FIELD OF THE INVENTION The present invention pertains to the field of pharmaceuticals, particularly to novel cholic acid derivatives, their process of synthesis, composition comprising of these compounds and use of the compounds for autoimmune diseases. BACKGROUND OF THE INVENTION Bile acids (BAs) are synthesized from cholesterol in the liver by two pathways: classical and alternative pathways. After each meal, bile acids are excreted to the intestinal tract, where they undergo bacteria-mediated transformation to generate a large pool of bioactive molecules. BAs activate GPCR1, and FXR receptors present on innate immune cells, which contribute to maintaining a tolerogenic phenotype in entero-hepatic tissues. Recently published studies have shown that the Clostridium species modified bile may signal liver sinusoidal endothelial cells to secrete CXCL16, a potent chemokine to recruit NK cells and perform anti-tumor surveillance of the liver. Several reports have shown that both dietary and microbial composition may alter the BAs pool and modulate the colonic regulatory T cells expressing the transcription factor RORγ. In addition, individuals with genetic abolition in BAs metabolism have reduced frequencies of colonic regulatory T cells, and which of these individuals are susceptible to inflammatory bowel disease (IBD). Restoration of the intestinal BAs pool increases the frequency of colonic RORγ+ Treg cell and reduces host susceptibility to inflammatory colitis. Th17 cells play a critical role in host defense against extracellular pathogens. However, Th17 cells with distinct effector functions act as an inducer of autoimmune inflammation/inflammatory conditions in psoriasis, rheumatoid arthritis (RA), multiple sclerosis (MS), inflammatory bowel diseases (IBD) and other inflammatory diseases. The pathogenic functions of Th17/T cells and inflammatory cells in autoimmune diseases are mediated by pro- inflammatory cytokines like IL-17A, IL-17F, IL-21, IL-22, IL-6 etc. In addition, the imbalance between Th17 and Tregs favors the effector functions of Th17 cells, which contribute to the inflammation and exacerbation of autoimmune diseases/inflammatory conditions. Therapies based on the increase in IL-10 production, a major anti-inflammatory cytokine, are novel to control inflammation in autoimmune/inflammatory conditions. These therapies may be implicated to enhance the frequency and functions of regulatory T cells (Tr1, Foxp3+ T regulatory cells, and RORγ+ T regs) while suppressing the functions of proinflammatory T cells like Th17 cells. Based on our results, we propose novel synthetic cholic acid derivatives as potent inhibitors of Th17 and other inflammatory T cells and inducers of IL-10-producing regulatory T cells. Hence, there is a need to have novel compounds having effect on auto immune disorders OBJECT OF THE INVENTION An object of the invention is to design and develop novel synthetic cholic acid derivatives for autoimmune disorders/inflammatory conditions, process of synthesis of the compounds, compositions comprising the said compounds and use of the compounds and treatment comprising the compounds of the present invention. SUMMARY OF THE INVENTION: The Invention provides a synthetic cholic acid compound for autoimmune disorders/inflammatory conditions comprising the compounds of Formula I Formula I Where X is selected from -OH or -NH-R, R is selected from the group consisting of mono, di-, tri- or tetra-peptide moiety having glutamic acid, wherein the terminal amino group of the glutamic acid is either in the salt form or protected form and the carboxylic acid group in the side chain of the glutamic acid is in the protected form; or R is selected from tetra peptide moiety having leucine, wherein the terminal amino group of the leucine is either in the salt form or protected form, Y is selected from OR, NHR or lysine moiety, wherein both the carboxylic acid group and the side chain amino group of the lysine are protected or in the salt form, R is independently, H or C1 to C6 straight chained or branched alkyl, alkenyl or alkynyl groups. R1 and R2 are independently H or OH. The Invention also provides a process of preparing the Cholic Acid Derivatives of compounds of Formula I, comprising the following steps: Preparation of amino-cholic acid: Protection of C24 carboxylic acid of cholic acid to its methyl ester in methanol using p-TSA followed by selective activation of the 3α- hydroxyl functionality of methyl cholate to respective mesylate using methane sulfonyl chloride, triethylamine in DCM followed by substitution using sodium azide in DMF to yield 3β-azido-methyl cholate and further reduction via Staudinger reaction using PPh3 in THF and water. Preparation Leucine-Cholic acid conjugates: Selective protection of carboxylic acid functionality of leucine in benzyl alcohol using p-TSA followed by protection of amino functionality of another fragment using Boc-anhydride and further coupling in DMF using EDCI/HOBt as coupling reagent to furnish dipeptide. Selective deprotection of the Boc group and benzyl ester functionalities of dileucine fragments using trifluoroacetic acid (TFA/DCM) and triethylsilane (TES), Pd-C in methanol, respectively and coupling in DMF using EDCI/HOBt to furnish tetrapeptide. Further, selective deprotection of benzyl group followed by subsequent coupling with amino cholic acid derivativeto furnish desired cholic acid-tetraleucine conjugate. Preparation of Cholic acid-Glutamic acid and Cholic acid-Lysine Conjugates: Boc- Glu(OBzl)-OH was coupled to C3-amino functionality of cholic acid derivative usingEDCI/HOBt, and triethylamine in DMF to furnis fully protected cholic acid- monoglutamic acid conjugate followed by selective deprotection of Boc-group at α- position of glutamic acid using HCl in dioxane and further coupling with Boc-Glu(OBzl)- OH furnished fully protected di-glutamic acid conjugated cholic acid derivative. By similar couplings with Boc-Glu(OBzl)-OH and deprotections of Boc-group furnished the tetra-glutamic linked cholic acid derivative. Similar procedure was opted for the synthesis of Cholic acid - lysine conjugates. BRIEF DESCRIPTION OF FIGURES Figure 1: Depicts contour flow plots showing quantification of IL-17 and IL-10 from the naïve T cells differentiated under Th17 conditions in the presence of various cholic acid derivatives. Figure 2: Depicts Fluorescence-activated cell sorting (FACS) showing inhibition of IL-17 cytokine and increase in IL-10 cytokine by various cholic acid derivatives during Th17 differentiation in-vitro. Figure 3: Molecular docking of cholic acid derivatives with ROR-γt (Retinoic acid-related orphan receptor γt). Figure 4: In-vitro testing of cholic acid derivatives in blocking of ROR-γt functions. Figure 5: Depicts colitis associated body weight changes post cholic acid derivatives treatment. Figure 6: Depicts colitis associated colon length reduction post cholic acid derivatives treatment. Figure 7: Depicts colitis associated diarrheal and rectal bleeding post cholic acid derivatives treatment. Figure 8: Depicts colitis associated histopathological changes post cholic acid derivatives treatment. Figure 9: Depicts FACS showing increase in IL-10 cytokine post cholic acid derivatives treatment in experimental colitis mice. Figure 10: Depicts FACS showing inhibition of IL-17 and IFN-γ post cholic acid derivatives treatment in experimental colitis mice. DETAILED DESCRIPTION OF THE INVENTION The present invention discloses compounds of formula (I), including any configurational and conformational isomeric form, salts and solvates thereof: Formula I X is selected from -OH or -NH-R, R is selected from the group consisting of mono, di-, tri- or tetra-peptide moiety having glutamic acid, wherein the terminal amino group of the glutamic acid is either in the salt form or protected form and the carboxylic acid group in the side chain of the glutamic acid is in the protected form; or R is selected from tetra peptide moiety having leucine, wherein the terminal amino group of the leucine is either in the salt form or protected form, Y is selected from OR, NHR or lysine moiety, wherein both the carboxylic acid group and the side chain amino group of the lysine are protected or in the salt form, R is independently, H or C1 to C6 straight chained or branched alkyl, alkenyl or alkynyl groups. R1 and R2 are independently H or OH. Certain illustrative compounds of the present invention are exemplified at Table 1. Table 1: Illustrative compounds of the present invention.

The compounds of the present invention include: i. methyl (4R)-4-((3S,5S,7R,10S,12S,13R,17R)-3-((S)-2-((S)-2-((S)-2-(( S)-2-amino-4- methylpentanamido)-4-methylpentanamido)-4-methylpentanamido) -4- methylpentanamido)-7,12-dihydroxy-10,13-dimethylhexadecahydr o-1H- cyclopenta[a]phenanthren-17-yl)pentanoate hydrochloride ii. benzyl (S)-4-((tert-butoxycarbonyl)amino)-5-(((3S,5S,7R,8R,9S,10S,1 2S,13R,14S,17R)- 7,12-dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dim ethylhexadecahydro- 1H-cyclopenta[a]phenanthren-3-yl)amino)-5-oxopentanoate iii. benzyl (S)-4-amino-5-(((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-di hydroxy-17- ((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dimethylhexadecahydro -1H- cyclopenta[a]phenanthren-3-yl)amino)-5-oxopentanoate hydrochloride iv. benzyl (S)-4-amino-5-(((S)-5-(benzyloxy)-1-(((3S,5S,7R,8R,9S,10S,12 S,13R,14S,17R)- 7,12-dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dim ethylhexadecahydro- 1H-cyclopenta[a]phenanthren-3-yl)amino)-1,5-dioxopentan-2-yl )amino)-5- oxopentanoate hydrochloride v. tert-butyl N ⁶ -(tert-butoxycarbonyl)-N ² -((R)-4-((3R,5S,7R,8R,9S,10S,12S,13R,14S,17R)- 3,7,12-trihydroxy-10,13-dimethylhexadecahydro-1H-cyclopenta[ a]phenanthren-17- yl)pentanoyl)-L-lysinate vi. ((R)-4-((3R,5S,7R,8R,9S,10S,12S,13R,14S,17R)-3,7,12-trihydro xy-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pent anoyl)-L-lysine hydrochloride vii. methyl (4R)-4-((3S,5S,7R,10S,12S,13R,17R)-7,12-dihydroxy-10,13-dime thyl-3- ((6S,9S,12S,15S)-6,9,12,15-tetraisobutyl-2,2-dimethyl-4,7,10 ,13-tetraoxo-3-oxa- 5,8,11,14-tetraazahexadecan-16-amido)hexadecahydro-1H-cyclop enta[a]phenanthren- 17-yl)pentanoate viii. benzyl (S)-5-(((S)-5-(benzyloxy)-1-(((3S,5S,7R,8R,9S,10S,12S,13R,14 S,17R)-7,12- dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dimethyl hexadecahydro-1H- cyclopenta[a]phenanthren-3-yl)amino)-1,5-dioxopentan-2-yl)am ino)-4-((tert- butoxycarbonyl)amino)-5-oxopentanoate ix. benzyl (6S,9S,12S)-6,9-bis(3-(benzyloxy)-3-oxopropyl)-12- (((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-dihydroxy-17-((R )-5-methoxy-5- oxopentan-2-yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a] phenanthren-3- yl)carbamoyl)-2,2-dimethyl-4,7,10-trioxo-3-oxa-5,8,11-triaza pentadecan-15-oate x. benzyl (S)-4-amino-5-(((S)-5-(benzyloxy)-1-(((S)-5-(benzyloxy)-1- (((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-dihydroxy-17-((R )-5-methoxy-5- oxopentan-2-yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a] phenanthren-3- yl)amino)-1,5-dioxopentan-2-yl)amino)-1,5-dioxopentan-2-yl)a mino)-5-oxopentanoate hydrochloride xi. benzyl (S)-4-amino-5-(((6S,9S,12S)-9-(3-(benzyloxy)-3-oxopropyl)-6- (((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-dihydroxy-17-((R )-5-methoxy-5- oxopentan-2-yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a] phenanthren-3- yl)carbamoyl)-3,8,11,15-tetraoxo-1,17-diphenyl-2,16-dioxa-7, 10-diazaheptadecan-12- yl)amino)-5-oxopentanoate hydrochloride The compounds of the present invention may preferably be: i. benzyl (S)-4-((tert-butoxycarbonyl)amino)-5-(((3S,5S,7R,8R,9S,10S,1 2S,13R,14S,17R)- 7,12-dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dim ethylhexadecahydro-1H- cyclopenta[a]phenanthren-3-yl)amino)-5-oxopentanoate ii. benzyl (S)-4-amino-5-(((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-di hydroxy-17-((R)-5- methoxy-5-oxopentan-2-yl)-10,13-dimethylhexadecahydro-1H-cyc lopenta[a]phenanthren- 3-yl)amino)-5-oxopentanoate hydrochloride The compounds of the present invention when present as their pharmaceutically acceptable salts or stereoisomers. The present invention provides for pharmaceutically acceptable acid addition salts of compounds of formula (I) as well as pharmaceutically acceptable or present as their free base form. The non- toxic acids which are used to prepare the pharmaceutically acceptable acid addition salts of above-mentioned base compounds of this invention. Appropriate acids comprise, for example, the inorganic acids such as the Hydrochloride, Hydrobromide, Hydroiodide, Phosphorates, Nitric acid and Sulfuric acid; or organic acids such as Methanesulfonate, Acetate, Fumarate, Saccharate, p-toluenesulfonate, Benzenesulfonate, Lactate, Succinate, Citrate, Tartrate, Succinate, Gluconate, Benzoate, etc. The base addition salts of formula (I) were prepared by using the pharmaceutically acceptable chemical bases. The pharmaceutically acceptable base addition salts of those compounds of formula (I) that are acidic in nature and may form non-toxic base salts, such as pharmaceutically acceptable alkali metal cations, like potassium, sodium, and alkali earth metal cations, (e.g., calcium, magnesium), ammonium or water-soluble amine addition salts, like N- methylglucamine, and lower alkanolammonium and other pharmaceutically acceptable organic amine salts. The compounds of present invention may exist in more than one form of crystal structure is called polymorph. The compounds may be existing as crystalline or amorphous form. Without being limited by theory the peptide conjugates (synthesized compounds in the present application) may not be a prodrug. Even though, bile acid itself is known to show similar effect, the amide linked conjugates will not easily get deprotected to give a parent bile acid in the biological system. Infact, the bile acid itself is converted to amino derivative so there is no chance to get the parent bile acid from the active compounds in-vivo. Computational docking results demonstrate that the compounds of the present invention have enhanced therapeutic efficacy. In addition, the peptide conjugates of the present invention 16 and17 are found to be very active. The compounds of the present invention show activity as illustrated in the present invention. B. Process for preparation of the compounds of the present invention In another aspect, the present invention also discloses a process of preparing the compounds of the present invention. The compounds of the present invention may be prepared by the general synthetic schemes 1, presented here below. Synthesis of Cholic Acid Derivatives: 3α-Hydroxyl functionality of cholic acid was converted to β-amino functionality to form the building block required for the synthesis of desired cholic acid-leucine and cholic acid-glutamic acid conjugates (Scheme 1). Scheme 1. Synthesis of steroid backbone. Carboxylic acid at C24 position of cholic acid may be converted to respective ester by overnight stirring of cholic acid in alcohol using an acid catalyst (Scheme 1). The ester may also be obtained by a coupling reaction of carboxylic acid with different alcohols. Selective activation of the C3-α-hydroxyl group of methyl cholate can be carried out using organic sulfonyl chloride which can be further reacted with azide source to yield 3β-azido derivatives. The respective 3β- azido derivatives can be synthesized using Mitsunobutype reaction. Reduction of 3β-azido functionality via Staudinger reaction can be carried out to yield the respective 3-amino-cholic acid derivatives (Scheme 1). For the synthesis of leucine conjugates of cholic acid, tetrapeptides of leucine were prepared and then coupled with cholic acid scaffold. The tetrapeptide Boc-(Leu)4-OBzl can be synthesized from L-leucine 6 in total 7 steps as shown in Scheme 2. Selective protection of carboxylic acid functionality of L-leucine 6 can be achieved using benzyl alcohol in acid catalyst and protection of amino functionality can be achieved using Boc-anhydride to yield the protected monomers 7 and 8, respectively which can be further coupled in polar aprotic solvent using peptide coupling reagents to furnish dipeptide, Boc-(Leu) ₂ -OBzl 9 (Scheme 2). Selective deprotection of the Boc group and benzyl group from dileucine 9 using organic acid and transfer hydrogenation, respectively yielded dileucine derivatives 10 and 11, which may be coupled to yield the fully protected tetraleucine derivative 12 (Scheme 2). Scheme 2. Synthesis of tetrapeptide fragment. Selective deprotection of benzyl group in compound 12 as discussed above may yield the desired tetrapeptide derivative 13 (Scheme 2) which on subsequent coupling with amino cholic acid derivative 5will furnish cholic acid-tetraleucine conjugate 14 (Scheme 3).Further, deprotection of Boc-group using acidic conditions will result in the formation of conjugate 15 (Scheme 3). Scheme 3. Synthesis of tetraleucine cholic acid conjugates.

Synthesis of Cholic acid-Glutamic Acid Conjugates In the another process, commercially available Boc-Glu(OBzl)-OH was coupled to C3-amino functionality of cholic acid derivative 5in polar aprotic solvent using typical coupling condition to synthesize fully protected cholic acid-monoglutamic acid conjugate 16 (Scheme 4). Scheme 4. Synthesis of mono- and di-glutamic acid derived cholic acid conjugates. ^a Selective deprotection of Boc-group at α-position of glutamic acid in intermediate 16may be achieved by using acidic conditions to yield intermediate 17 (Scheme 4). Further, coupling of compound 17 with Boc-Glu(OBzl)-OH may yield the fully protected di-glutamic acid conjugated cholic acid derivative 18, which on selective deprotection of Boc-group will furnish the intermediate 19 (Scheme 4). By similar couplings with Boc-Glu(OBzl)-OH and deprotections of Boc-group will yield the fully protected tetra-glutamic linked cholic acid derivative 22 with intermediate formation of compound 20 and 21(Scheme 5). Scheme 5. Synthesis of tri- and tetra-glutamic acid derived cholic acid conjugates. ^a Similar selective deprotection of Boc-group at α-position will yield cholic acid-tetra-glutamic acid conjugate 23 (Scheme 5) and subsequent deprotections of four benzylic groups in compound 23via hydrogenation will yield the totally deprotected desired analogue 24 (Scheme 5). Synthesis of Cholic Acid-Lysine Conjugates: Lysine derivative 25will be coupled to C-24 acid functionality of cholic acid in organic solvent using peptide coupling protocol to yield fully protected cholic acid-lysine conjugate26 (Scheme 6). Deprotection of Boc-group at amine position and tertiary butyl group in acidic conditions may yield cholic acid-lysine conjugate 27 (Scheme 6). Scheme 6. Synthesis of Lysine derived cholic acid conjugates. ^a Administration of the compounds of this disclosure, or their pharmaceutically acceptable salts, in pure form or in an appropriate pharmaceutical composition, may be carried out via any of the accepted modes of administration or agents for serving similar utilities. Thus, administration may be, orally, nasally, parenterally (intravenous, intramuscular, or subcutaneous), topically, transdermally, intravaginally, intravesically, intracistemally, or rectally, in the form of solid, semi-solid, lyophilized powder, or liquid dosage forms, such as for example, tablets, suppositories, pills, soft elastic and hard gelatin capsules, powders, solutions, suspensions, or aerosols, or the like, preferably in unit dosage forms suitable for simple administration of precise dosages. Solid dosage forms for oral administration include capsules, tablets, pills, powders, and granules. Solid dosage forms, as described above, may be prepared with coatings and shells, such as enteric coatings. Liquid dosage forms for oral administration include pharmaceutically acceptable emulsions, solutions, suspensions, syrups, and elixirs. Compositions for rectal administrations are, for example, suppositories that may be prepared by mixing the compounds of this disclosure with, for example, suitable non-irritating excipients or carriers. The compounds of the present invention may also parenteral and administered as sterile powders for reconstitution into sterile injectable solutions or dispersions. Dosage forms for topical administration of a compound of this disclosure include ointments, powders, sprays, and inhalants. Ophthalmic formulations, eye ointments, powders, and solutions are also contemplated for the compounds in this disclosure. Compressed gases may be used to disperse a compound of this disclosure in aerosol form. In another embodiment, compounds or compositions comprising the compound may be administered orally or via injection at a dose of from 0.1 to 500 mg/kg per day. The dose range for adult humans is generally from 5mg to 2g/day. Tablets or other forms of presentation provided in discrete units may conveniently contain an amount of one or more compounds which is effective at such dosage or as a multiple of the same, for instance, units containing 5 mg to 500 mg, usually around 10mg to 200mg. The amount of active ingredient that may be combined with the carrier materials to produce a single dosage form will vary depending upon the host treated and the particular mode of administration. The compounds of the present invention may be administered in a dose ranging from 0.1 to 500 mg/kg per day, preferably 5mg to 500mg, more preferably 10mg to 200mg. In an embodiment the compounds of the present invention may be used to treat and prevent autoimmune diseases and inflammatory conditions like Inflammatory Bowel diseases (IBD), Sjogren’s syndrome (SjS), Multiple sclerosis (MS), Rheumatoid arthritis (RA), Psoriasis, Type 1 diabetes, systemic lupus disease, Hashimoto’s thyroiditis, Autoimmune hemolytic anemia, and Autoimmune-associated uveitis. The said derivatives have potent inhibitory activity against in-vitro differentiated Th17 cells and induce the IL-10-secreting cells that make these derivatives very attractive in restoration of Th17/T regulatory axis in autoimmune and inflammatory conditions. It is expected that the use of these novel cholic acid derivatives may lead to suppression of Th17 cells and induction of IL-10 producing T regulatory cells (Foxp3+ T cells, Tr1 cells and RORγ+ T reg cells) in clinical settings also. The examples and scheme below follow the general synthetic procedure for the compounds disclosed herein. Synthesis of the compounds of Formulae I disclosed herein, and embodiments thereof, are not limited by these examples and schemes. One skilled in the art will know that other procedures may be used to synthesize the compounds of Formulae I disclosed herein, and that the procedures described in the examples and schemes is only one such procedure. In the descriptions below, one of ordinary skill in the art would recognize that specific reaction conditions, added reagents, solvents, and reaction temperatures may be modified for the synthesis of specific compounds that fall within the scope of this disclosure. All intermediate compounds described below, for which there is no description of how to synthesize such intermediates within these examples below, are commercially available compounds unless otherwise specified. EXPERIMENTAL SECTION: Synthesis of the compounds of the present invention Methyl (4R)-4-((3S,5S,7R,10S,12S,13R,17R)-7,12-dihydroxy-10,13-dime thyl-3- ((6S,9S,12S,15S)-6,9,12,15-tetraisobutyl-2,2-dimethyl-4,7,10 ,13-tetraoxo-3-oxa-5,8,11,14- tetraazahexadecan-16-amido)hexadecahydro-1H-cyclopenta[a]phe nanthren-17- yl)pentanoate (14): 10% Pd/C (0.3 g) was added to a solution of compound 12 (700 mg, 1.06 mmol) in methanol. Triethylsilane (1.69 mL, 10.6 mmol) was added to reaction mixture dropwise and reaction mixture was stirred for 30 min. After completion of the reaction, solution was filtered through celite and solvent was evaporated. The crude compound 13 obtained was used as such without further purification. Methyl 3 ^-amino-7 ^,12 ^-dihydroxy-5 ^-cholane-24-oate(5) (400 mg, 0.95 mmol) and Boc-(Leu) ₄ -OH 13 (571 mg, 1.04 mmol) were dissolved in dry DMF (10 mL) under nitrogen atmosphere and the solution was cooled to 0 ºC. HOBt (64 mg, 0.47 mmol) and triethylamine (264 μL, 1.90 mmol) were added to the reaction mixture. After 15 min of stirring, EDCI (272 mg, 1.42 mmol) was added. The reaction mixture was allowed to warm to room temperature and was stirred for 6h. The solvent was evaporated under reduced pressure and the residue was dissolved in ethylacetate (300 mL). The organic phase was washed successively with H ₂ O, 5 % citric acid, H ₂ O, sat. NaHCO ₃ and brine, dried with anhydrous Na ₂ SO ₄ and the solvent was evaporated. The residue was purified by flash chromatography on silica gel to afford compound 14 as white amorphous powder in 62% yield. ¹ H NMR (400 MHz, CDCl3) δ 7.07 (d, J = 8.3 Hz, 1H), 7.00 (d, J = 7.4 Hz, 1H), 6.72 (d, J = 6.9 Hz, 1H), 6.56 (d, J = 4.8 Hz, 1H), 5.02 (d, J = 2.6 Hz, 1H), 4.38-4.45 (m, 2H), 4.14 (m, 1H), 4.05 (m, 1H), 3.95 (m, 1H), 3.84-3.90 (m, 2H), 3.65 (s, 3H), 1.46 (s, 9H), 0.87-0.98 (m, 30H), 0.68 (s, 3H). ¹³ C NMR (101 MHz, CDCl3) δ 174.94, 174.09, 172.5, 172.3, 171.9, 156.8, 81.4, 73.2, 68.5, 55.1, 52.6, 52.5, 51.6, 47.3, 46.7, 45.7, 42.1, 40.7, 40.6, 40.5, 40.1, 39.6, 36.5, 35.3, 35.2, 34.7, 33.4, 31.2, 31.0, 30.6, 28.7, 28.3, 27.6, 26.2, 25.2, 25.1, 25.0, 24.9, 24.6, 23.5, 23.3, 23.2, 23.1, 22.9, 22.8, 22.0, 21.9, 21.4, 21.2, 17.4, 12.7. (HRMS) m/z calculated for C54H96N5O10 ⁺ [M+H] ⁺ : 974.7152, found: 974.7141. (2S)-1-(((2S)-1-(((2S)-1-(((2S)-1-(((3S,5S,7R,10S,12S,13R,17 R)-7,12-dihydroxy-17-((R)-5- methoxy-5-oxopentan-2-yl)-10,13-dimethylhexadecahydro-1H-cyc lopenta[a]phenanthren- 3-yl)amino)-4-methyl-1-oxopentan-2-yl)amino)-4-methyl-1-oxop entan-2-yl)amino)-4- methyl-1-oxopentan-2-yl)amino)-4-methyl-1-oxopentan-2-aminiu m chloride (15): A solution of compound 14 (100 mg, 0.03 mmol) in HCl/dioxane (5 mL) was stirred at 25 ºC for 30 min. The volatiles were removed under vacuum, and the residue was dried thoroughly to afford compound15 as a white amorphous solid. Yield: 95%; ¹ H NMR (500 MHz, DMSO-d ₆ ) δ 8.63 (d, J = 8.2 Hz, 1H), 8.26 (m, 3H), 7.98 (d, J = 8.5 Hz, 1H), 7.39 (d, J = 7.1 Hz, 1H), 4.27- 4.42 (m, 3H), 3.82 (m, 1H), 3.77 (m, 2H), 3.57 (s, 3H), 0.80-0.92 (m, 30H), 0.58 (s, 3H). ¹³ C NMR (126 MHz, DMSO-d6) δ 173.8, 171.4, 171.1, 171.0, 168.5, 79.3, 79.0, 78.8, 72.2, 71.0, 70.5, 66.4, 66.2, 62.8, 60.2, 51.2, 51.0, 50.8, 50.7, 48.6, 46.0, 45.8, 44.6, 43.6, 41.4, 40.9, 40.6, 40.3, 36.6, 35.0, 34.7, 34.4, 33.3, 30.7, 30.5, 28.7, 27.2, 25.6, 24.3, 24.1, 24.1, 24.0, 23.5, 23.05, 23.02, 22.97, 22.86, 22.78, 22.5, 22.3, 21.9, 21.64, 21.58, 16.9, 12.3. (HRMS) m/z calculated for C ₄₉ H ₈₈ N ₅ O ₈ + [M+H] ⁺ : 874.6627, found: 874.6627. Benzyl (S)-4-((tert-butoxycarbonyl)amino)-5-(((3S,5S,7R,8R,9S,10S,1 2S,13R,14S,17R)-7,12- dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dimethyl hexadecahydro-1H- cyclopenta[a]phenanthren-3-yl)amino)-5-oxopentanoate (16): To a solution of cholic acid derivative 5 (330 mg, 0.78 mmol) in dry DMF (5 mL), Boc- Glu(OBzl)-OH (237 mg, 0.70 mmol), HOBt (53 mg, 0.39 mmol) and triethylamine (218 µL, 1.56 mmol) were added at 0 ^o C under nitrogen atmosphere. After 10 minutes of stirring at 0 ^o C, EDCI (300 mg, 1.56 mmol) was added to the reaction mixture. The reaction mixture was allowed to warm to room temperature and stirred for 6h. Completion of the reaction was monitored by TLC. After completion of the reaction, solvent was removed under reduced pressure. The residue was dissolved in 50 mL of ethyl acetate and further washed with water, brine and dried over sodium sulfate. The solvent was removed under vacuum and residue was purified by flash column chromatography using 230-400 Mesh silica gel using MeOH/DCM as eluents to obtain compound 16 (457 mg, 88% yield) as amorphous white solid. ¹ H NMR (500 MHz, DMSO-d ₆ ) δ 7.43 (d, J = 7.2 Hz, 1H), 7.33-7.39 (m, 5H), 6.91 (d, J = 8.3 Hz, 1H), 5.09 (s, 2H), 4.12 (d, J = 3.6 Hz, 1H), 4.06 (d, J = 3.2 Hz, 1H), 3.96-4.00 (m, 1H), 3.84 (m, 1H), 3.78 (m, 1H), 3.62 (m, 1H), 3.58 (s, 3H), 1.38 (s, 9H), 0.92 (d, J = 6.3 Hz, 3H) 0.86 (s, 3H), 0.59 (s, 3H). ¹³ C NMR (126 MHz, DMSO-d ₆ ) δ 173.9, 172.3, 170.7, 155.4, 136.2, 128.5, 128.0, 127.9, 78.2, 71.1, 66.3, 65.5, 53.4, 51.2, 46.1, 45.8, 44.7, 41.4, 36.7, 35.1, 34.8, 34.4, 33.3, 30.8, 30.5, 30.3, 28.7, 28.2, 27.4, 27.3, 25.6, 24.4, 22.9, 22.8, 16.9, 12.3. (HRMS) m/z calculated for C42H65N2O9 ⁺ [M+H] ⁺ : 741.4680, found: 741.4685. Benzyl (S)-4-amino-5-(((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-di hydroxy-17-((R)-5- methoxy-5-oxopentan-2-yl)-10,13-dimethylhexadecahydro-1H-cyc lopenta[a]phenanthren- 3-yl)amino)-5-oxopentanoate hydrochloride (17): Compound 6 (250 mg, 0.34 mmol) was stirred in HCl/dioxane (3 mL) for 30 min at 25 ºC, followed by purging of nitrogen gas. Remaining HCl/dioxane was co-evaporated with DCM (5 mL × 3) in order to obtain compound 17 (220 mg, 96%) as amorphous white solid. ¹ H NMR (500 MHz, DMSO-d ₆ ) δ 8.28-8.39 (m, 4H), 7.31-7.39 (m, 5H), 5.10 (s, 2H), 3.90-3.95 (m, 2H), 3.78 (m, 2H), 3.60 (m, 2H), 3.57 (s, 3H), 0.92 (d, J = 6.3 Hz, 1H), 0.86 (s, 3H), 0.59 (s, 3H). (ESI-MS) m/z calculated for C37H57N2O7 ⁺ [M+H] ⁺ : 641.4, found: 641.3. III-4.1.3.benzyl (S)-5-(((S)-5-(benzyloxy)-1-(((3S,5S,7R,8R,9S,10S,12S,13R,14 S,17R)-7,12- dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dimethyl hexadecahydro-1H- cyclopenta[a]phenanthren-3-yl)amino)-1,5-dioxopentan-2-yl)am ino)-4-((tert- butoxycarbonyl)amino)-5-oxopentanoate (18): Amphiphilic cholic acid-glutamic acid conjugate 18 was synthesized and characterized as described for compound 6 starting from compound 17. Amorphous white solid; Yield: 76%; ¹ H NMR (400 MHz, DMSO-d6) δ 7.84 (d, J = 8.0 Hz, 1H), 7.68 (d, J = 6.9 Hz, 1H), 7.30-7.38 (m, 10H), 7.08 (d, J = 8.1 Hz, 1H), 5.07 (s, 4H), 4.34-4.39 (m, 1H), 4.11 (m, 1H), 4.04-4.06 (m, 1H), 3.91-3.96 (m, 1H), 3.83 (m, 1H), 3.77 (m, 1H), 3.60 (m, 1H), 3.57 (s, 3H), 1.35 (s, 9H), 0.92 (d, J = 6.1 Hz, 3H), 0.83 (s, 3H), 0.59 (s, 3H). ¹³ C NMR (101 MHz, DMSO-d6) δ 173.8, 172.2, 172.2, 169.9, 155.3, 136.2, 128.4, 127.9, 127.84, 127.81, 78.2, 71.0, 66.2, 65.4, 53.5, 51.5, 51.2, 46.0, 45.8, 44.8, 41.4, 36.6, 35.0, 34.7, 34.3, 33.3, 30.7, 30.5, 30.4, 302, 29.8, 28.6, 28.1, 27.8, 27.2, 26.9, 25.6, 24.3, 22.8, 16.9, 12.2. (HRMS) m/z calculated for C54H78N3O12 ⁺ [M+H] ⁺ : 960.5580, found: 960.5572. Benzyl (S)-4-amino-5-(((S)-5-(benzyloxy)-1-(((3S,5S,7R,8R,9S,10S,12 S,13R,14S,17R)-7,12- dihydroxy-17-((R)-5-methoxy-5-oxopentan-2-yl)-10,13-dimethyl hexadecahydro-1H- cyclopenta[a]phenanthren-3-yl)amino)-1,5-dioxopentan-2-yl)am ino)-5-oxopentanoate hydrochloride (19): Amphiphilic cholic acid-glutamic acid conjugate 19 was synthesized and characterized as described for compound 17 starting from compound 18. Amorphous white solid; Yield: 95%; ¹ H NMR (400 MHz, DMSO-d ₆ ) δ 8.73 (d, J = 7.5 Hz, 1H), 8.30 (m, 3H), 7.85 (d, J = 7.0 Hz, 1H), 7.31-7.39 (m, 10H), 5.09 (s, 4H), 4.42-4.43 (m, 1H), 3.84 (m, 3H), 3.77 (m, 1H), 3.57-3.60 (m, 5H), 0.92 (d, J = 6.0 Hz, 3H), 0.83 (s, 3H), 0.58 (s, 3H). ¹³ C NMR (101 MHz, DMSO-d6) δ 173.8, 172.1, 171.6, 169.6, 167.8, 136.1, 136.0, 128.4, 128.1, 128.0, 127.9, 126.4, 71.0, 66.3, 66.2, 65.7, 65.6, 51.9, 51.3, 51.2, 46.0, 45.8, 44.9, 43.6, 41.4, 36.5, 35.0, 34.7, 34.3, 33.2, 30.7, 30.5, 30.4, 30.1, 29.0, 28.7, 27.8, 27.2, 26.5, 26.3, 25.6, 24.3, 22.8, 16.9, 12.3. (HRMS) m/z calculated for C49H70N3O10 ⁺ [M+H] ⁺ : 860.5056, found: 860.5050. Benzyl(6S,9S,12S)-6,9-bis(3-(benzyloxy)-3-oxopropyl)-12- (((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-dihydroxy-17-((R )-5-methoxy-5-oxopentan-2- yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren- 3-yl)carbamoyl)-2,2- dimethyl-4,7,10-trioxo-3-oxa-5,8,11-triazapentadecan-15-oate (20): Amphiphilic cholic acid-glutamic acid conjugate 20 was synthesized and characterized as described for compound 16 starting from compound 19. Amorphous white solid; Yield: 71%; ¹ H NMR (400 MHz, DMSO-d ₆ ) δ 8.04 (d, J = 8.0 Hz, 1H), 7.95 (d, J = 7.5 Hz, 1H), 7.60 (d, J = 7.0 Hz, 1H), 7.32-7.38 (m, 15H), 7.05 (d, J = 7.8 Hz, 1H), 5.07 (s, 6H), 4.30-4.34 (m, 2H), 4.12 (d, J = 3.2 Hz, 1H), 4.05 (d, J = 2.9 Hz, 1H), 3.90-3.96 (m, 1H), 3.83 (m, 1H), 3.78 (m, 1H), 3.60 (m, 1H), 3.58 (s, 3H), 1.34 (s, 9H), 0.92 (d, J = 6.0 Hz, 3H), 0.83 (s, 3H), 0.59 (s, 3H). ¹³ C NMR (101 MHz, DMSO-d ₆ ) δ 173.8, 172.2, 172.1, 171.5, 170.7, 169.9, 155.4, 136.2, 128.4, 128.0, 127.9, 127.85, 127.77, 78.3, 71.0, 66.2, 65.44, 65.38, 53.5, 51.7, 51.2, 46.0, 45.8, 44.8, 41.4, 36.5, 35.0, 34.7, 34.3, 33.3, 30.7, 30.5, 30.3, 30.1, 29.9, 28.6, 28.1, 27.5, 27.2, 26.8, 25.6, 22.8, 16.9, 12.3. (HRMS) m/z calculated for C ₆₆ H ₉₀ N ₄ NaO ₁₅ ⁺ [M+Na] ⁺ : 1201.6295, found: 1201.6279. Benzyl(S)-4-amino-5-(((S)-5-(benzyloxy)-1-(((S)-5-(benzyloxy )-1- (((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-dihydroxy-17-((R )-5-methoxy-5-oxopentan-2- yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren- 3-yl)amino)-1,5- dioxopentan-2-yl)amino)-1,5-dioxopentan-2-yl)amino)-5-oxopen tanoate hydrochloride (21): Amphiphilic cholic acid-glutamic acid conjugate 21 was synthesized and characterized as described for compound 17 starting from compound 20. Amorphous white solid; Yield: 96%; ¹ H NMR (400 MHz, DMSO-d ₆ ) δ 8.74 (d, J = 7.3 Hz, 1H), 8.28-8.34 (m, 4H), 7.69 (d, J = 7.0 Hz, 1H), 7.30-7.39 (m, 15H), 5.08 (s, 2H), 5.07 (s, 2H), 5.06 (s, 2H), 4.31-4.36 (m, 2H), 3.82-3.87 (m, 3H), 3.77 (m, 1H), 3.65-3.71 (m, 1H), 3.59 (m, 1H), 3.57 (s, 3H), 3.56 (m, 1H) 0.92 (d, J = 6.1 Hz, 3H), 0.81 (s, 3H), 0.58 (s, 3H). ¹³ C NMR (101 MHz, DMSO-d ₆ ) δ 173.8, 172.10, 172.08, 171.7, 170.3, 170.0, 167.9, 136.12, 136.06, 136.00, 128.4, 128.01, 127.95, 127.91, 127.86, 126.6, 126.4, 71.0, 66.3, 66.2, 65.6, 65.52, 65.47, 62.8, 52.0, 51.7, 51.2, 46.0, 45.8, 44.7, 41.3, 36.5, 35.0, 34.6, 34.3, 33.2, 30.7, 30.4, 30.3, 30.1, 29.0, 28.9, 28.6, 28.4, 27.5, 27.3, 27.2, 26.2, 25.6, 22.7, 16.9, 12.3. (HRMS) m/z calculated for C ₆₁ H ₈₃ N ₄ O ₁₃ ⁺ [M+H] ⁺ : 1079.5951, found: 1079.5953. Benzyl(S)-4-amino-5-(((6S,9S,12S)-9-(3-(benzyloxy)-3-oxoprop yl)-6- (((3S,5S,7R,8R,9S,10S,12S,13R,14S,17R)-7,12-dihydroxy-17-((R )-5-methoxy-5-oxopentan-2- yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren- 3-yl)carbamoyl)- 3,8,11,15-tetraoxo-1,17-diphenyl-2,16-dioxa-7,10-diazaheptad ecan-12-yl)amino)-5- oxopentanoate hydrochloride (23): Amphiphilic cholic acid-glutamic acid conjugate 23 was synthesized and characterized as described for compound 17 starting from compound 22. Amorphous white solid; Yield: 95%; ¹ H NMR (500 MHz, DMSO-d ₆ ) δ 8.65 (d, J = 7.5 Hz, 1H), 8.29 (d, J = 7.6 Hz, 1H), 8.17 (m, 3H), 8.06 (d, J = 7.9 Hz, 1H), 7.64 (d, J = 7.1 Hz, 1H), 7.34 (m, 20H), 5.06 (m, 8H), 4.25-4.35 (m, 3H), 3.82 (m, 2H), 3.76 (m, 1H), 3.65-3.70 (m, 1H), 3.59 (m, 1H), 3.57 (s, 3H), 3.45-3.50 (m, 1H), 0.91 (d, J = 6.3 Hz, 3H), 0.81 (s, 3H), 0.58 (s, 3H). (ESI-MS) m/z calculated for C ₇₃ H ₉₆ N ₅ O ₁₆ ⁺ [M+H] ⁺ : 1298.7, found: 1298.4. Tert-butyl N ⁶ -(tert-butoxycarbonyl)-N ² -((R)-4-((3R,5S,7R,8R,9S,10S,12S,13R,14S,17R)- 3,7,12-trihydroxy-10,13-dimethylhexadecahydro-1H-cyclopenta[ a]phenanthren-17- yl)pentanoyl)-L-lysinate (26): To a solution of cholic acid(330 mg, 0.78 mmol) in dry DMF (5 mL), Lysine derivative 5(237 mg, 0.70 mmol, HOBt (53 mg, 0.39 mmol) and triethylamine (218 µL, 1.56 mmol) were added at 0 ^o C under nitrogen atmosphere. After 10 minutes of stirring at 0 ^o C, EDCI (300 mg, 1.56 mmol) was added to the reaction mixture. The reaction mixture was allowed to warm to room temperature and stirred for 6hours. Completion of the reaction was monitored by TLC. After completion of the reaction, solvent was removed under reduced pressure. The residue was dissolved in 50 mL of ethyl acetate and further washed with water, brine and dried over sodium sulfate. The solvent was removed under vacuum and residue was purified by flash column chromatography using 230-400 Mesh silica gel using MeOH/DCM as eluents to obtain compound 26.Yield: 87%; ¹ H NMR (400 MHz, CDCl ₃ ) δ 6.24 (d, J = 7.9 Hz, 1H), 4.63 (s, 1H), 4.47 (dd, J = 12.8, 7.5 Hz, 1H), 4.12 (q, J = 7.2 Hz, 1H), 3.98 (s, 1H), 3.85 (d, J = 2.5 Hz, 1H), 3.51 – 3.40 (m, 1H), 3.09 (s, 2H), 1.46 (s, 10H), 1.44 (s, 9H), 0.99 (d, J = 6.2 Hz, 4H), 0.89 (s, 3H), 0.68 (s, 3H). ¹³ C NMR (126 MHz, DMSO) δ 172.66, 171.47, 155.45, 80.00, 77.19, 70.91, 70.33, 66.13, 52.43, 46.13, 45.62, 41.42, 41.25, 35.20, 34.98, 34.77, 34.27, 32.05, 31.59, 30.58, 30.29, 28.96, 28.43, 28.15, 27.51, 27.19, 26.09, 22.68, 22.60, 22.51, 17.01, 12.22. ((R)-4-((3R,5S,7R,8R,9S,10S,12S,13R,14S,17R)-3,7,12-trihydro xy-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pent anoyl)-L-lysine hydrochloride (27): A solution of compound 26 (100 mg, 0.03 mmol) in HCl/dioxane (5 mL) was stirred at 25 ºC for 30 min. The volatiles were removed under vacuum, and the residue was dried thoroughly to afford compound27 as a white amorphous solid. Yield: 95%; ¹ H NMR (500 MHz, DMSO) δ 7.96 (d, J = 5.5 Hz, 1H), 7.78 (s, 1H), 4.51 – 4.43 (m, 1H), 4.19 (t, J = 4.0 Hz, 1H), 3.78 (d, J = 3.5 Hz, 1H), 3.34 – 3.20 (m, 1H), 3.20 – 3.12 (m, 1H), 2.89 (s, 1H), 2.76 – 2.67 (m, 1H), 1.08 – 0.96 (m, 1H), 0.95 – 0.88 (m, 1H), 0.85 (d, J = 11.3 Hz, 1H), 0.59 (d, J = 5.4 Hz, 1H). ¹³ C NMR (126 MHz, DMSO) δ 174.81, 173.65, 80.15, 70.91, 70.30, 66.07, 51.44, 45.99, 45.62, 41.40, 41.27, 38.25, 35.19, 35.05, 35.02, 34.78, 34.27, 34.03, 32.07, 31.19, 30.27, 28.44, 27.53, 27.21, 26.38, 26.10, 22.51, 17.04, 12.23. Experimental Biology: Example 1: Efficacy check of cholic acid derivatives using in-vitro Th17 cells differentiation. Step 1: Isolation of Splenocytes and lymph node cells from mice: Inventors used IL-10-GFP mice (6-8 weeks old) for isolating spleen and lymph nodes with prior ethical committee approval. Isolated spleen and lymph nodes were homogenized into single cell suspension and RBCs were lysed in Splenocytes using RBC lysis buffer. Step 2: In vitro differentiation of Th17 cells and effect of cholic acid derivatives on Th17 differentiation Splenocytes and lymph node cells were pooled and seeded in 96 well plates with density of 0.2 million cells/ well. Soluble mouse anti-CD3 (2.0 μg/mL) was added for the activation of T cells. For differentiation of T cells into Th17 cells, recombinant mouse TGF-beta (2.0 ng/mL) and recombinant mouse IL-6 cytokine (25.0 ng/mL) was added. Various cholic acid derivatives were added in individual wells along with Th17 differentiating cytokines at the start of culture. The culture was done for 3 days. Intracellular cytokine staining was done to check the expression of IL-17 and IL-10 cytokine in Th17 differentiated cells. The effect of various cholic acid derivatives was compared to a Th17 control condition. The results are provided at Figure 1 and figure 2. From the figure 1 and figure 2, it may be seen that Spleen and Lymph nodes were isolated from IL-10 GFP mice and their single cell suspension was prepared. Total cells were activated using soluble anti-CD3 monoclonal antibodies and differentiated into Th17 cells using recombinant mouse IL-6 and TGF-beta cytokines. Cholic acid derivatives were added at the start of the culture (for details see table 1) with dose 200 μM. Cells were differentiated for 72 hours. IL-17 production was measured by Intracellular cytokine staining and IL-10 was measured as GFP signal by FACS. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 was calculated by one-way ANOVA. The results of the present invention were arrived by the calculation below and presented at Table 2 below: Here, ‘f10’ refers to ‘percentage change of IL10’. ‘f17’ refers to ‘percentage change of IL17’. ‘f10/17’ refers to ‘efficacy factor’. ‘IL10i’ refers to ‘unintervened levels of IL10’. ‘IL10n’ refers to ‘levels of IL10 post intervention’. ‘IL17i’ refers to ‘unintervened levels of IL17’. ‘IL17n’ refers to ‘levels of IL17 post intervention’. Higher the value of efficacy factor, more active is the compound. Table 2: In-vitro activities of the compound of the present invention Compound Efficacy factor No. ( f10/17) 14 0.976096 15 0.116729 16 4.650073 17 3.140058 18 0.346603 19 1.2372 20 0.478639

Higher the value of efficacy factor (f10/17) more IL-10 and lesser IL-17 production by a compound when given to the in-vitro differentiated CD4 ⁺ T cells under Th17 conditions. So, a positive value of f10/17 for a compound indicates that the particular compound is more active, and activity increases as the values of f10/17 increase further and vice versa. Hence, the compounds of the present invention are found to be active. Example 2: DOCKING STUDIES Co-crystal of digoxin bound ROR-γt was taken from Protein Data Bank (Pdb Id- 3B0W). To prepare protein for binding studies, bound ligand digoxin was removed, and missing side chains were added. Hydrogens were added, charges were assigned, and bond orders were corrected using parameters from OPLS 3.0 forcefield. This was followed by protonation of Histidine and complete structure minimization using Polak-Ribière-Conjugate Gradient algorithm implemented in Protein Preparation Wizard module of Schrodinger-2017-2 suite (Schrodinger here after). Coordinates for ligand of interest- various cholic acid derivatives including Cholic acid (CA) and Lithocholic acid (LCA) were taken from PubChem. Structure of Digoxin was extracted from co-crystal of digoxin bound complex-3B0W. Possible conformations of ligands were generated using the LigPrep module in Schrodinger. Molecular docking was accomplished using GlideXp module of Schrodinger-2017-2. Binding free energies of all ligands were computed using Prime MM-PBSA method implemented in Schrodinger. The results are presented at Figure 3 Figure 3 shows the binding energy of Novel compounds of the present invention when compared with known existing compounds such as Lithocholic acid (LCA), Cholic acid (CA) and digoxin (As a positive control). Predicted binding scores indicate that novel CA derivatives have a better affinity towards ROR-γt in comparison to different known compounds and could suppress the activity of the Th17 cells and their respective cytokines. Example 3:In-vitro testing of cholic acid derivatives in blocking of ROR-γt functions. To study the efficacy of the best three synthetic cholic acid derivatives, C-26, C-17, and C-16, shortlisted from the docking and in-vitro differentiation-based assays for Th17 cells, inventors performed luciferase assay to confirm whether these three derivatives can block ROR-γt function in the IL-17 luciferase assay. For which inventors seeded 20,000 HEK 293 per well in a 96-well plate. After overnight culture, those cells were transfected with pMIG-RORyt (80 ng/well), pGL4 mIL172kb promoter (50 ng/well), and pRL-Tk plasmid (Promega, 20 ng/well) separately and in combination using the X-tremeGENE™ 9 DNA Transfection Reagent (Roche). After 24 hours of transfection, test compounds (C-26, C-17, and C-16) were added. Twenty-four hours later, those cells were lyzed and analyzed for Renilla and Firefly measurements using the Dual- Glo® Luciferase Assay System (Promega) with a luminometer (Biotek Multimode plate reader). Renilla luciferase was used to normalize luciferase activity and transfection efficiency. As a result, inventors found that all three synthetic derivatives were able to bind to the ROR-γt element in the IL‑17 promoter efficiently and significantly decreased the luminescence intensity. These results are presented in figure 4. Example 4: Efficacy of cholic acid derivatives in prevention of experimental colitis in mice. Step 1: Experimental Colitis induction and dosing regimen used for cholic acid derivatives treatment in mice: For experimental colitis induction, the inventor gave 2.0 % (w/v) Dextran Sodium Sulfate (DSS) to mice in drinking water for six days. Selected three derivatives (C-26, C-17, and C-16; Dose 100 mg/kg) were given to DSS colitis mice using enema on days 3, 5, and 7. Each enema volume was 150 μl. On day 9, mice were sacrificed, and body parameters for colitis were measured and compared with the control (healthy) and DSS-treated group of animals. Step2: In-vivo study showing protective effect of cholic acid derivatives in experimental colitis: The inventors tested these derivatives (C-26, C-17, and C-16) in experimental colitis and found a delay in the signs of colitis indicated by body weight reduction, diarrhea, rectal bleeding, and colon length recovery. Histologically, that derivative suppresses leukocyte infiltration, edema, and inflammation in experimental colitis. The immunological analysis identifies that these derivatives efficiently promote IL-10 while suppressing pro-inflammatory cytokines, IL-17, and IFN-γ from CD4 ⁺ T cells isolated from mesenteric lymph nodes. Altogether, data indicated that bile acid synthetic derivatives effectively mediate protection in experimental colitis. The inventors proposed that these synthetic derivatives could be a promising therapy for colitis and other gut-related pathologies in humans. These results are presented in figure 5 to 10.