated with a second antibody. The reaction is started by adding 50 ^L, peroxidase-labeled cAMP to the sample (100 |iL) pre-incubated with the antiserum (100 mL) for 2 hours at 4 °C. Following 1 hour incubation at 4 °C, the unbound ligand is separated by a simple washing procedure. Then an enzyme substrate, trimethylbenzidine (1), is added and incubated at room temperature for 60 minutes. The reaction is stopped by the addition of 100 mL 1.0 M sulphuric acid and the resultant color read by a microtitre plate spectrophotometer at 450 nm within 30 minutes.
In the functional adenylyl cyclase assay, some of the compound of this invention was found to be a competitive antagonist with good selectivity over a number of other receptors including other serotonin receptors such as 5-HTjA and 5-HT7. Example 67: Rodent Pharmacokinetic Study

Male wistar rats (230 - 280 grams) obtained from NIN (National Institute of Nutrition, Hyderabad, India) were used as an experimental animal.
Three to five animals were housed in each cage. Animals were kept fasted over night and maintained on a 12 hours light/dark cycle. Three rats were dosed__NCE (10 mg/Kg) orally and intravenously on day 0 and day 2
At each time point blood was collected by jugular vein. Plasma was stored frozen at -20°C until analysis. The concentrations of the NCE compound in plasma were determined using LC-MS/MS method.
Schedule time points: Pre dose 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 10, 12 and 24 hours after dosing (n"3). The NCE compounds were quantified in plasma by validated LC-MS/MS method using solid phase extraction technique. NCE compounds were quantified in Ihe calibration range of 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, AUCt, AUCinf, half life, volume of distribution, clearance, mean residence time and thereby oral bioavailability were calculated by non-compartmental model using software WinNonlin version 5.1.

Example 68: Rodent Brain Penetration Study
Male Wister rats (230 - 280 grams) obtained from NIN (National Institute of Nutrition, Hyderabad, India) were used as an experimental animal. 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 at steady state in rat. One day prior to dosing day, male wistar rats (225 - 250 grams) were anesthetized with halothane for surgical placement of jugular and femoral vein catheters. After surgery, the rats were housed in individual rat infusion cage connected with infusion components (Instech Solomon; Plymouth Meeting, PA. USA) and allowed free access to food and water

NCE compound was dissolved in water and administered at a constant infusion rate (5 ml/kg/hr) over 6-10 hours at a target dose rate of 1.0 mg free base/kg/h. Blood samples were removed during the latter part of the infusion to confirm steady-state blood concentrations, brain and blood was collected and estimated. Animals will be sacrificed to collect the plasma and brain tissue and was homogenized. Plasma and Brain was stored frozen at -20 °C until analysis. The concentrations of the NCE compound in plasma and Brain were determined using LC-MS/MS method.
The NCE compounds were quantified in plasma and brain homogenate by validated LC-MS/MS method using solid phase extraction technique. NCE compounds 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. Extents of brain-blood ratio were calculated (Cb/Cp).

Example 69: Rodent Brain Micro dialysis Study for possible modulation of Neurotransmitters,
Male Wister rats (230 - 280 grams) obtained from N. I. N. (National Institute of Nutrition, Hyderabad, India) were used as experimental animals.
Group allocation Group 1: Vehicle (Water; 5 mL/kg; p.o.), Group 2: NCE (3 mg/kg; p.o.), Group 3: NCE (10 mg/kg; p.o.)
Surgical Procedure: Rats were anesthetized with chloral hydrate and placed in Stereotaxic frame. Guide cannula (CMA/12) was placed at AP: -5.2 mm, ML: +5.0 mm relative from bregma and DV: -3.8 mm from the brain surface according to the atlas of Paxinos and Watson (1986). While the animal was still anesthetized, a micro dialysis probe (CMA/12, 4 mm, PC) was inserted through the guide cannula and secured in place. After surgery recovery period of 48 - 72 hours was maintained before subjecting the animal for study.
A day prior to study animals were transferred to home cages for acclimatization and implanted probe was perfused overnight with a modified Ringer's solution comprised of: 1.3 pM CaC12 (Sigma), 1.0 jaM MgCI2 (Sigma), 3.0 pM KC1 (Sigma), 147.0 pM NaCl (Sigma), 1.0 pM Na2HP04.7H20 and 0.2 pM NaH2P04.2 H20 and and 0.3 pM neostigmine bromide (Sigma) (pH to 7.2) at a rate of 0.2 fiL/minute set by a microinfusion pump (PicoPlus, Harward). On the day of experiment perfusion rate was changed to 1.2 pL/minutes and allowed for 3 hours stabilization. After

stabilization period, four basals were collected at 20 minutes intervals before dosing. Dialysate samples were collected in glass vials using CMA/170 refrigerated fraction collector.
Vehicle or NCE (3 mg/kg or 10 mg/kg) was administered by gavage after four fractions had been collected. The perfusate was collected until 6 hours after administration.
Acetylcholine concentrations in dialysate samples were measured by LC-MS/MS (API 4000, MDS SCIEX) method. Acetylcholine is quantified in the calibration range of 0.250 to 8.004 ng/mL in dialysates.
On completion of the microdialysis experiments, the animals were sacrificed and their brains were removed and stored in a 10% formaJin solution. Each brain was sliced at 50 p on a cryostat (Leica) stained and examined microscopically to confirm probe placement. Data from animals with incorrect probe placement were discarded.
Microdialysis data were expressed as percent changes (Mean ± S.E.M.) of baseline that was defined as the average absolute value (in fM/10 \xL) of the four samples before drug administration.
Effects of NCE (3 & 10 mg/kg) and Vehicle treatments were statistically evaluated by oneway ANOVA followed by Dunnett's multiple comparison tests. In all statistical measures, a p < 0.05 was considered significant. The Graph Pad Prism program statistically evaluated the data Example 70: Food Intake Measurement
Male Wister rats (120-140 grams) obtained from N. I. N. (National Institute of Nutrition, Hyderabad, India) were used. The chronic effect of the compounds of general formula (I) on food intake in well-fed rats was then determined as follows.
The rats were housed in single home cages for 28 days. During this period, the rats were either dosed orally or ip, with a composition comprising a compound of formula (1) or a corresponding composition (vehicle) without the said compound (control group), once a day. The rat is provided with ad libitum food and water.
On 0, 1st, 7th, 14th, 21st and 28th day the rats were left with the pre-weighed amounts of food. Food intake and weight gain were measured on a routine basis. Also a food ingestion method is disclosed in the literature (Kask et al., European Journal of Pharmacology, 414, 2001, 215-224 and Turnball et. al., Diabetes, vol 51, August, 2002, and some in-house modifications.). The respective parts of the descriptions are herein incorporated as a reference and they form part of the disclosure.
Some representative compounds have shown the statistically significant decrease in food intake, when conducted in the above manner at the doses of either 10 mg/Kg or 30 mg/Kg or both Example 71: Object Recognition Task Model
The cognition-enhancing properties of compounds of this invention were estimated using a model of animal cognition: the object recognition task model.
Male Wister rats (230 - 280 grams) obtained from N. I. N. (National Institute of Nutrition, Hyderabad, India) 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 corners, 10 cm. 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 Ennaceur, A., Delacour, J., 1988, A new one-trial test for neurobiological studies of memory in rats - Behavioral data, Behav. Brain Res., 31, 47-59.
Some representative compounds have shown positive effects indicating the increased novel object recognition viz; increased exploration time with novel object and higher discrimination index.

Example 72: Water Maze
The water maze apparatus consisted of a circular pool (1.8 m diameter, 0.6 m high) constructed in black Perspex (TSE systems, Germany) filled with water (24 ± 2°C) and positioned underneath a wide-angled video camera to track animal. The 10 cm perspex platform, lying 1 cm

below the water surface, was placed in the centre of one of the four imaginary quadrants, which remained constant for all rats. The black Perspex used in the construction of the maze and platform offered no intramaze cues to guide escape behavior. By contrast, the training room offered several strong extramaze visual cues to aid the formation of the spatial map necessary for escape learning. An automated tracking system, [Videomot 2 (5.51), TSR systems, Germany] was employed. This program analyzes video images acquired via a digital camera and an image acquisition board that determined path length, swim speed and the number of entries and duration of swim time spent in each quadrant of the water maze.

Example 73: Chewing/Yawning/Stretching induction by 5-HT6 R antagonists
Male Wister rats weighing 200-250 grams were used. Rats were given vehicle injections and placed in individual, transparent chambers for 1 hour each day for 2 days before the test day, to habituate them to the observation chambers and testing procedure. On the test day, rats were placed in the observation chambers immediately after drug administration and observed continuously for yawning, stretching, and chewing behaviors from 60 to 90 minutes after drug or vehicle injections. 60 minutes prior to the drug administration Physostigmine, 0.1 mg/kg i.p, was administered to all the animals. Average number of yawns, stretches and vacuous chewing movements during the 30 minutes observation period were recorded.
Reference: (A) King M. V., Sleight A., J., Woolley M. L., and et. al., Neuropharmacology, 2004, 47, 195-204. (B) Bentey J. C, Bourson A., Boess F. G., Fone K. C. F., Marsden C. A., Petit N., Sleight A. J., British Journal of Pharmacology, 1999, 126 (7), 1537-1542). Example 74: Passive avoidance
Animals were trained in a single-trial, step through, light-dark passive avoidance paradigm. The training apparatus consisted of a chamber 300 mm in length, 260 mm wide, and 270 mm in height, constructed to established designs. The front and top were transparent, allowing the experimenter to observe the behavior of the animal inside the apparatus. The chamber was divided into two compartments, separated by a central shutter that contained a small opening 50 mm wide and 75 mm high set close to the front of the chamber. The smaller of the compartments measured 9 mm in width and contained a low-power (6V) illumination source. The larger compartment measured 210 mm in width and was not illuminated. The floor of this dark compartment consisted of a grid of 16 horizontal stainless-steel bars that were 5 mm in diameter and spaced 12.5 mm apart. A current generator supplied 0.75 mA to the grid floor, which was scrambled once every 0.5 seconds across the 16 bars. A resistance range of 40-60 micro ohms was calculated for a control group of rats and the

apparatus was calibrated accordingly. An electronic circuit detecting the resistance of the animal ensured an accurate current delivery by automatic variation of the voltage with change in resistance. Experimental procedure:
This was carried out as described previously. Adult male Wister rats weighing 200-230 grams were used. Animals were brought to the laboratory 1 hour before the experiment. On the day of training, animals were placed facing the rear of the light compartment of the apparatus. The timer was started once the animal has completely turned to face the front of the chamber. Latency to enter the dark chamber was recorded (usually < 20 seconds) and having completely entered the dark compartment an inescapable foot shock of 0.75 mA for 3 seconds was administered to the animal. Animals were then returned to their home cages. Between each training session, both compartments of the chamber were cleaned to remove any confounding olfactory cues. Recall of this inhibitory stimulus was evaluated 24 hours, 72 hours and on 7 day post-training by returning the animal into the light chamber and recording their latency to enter the dark chamber, a criterion time of 300 seconds was employed.
Reference: (A) Callahan P.M., Rowe N. B., Tehim A., Abst. 776.19.2004, Society for neuroscience, 2004. (B) Fox G. B., Connell A. W. U., Murphy K. J., Regan C. M., Journal of Neurochemistry, 1995, 65, 6, 2796-2799

r
We claim:
1. A compound of formula (I)

Wherein R represents hydrogen, (CrC3) alkyl or (C3-C6) cycloalkyl;
Ri, R2 and R3 may be same or different and each independently represent hydrogen, halogen, (CrC3)alkyl, halo(CrC3)alkyl, (C3-C6) cycloalkyl, (CrC3)alkoxy or halo (CrC3)alkoxy;
R4 represents hydrogen, (CrC3)alkyl, halo(CrC3)aIkyI, aryl, aralkyl, (C3-C6) cycloalkyl or t-butyloxy carbonyl;
"m" represents 0 to 4;
"n" represents 0 to 5;
"p" represents 0 to 5;
2. The compound as claimed in claim 1, wherein R is hydrogen, (C1-C3) alkyl or (C3-C6) cycloalkyl;
3. The compound as claimed in claim 1, wherein R{ is hydrogen, halogen, (CVCyalkyl, (C^-C6) cycloalkyl, halo(CrC3)aIkyI, (CrC3)aikoxy or halo (CrC3)alkoxy;
4. The compound as claimed in claim 1, wherein R2 is hydrogen, halogen, (CrC3)aIkyl, (C3-C6) cycloalkyl, haIo(CrC3)alkyI, (CrC3)alkoxy or halo (CrC3)alkoxy;
5. The compound as claimed in claim 1, wherein R3 is hydrogen, halogen, (CrC3) alkyl, (C3-C6) cycloalkyl, ha!o(CrC3)alkyl, (CrC3)alkoxy or halo(CrC3)alkoxy;
6. The compound as claimed in claim 1, wherein R4 ;s hydrogen, halogen, (CrC3)aikyl, (Cz-Ce)
cycloalkyl, aryl, aralkyl or t-butyloxy carbonyl.

7. The compound as claimed in claim 1, which is selected from the group consisting of: l-(2'-Bromo benzenesulfonyl)-4-[N-(l-methyl piperidin-4-yl)] amino-lH-indole; l-(2'-Bromo benzenesulfonyl)-4-[N-(piperidin-4-yl)] amino- IH-indole dihydrochloride; l-(2'-Bromobenzenesulfonyl)-4-[N-methyl-N-(piperidin-4-yl)] amino-IH-indole dihydrochloride;
l-(2'-Bromo benzenesulfonyl)-4-[N-ethyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole; 4-[N-Ethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methyl benzenesulfonyl)-IH-indole; l-(2'-Chloro benzenesulfonyl)-4-[N-ethyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole; 1-(3'-Chloro benzenesulfonyl)-4-[N-(l-t-butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-IH-indole;
4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-l-(4'-isopropyl benzenesulfonyl)-lH-indole;
4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)-N-methyl] amino-l-(4'-fluoro benzenesulfonyl)-1H-indole;
4-[N-( 1 -t-Butyloxycarbony 1 piperidin-4-yl)-N-methyl] amino-1 -(3 '-trifluoromethyl benzenesulfonyl)-IH-indole;
4-[N-(l-t-Butyloxycarbonyl piperidin-4-yl)] amino-l-(3'-chloro benzenesulfonyl)-IH-indole; 1 -(3'-Chloro benzenesulfonyl)-4-[N-methyl-N-(piperidin-4-yl)] amino-1 H-indole dihydrochloride;
l-(3'-Chloro benzenesulfonyl)-4-[N-(piperidin-4-yl)] amino-IH-indole dihydrochloride; 1-(3'-Chloro benzenesulfonyl)-4-[N-(l-methyl piperidin-4-yl)] amino-IH-indole; l-(4'-Fluoro benzenesulfonyl)-4-[N-methyl-N-(piperidin-4-yl)] amino-IH-indole dihydrochloride;
l-(4'-Isopropyl benzenesuIfonyl)-4-[N-methyl-N-(piperidin-4-yl)] amino-IH-indole dihydrochloride;
4-[N-(l-Benzyl piperidin-4-yl) amino-l-(4'-fluoro benzenesulfonyl)-IH-indole; l-(2\ 5'-Dimethoxy benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(4'-Methyl benzenesulfonyI)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole; l-(2'-Chloro benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole; l-(4'-Fluoro benzenesulfonyl)-4-[N-methyI-N-(l-methyl piperidin-4-yl)] amino-IH-indole; l-(3'-Chloro benzenesulfonyI)-4-[N-methyl-N-(l-methyl piperidin-4-yI)] amino-IH-indole; 4-[N-MethyI-N-( 1 -methyl piperidin-4-yl)] amino-1 -(3 "-trifluoromethyl benzenesulfonyl)-1H-indole; l-(4'-Isopropyl benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-IH-indole;

l-(2'-Bromo benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-lH-indole;
l-(4'-Methoxy benzenesulfonyl)-4-[N-methyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methyl benzenesulfonyl)-1H-
indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-lH-
indole;
l-(2*-Chloro benzenesulfonyl)-4-[N-cyc!opropylmethyl-N-(l-methyl piperidin-4-yl)] amino-lH-
indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-fluoro benzenesulfonyl)-1H-
indole;
l-(3'-Chloro benzenesulfonyl)-4-[N-cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-lH-
indole;
4-[N-Cyclopropylmethyl-N-( 1 -methyl piperidin-4-yl)] amino-1 -(3' -trifluoromethyl
w
benzenesulfonyl)-1 H-indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methoxy benzenesulfonyl)-
1 H-indole;
4-[N-Cyclopropylmethyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-isopropyl benzenesulfonyl)-
1 H-indole;
4-[N-Isopropyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methyl benzenesulfonyl)-!H-indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;
l-(2'-Chloro benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;
l-(4'-Fluoro benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;
l-(3'-Chloro benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;
4-[N-Isopropyl-N-(l-methyl piperidin-4-yl)] amino-1-(3'-trifluoromethyl benzenesulfonyl)-1H-
indole;
4-[N-Isopropyl-N-(l-methyl piperidin-4-yl)] amino-l-(4'-methoxy benzenesulfonyl)-!H-indole;
l-(4'-Isopropyl benzenesulfonyl)-4-[N-isopropyl-N-(l-methyl piperidin-4-yl)] amino-1 H-indole;
4-[N-(l-Ethyl piperidin-4-yl)] amino-1-(4'-methyl benzenesulfonyl)-!H-indole;
l-(2'-Bromo benzenesulfonyl)-4-[N-(l-ethyl piperidin-4-y!)] amino-1 H-indole;
l-(2'-Chloro benzenesulfonyl)-4-[N-(!-ethyl piperidin-4-yl)] amino-1 H-indole;
I-(4'-Fluoro benzenesulfonyl)-4-[N-(l-ethyl piperidin-4-yl)] amino--1 H-indole;
l-(3'-Ch!oro benzenesulfonyI)-4-[N-(l-ethyl piperidin-4-yl)] amino-1 H-indole;
4-[N-(l-Ethyl piperidin-4-yl)] amino-1-(3'-trifluoromethyl benzenesulfonyl)-!H-indole;
4-[N-(l -Ethyl piperidin-4-yl)] amino-l-(4'-methoxy benzenesulfonyl)-1 H-indole;
4-[N-(l -Ethyl piperidin-4-yl)] amino-l-(4'-isopropyl benzenesulfonyl)-1 H-indole;
l-(4'-Methyl benzenesulfonyl)-4-[N-(l-propyl piperidin-4-yi)] amino-!H-indole;

l-(2'-Bromo benzenesulfonyl)-4-[N-(1 -Propyl pipcridin-4-yl)] amino-lH-indole; l-(2'-Chloro bcnzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole; l-(4'-Fluoro benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-IH-indole; l-(3'-Chloro benzenesulfonyl)-4-[N-(l- propyl piperidin-4-yl)] amino-lH-indole; 4-[N-(l- Propyl piperidin-4-yl)] amino-l-(3'-trifluoromethyl benzenesulfonyl)-lH-indole; l-(4'-Methoxy benzenesulfonyl) 4-[N-(l- propyl pipcridin-4-yl)] amino-III-indole and 1 -(4'-Isopropyl benzenesulfonyl)-4-[N-( 1 - propyl piperidin-4-yl)] amino- IH-indole; the stereoisomer thereof; and the pharmaceutically acceptable salt thereof;.
8. A process for the preparation of compound of formula (I), wherein R represents (Cj-C3) alkyl or (C3-C6) cycloalkyl group and all other symbols are as defined in claim 1, which comprises: Contacting a compound of formula (a),

(a) with arylsulfonyl chloride derivatives, using a suitable base in presence of inert solvent and inert gases at ambient temperature to obtain a compound of formula (I).
9. A process for the preparation of compound of formula (I), wherein R represents hydrogen and all
other symbols are as defined in claim 1, which comprises:
Contacting a compound of formula (b)
tti 1

r
with piperidine-4-one derivatives, using a suitable reducing agent and base in presence of suitable solvent at ambient temperature to obtain a compound of formula (I).
10. A process for the preparation of compound of formula (I), wherein R and R4 represents hydrogen,
which comprises:
Conversion of compound of formula (II) in to formula (I) by convenient derivatization.

wherein all symbols are as defined in claim 1.
11. A process for the preparation of compound of formula (I), wherein R4 represents hydrogen, which
comprises:
Conversion of compound of formula (III) in to formula (I) by convenient derivatization.


wherein all symbols are as defined in claim 1.
12. Novel intermediate defined by general formula (II)
wherein all symbols are as defined in claim 1.
13. Novel intermediate defined by general formula (III)

wherein all symbols are as defined in claim 1;
14. A process for the preparation of novel intermediates of general formula (II), wherein all symbols are as defined in claim 1, which comprises: Contacting a compound of the following formula (b),


with 1-Boc piperidine-4-one derivatives, using a suitable reducing agent and base in presence of suitable solvent at ambient temperature to obtain a compound of formula (II).
15. A process for the preparation of novel intermediates of general formula (III), which comprises:
Conversion of compound of formula (II) in to the compound of formula (III) by reductive amination

using a suitable base in presence of inert solvent and inert gases at ambient temperature to obtain a compound of formula (III), wherein all symbols are as defined in claim 1.
16. A method for the treatment of a disorder of the central nervous system related to or affected by the
5-HT6 receptor, in a patient in need thereof, which comprises providing to said patient a
therapeutically effective amount of a compound of formula (I) as defined in any one of claims 1 to 7.
17. The method as claimed in claim 16, wherein the said disorder is a motor disorder, anxiety
disorder, a cognitive disorder or a neurodegenerative disorder.

18. The method as claimed in claim 17, wherein the said disorder is selected from a group consisting of attention deficit disorder, obsessive compulsive disorder, withdrawal from drug, alcohol or nicotine addiction, schizophrenia and depression.
19. The method as claimed in claim 16, wherein the said disorder is Alzheimer's disease, cognitive impairment associated with schizophrenia, Mild cognitive impairment and Parkinson's disease.
20. The method as claimed in claim 16, wherein the said disorder is attention deficit disorder or
obsessive compulsive disorder.
21. The method as claimed in claim 16, wherein the said disorder is stroke or head trauma.
22. The method as claimed in claim 16, wherein the said disorder is eating disorder or obesity.
23. A pharmaceutical composition which comprising a compound of formula (I) as defined in claims
1 to 7 and apharmaceutically acceptable carrier, diluent, excipent or solvate.
24. A pharmaceutical composition as claimed in claim 23 in the form of a tablet, capsule, powder,
syrup, solution, injectable or suspension, administered in, as a single dose or multiple dose units.
25. The pharmaceutical composition as claimed in claim 24, for use in the treatment of Alzheimer's
disease, Huntington's chorea, Gastrointestinal, cognitive impairment associated with schizophrenia,
Mild cognitive impairment, eating disorders, anxiety, depression, obesity and/or Parkinson's disease.
26. Use of a compound as claimed in any one of claims 1 to 7 in the manufacture of medicament for
treating or preventing diseases related to the serotonin related 5-HT6 receptor.
27. The use as claimed in claim 26 for the treatment of Alzheimer's disease, Huntington's chorea,
Gastrointestinal, cognitive impairment associated with schizophrenia, Mild cognitive impairment,
eating disorders, anxiety, depression, obesity and/or Parkinson's disease.
28. An agent for the prevention or treatment of Alzheimer's disease, Huntington's chorea,
Gastrointestinal, cognitive impairment associated with schizophrenia, eating disorders, anxiety,