SUBSTITUTED LITHOCHOLIC ACID AND METHODS THEREOF FIELD OF INVENTION [0001] The present disclosure relates to a compound of Formula I and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, metabolites thereof. It further relates to the preparation of a compound of Formula I. In addition, the present disclosure relates to the pharmaceutical composition comprising the compound of Formula I for topical application in skin disorders and methods thereof. BACKGROUND OF THE INVENTION [0002] Psoriasis is a chronic autoimmune skin disorder with a substantial negative impact on the patient’s quality of life. Over 70 million people are suffering from psoriasis globally. The worldwide prevalence of psoriasis is around 2%, but studies in developed countries have reported higher prevalence rates of, on average, about 4.6%. To date, a wide range of treatment options such as topical delivery of corticosteroids, vitamin D derivatives, phototherapy, and administration of biological agents as immune-modulators are available. However, these approaches have major limitations, such as a plethora of side effects, and skin develops resistance to treatments over time. In addition, the therapeutic outcome of psoriasis treatments also can be unpredictable. Thus, there exist a need to develop efficient and safer psoriasis therapeutics. In psoriatic condition, the overactive immune system triggers skin cells to grow in an uncontrolled manner that leads to the formation of psoriatic plaques on the surface of the skin. Basic characteristics of psoriatic plaques are i) thick epidermis, due to increased proliferation of keratinocytes, and ii) significantly infiltrated mononuclear leukocytes (T cells and dendritic cells) in the dermal region. Thus, a rational combination treatment that targets epidermal alterations and inflammation may synergistically provide enhanced efficacy. [0003] In psoriatic plaques EphA2 (Ephrin type-A receptor 2 precursor), a receptor tyrosine kinase (RTK) that contributes to epidermal architecture, keratinocytes differentiation, and proliferation, showed enhanced up-regulation. Incerti M. et al., (Amino acid conjugates of lithocholic acid as antagonists of the EphA2 receptor. J Med Chem. 2013; 56:2936-47) demonstrated that amino acid conjugates of lithocholic acid serve as antagonists for EphA2 and the antagonism increases with the increase in hydrophobicity of amino acid. Vitamin D receptor in the modulation of the immune system especially the Type 1 helper T cell (Th1) pathway, reveals its potential for treating Th1 inflammatory diseases such as psoriasis. [0004] Delivering therapeutic agents across the skin layers is the primary technical challenge as lipophilic stratum corneum (SC), limits the delivery of most therapeutic payloads into the deeper layers. To overcome the limitation, skin permeation enhancers such as N-Methyl Pyrrolidone (NMP), Azones were developed. However, their use is restricted due to local intolerance and difficulties in therapeutic feasibility. [0005] To address said issues novel lithocholic analogues were designed for uniform distribution across the inflamed skin layers to reduce EphA2 levels and activate vitamin D receptors (VDR) to combat keratinocyte hyper-proliferation and hyper-immune responses together. Dual targeting ability of lithocholic acid analogues restored the altered complex disease biology and lead to the development of a novel class of effective topical therapeutics for psoriasis. SUMMARY OF THE INVENTION [0006] In an aspect of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, Formul pharmaceutically acceptable salts, and metabolites thereof, wherein R _a is selected from hydrogen, SiR ₂ R ₃ R ₄ , C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or COR ₂ , wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1- 18 heteroalkyl is optionally substituted with one or more substituents selected from -OC _{1- 18} alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₂ , R ₃ , R ₄ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or -OC _1-18 alkyl, wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -OC _1-18 alkyl is optionally substituted with one or more substituents selected from -OC1-18 alkyl, hydroxyl, cyano, C1-6 haloalkyl, C3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₁ is NR ₅ R ₆ or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , or -CONHR ₈ , wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , -CONHR ₈ is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₈ is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, or C _1-18 heteroalkyl; and n is 1 to 18. [0007] In another aspect of the present disclosure, there is provided a process for the preparation of the compound of Formula (I), the process comprising: a) protecting a compound of Formula X with at least one protecting agent to obtain a compound of Formula XI; b) reacting the compound of Formula XI with a compound of Formula XII to obtain a compound of Formula XIII, and c) deprotecting the compound of Formula XIII to obtain the compound of Formula (I) wherein, the definition is same as above. [0008] In yet another aspect of the present disclosure, there is provided a pharmaceutical composition comprising the compound of Formula (I) or a pharmaceutically acceptable salt thereof with a pharmaceutically acceptable carrier, optionally in combination with one or more other pharmaceutical compositions or in combination with at least one active ingredient and at least one excipient. [0009] In another aspect of the present disclosure, there is provided a method of treatment of a condition mediated by a skin disease, said method comprising administering a combination of the compound of Formula (I) or the pharmaceutical composition comprising the compound of Formula (I), optionally with other clinically relevant immune modulator agents to a subject in need of thereof. BRIEF DESCRIPTION OF DRAWINGS [0010] The following drawings form a part of the present specification and are included to further illustrate aspects of the present disclosure. The disclosure may be better understood by reference to the drawings in combination with the detailed description of the specific embodiments presented herein. [0011] Figure 1 depicts the physicochemical characterization of self-assembled lipid nanoparticles. (A) Tabular representation of the diameter, surface charge and polydispersity of self-assembled nanoparticles in water and 10% serum-containing medium of LC6, LC8, LC10 and LC12 using Dynamic Light Scattering (DLS). (B) Hydrodynamic diameter (HDD) and Zeta potential (C) histograms of nanoparticles (D) Transmission Electron Microscopic (TEM) analysis showing the shape and particle size distribution of nanoparticles (scale bar 0.5µm), in accordance with an implementation of the present disclosure. [0012] Figure 2 illustrates the growth inhibition study of substituted lithocholic acid (LC) on human keratinocytes (A-D): Normal human epidermal keratinocytes (NHEK) treated with LC6(A), LC8(B), LC10(C) and LC12(D) nanoparticles with varying concentrations from 0nM to 100nM, in accordance with an implementation of the present disclosure. [0013] Figure 3 depicts the cytokine expression of RAW cell lines and human PBMNCs. (A) Quantification of TNF-α expression in RAW 264.7 cell line at 50nM concentration of LCA nanoparticles. (B-D) Quantification of TNF-α, IL-17 and IL-23 expression in human PBMCs treated with LC10 nanoparticles with varying concentration from 50 to 200nM, in accordance with an implementation of the present disclosure. [0014] Figure 4 illustrates the skin permeation of LC analogues, ex vivo and in vivo. (A) Ex vivo skin permeation studies with lithocholic acid analogues LC6-LC12 in rat skin in comparison to the reference permeation enhancers, (B) In vivo skin permeation studies, the confocal microscopic images of the mice skin that was treated with Rhodamine associated LC10 nanoparticles along with control, in accordance with an implementation of the present disclosure. [0015] Figure 5 depicts the therapeutic evaluation of LC10 formulations: (A) PASI scores of psoriatic skin after the treatment; (B) Representative dorsal region images of BALB/c mice and the effect of treatment groups; (C) Bodyweight variations of the vehicle (red), LC10 (blue) and Sorvate (grey) treated BALB/c mice post-induction of psoriasis using IMQ for 6 days, in accordance with an implementation of the present disclosure. [0016] Figure 6 illustrates the representative images of H&E (hematoxylin and eosin) analysis in mice skin and spleen after psoriasis treatment with LC10 formulation in comparison with Sorvate and normal mice, in accordance with an implementation of the present disclosure. [0017] Figure 7 depicts the representative images of IHC (Immunohistochemistry analysis) in mice skin: TNF-α, IL-17 and IL-23 cytokines expression in imiquimod-induce psoriatic skin and LC10 treated skin in comparison with Sorvate and healthy mice, in accordance with an implementation of the present disclosure. [0018] Figure 8 depicts the serum biochemical analysis of (A) SGPT (Serum glutamic pyruvic transaminase) (B) SGOT(Serum glutamic oxaloacetic transaminase) (C) ALP (Alkaline phosphatase) (D) Bilirubin (E) Proteins (Albumin, Globulin) and (F) Spleen weights, in accordance with an implementation of the present disclosure. [0019] Figure 9 depicts the quantification of anti-inflammatory and pro-inflammatory cytokines in serum, in vivo, (A) IL-1α, (B) IL-1β, (C) IL-6, (D) IL-10, (E) IL-12p70, (F) IL-17, (G) IL-23, (H) IL-27, (I) TNF-α, (J) IFN-β, (K) IFN-γ, (L) MCP-1 and (M) GM- CSF cytokine levels in imiquimod induced psoriasis, treatment with LC10 formulation in comparison with Sorvate and normal mice. ns indicates non-significant, in accordance with an implementation of the present disclosure. [0020] Figure 10 depicts the fold change expression levels of Vitamin D Receptor (VDR) and Ephrin type-A receptor 2 (EphA2), and anti-inflammatory and pro-inflammatory cytokine mRNAs in different treatments with respect to IMQ on skin tissues (A) VDR, (B) EphA2, (C) IL-10, (D) IL-17, (E) IL-23, (F) TNF-α and (G) GM-CSF mRNA expressions, Dotted line indicates normalization to untreated control (IMQ), in accordance with an implementation of the present disclosure. [0021] Figure 11 represents the cell cycle analysis in bone marrow cells of different treated groups (A) Histogram represents the percentage of cell population in different phase of cell cycle. Blue, Green and Red represents cells population in G1, S and G2/M phases respectively; (B) The graph indicates quantitation of histogram data assayed on isolated bone marrow cells from 3 respectively treated BALB/cmice, in accordance with an implementation of the present disclosure. [0022] Figure 12 depicts the (A) H&E and Masson trichrome stained skin sections of Wistar rats were dissected at the 6th day after 5 continuous applications of LC10 nanoparticles at 10, 20 and 50mg/Kg body weight, (B) Variation of rat’s spleen weights by five continuous applications of LC10 nanoparticles at 10, 20 and 50mg/Kg body weight compared to untreated rats. ns indicates nonsignificant, in accordance with an implementation of the present disclosure. [0023] Figure 13 depicts the H&E (A) and Masson trichrome (B) stained organ sections (Heart, Lung, Kidney, Spleen and Liver) of Wistar rats that were excised on the 6th day after 5 continuous applications of LC10 nanoparticles at 10, 20 and 50mg/Kg body weight along with control, in accordance with an implementation of the present disclosure. DETAILED DESCRIPTION OF THE INVENTION [0024] Those skilled in the art will be aware that the present disclosure is subject to variations and modifications other than those specifically described. It is to be understood that the present disclosure includes all such variations and modifications. The disclosure also includes all such steps, features, compositions and compounds referred to or indicated in this specification, individually or collectively, and any and all combinations of any or more of such steps or features. Definitions: [0025] For convenience, before further description of the present disclosure, certain terms employed in the specification, and examples are collected here. These definitions should be read in the light of the remainder of the disclosure and understood as by a person of skill in the art. The terms used herein have the meanings recognized and known to those of skill in the art, however, for convenience and completeness, particular terms and their meanings are set forth below. [0026] The articles “a”, “an” and “the” are used to refer to one or to more than one (i.e., to at least one) of the grammatical object of the article. [0027] The terms “comprise” and “comprising” are used in the inclusive, open sense, meaning that additional elements may be included. It is not intended to be construed as “consists of only”. [0028] Throughout this specification, unless the context requires otherwise the word “comprise”, and variations such as “comprises” and “comprising”, will be understood to imply the inclusion of a stated element or step or group of element or steps but not the exclusion of any other element or steps. [0029] The term “including” is used to mean “including but not limited to”, “including” and “including but not limited to” are used interchangeably. [0030] In the structural formulae given herein and throughout the present disclosure, the following terms have been indicated meaning, unless specifically stated otherwise. [0031] Furthermore, the catalyst of Formula (I) can be its derivatives, analogs, tautomeric forms, stereoisomer’s, diastereomers, geometrical isomers, polymorphs, solvates, intermediates, metabolites, prodrugs or pharmaceutically acceptable salts and compositions. [0032] As used herein, the term "substituted" is contemplated to include all permissible substituents of organic compounds. In a broad aspect, the permissible substituents include acyclic and cyclic, branched and unbranched, carbocyclic and heterocyclic, aromatic and nonaromatic substituents of organic compounds. Illustrative substituents, for example, include those described hereinabove. The permissible substituents can be one or more and the same or different for appropriate organic compounds. For purposes of this disclosure, the heteroatoms such as nitrogen may have hydrogen substituents, and/or any permissible substituents of organic compounds described herein which satisfy the valences of the heteroatoms. [0033] The term “alkyl” refers to straight or branched aliphatic hydrocarbon groups having 1 to 18 carbon atoms, which are attached to the rest of the molecule by a single atom, which may be optionally substituted by one or more substituents. Preferred alkyl groups include, without limitation, methyl, ethyl, n-propyl, isopropyl, butyl, isobutyl, t- butyl, pentyl, hexyl, heptyl, octyl and the like. [0034] The term “haloalkyl” refers to straight or branched aliphatic hydrocarbon groups having 1 to 6 carbon atoms, which are attached to the rest of the molecule by a single atom, substituted with halogens, not limited to fluorine, chlorine, bromine, iodine. [0035] The term “alkenyl” refers to straight or branched aliphatic hydrocarbon groups having 2 to 18 carbon atoms with at least one carbon-carbon double bond, which are attached to the rest of the molecule by a single atom, which may be optionally substituted by one or more substituents. Preferred alkenyl groups include, without limitation, ethenyl, propenyl, butenyl, 1-methyl-2-buten-1-yl, and the like. [0036] The term “alkynyl” refers to straight or branched aliphatic hydrocarbon groups having 2 to 18 carbon atoms with at least one carbon-carbon triple bond, which are attached to the rest of the molecule by a single atom, which may be optionally substituted by one or more substituents. Preferred alkyl groups include, without limitation, ethynyl, 2-propynyl (propargyl), 1-propynyl, and the like. [0037] The term “aryl” refers to aromatic radicals having 6 to 10 carbon atoms, which may be optionally substituted by one or more substituents. Preferred aryl groups include, without limitation, phenyl, naphthyl, indanyl, biphenyl, and the like. [0038] The term "heteroalkyl" refers to an alkyl radical having 1 to 18 carbon atoms and one or more skeletal carbon atoms replaced by heteroatoms selected from oxygen, nitrogen and sulfur. The alkyl chain may be optionally substituted. [0039] The term “heterocyclyl” refers to a heterocyclic ring radical having 3 to 10 carbon atoms which may be optionally substituted by one or more substituents. The heterocyclyl ring radical may be attached to the main structure at any heteroatom or carbon atom that results in the creation of a stable structure. [0040] Furthermore, the term “heterocyclyl” refers to a stable 3 to 10 membered rings radical, which consists of carbon atoms and from one to five heteroatoms selected from nitrogen, phosphorus, oxygen, and sulfur. For purposes of this invention the heterocyclic ring radical may be monocyclic, bicyclic or tricyclic ring systems, and the nitrogen, phosphorus, carbon, or sulfur atoms in the heterocyclic ring radical may be optionally oxidized to various oxidation states. In addition, the nitrogen atom may be optionally quaternized; and the ring radical may be partially or fully saturated. [0041] The term “heteroaryl” refers to an aromatic heterocyclic ring radical as defined above. The heteroaryl ring radical may be attached to the main structure at any heteroatom or carbon atom that results in the creation of a stable structure. [0042] The term “cycloalkyl” refers to non-aromatic mono or polycyclic ring system of about 3 to 6 carbon atoms, which may be optionally substituted by one or more substituents. The polycyclic ring denotes hydrocarbon systems containing two or more ring systems with one or more ring carbon atoms in common, i.e., a spiro, fused or bridged structures. Preferred cycloalkyl groups include, without limitation, cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, groups. [0043] It is understood that included in the family of compounds of Formula (I) are isomeric forms including diastereoisomers, enantiomers, tautomers, and geometrical isomers in “E” or “Z” configurational isomer or a mixture of ‘E’ and ‘Z’ isomers. It is also understood that some isomeric form such as diastereomers, enantiomers and geometrical isomers can be separated by physical and/or chemical methods and by those skilled in the art. [0044] Compounds disclosed herein may exist as single stereoisomers, racemates and or mixtures of enantiomers and/or diastereomers. All such single stereoisomers, racemates and mixtures thereof are intended to be within the scope of the subject matter described. [0045] The phrase “pharmaceutically acceptable” refers to compounds or compositions that are physiologically tolerable and do not typically produce allergic or similar untoward reaction, including but not limited to gastric upset or dizziness when administered to subjects. [0046] Pharmaceutically acceptable salts forming part of this invention include salts derived from inorganic bases such as like Li, Na, K, Ca, Mg, Fe, Cu, Zn and Mn and ammonium, substituted ammonium salts, aluminum salts and the like.; salts of organic bases such as N, N’-diacetylethylenediamine, glucamine, triethylamine, choline, dicyclohexylamine, benzylamine, trialkylamine, thiamine, guanidine, diethanolamine, ^- phenylethylamine, piperidine, morpholine, pyridine, hydroxyethylpyrrolidine, hydroxyethylpiperidine and the like, salts also include amino acid salts such as glycine, alanine, cystine, cysteine, lysine, arginine, phenylalanine, guanidine etc. Salts may include acid addition salts where appropriate which are sulphates, nitrates, phosphates, perchlorates, borates, hydrohalides, acetates, tartrates, maleates, fumarates, citrates, succinates, palmoates, methanesulphonates, tosylates, benzoates, salicylates, hydroxynaphthoates, benzenesulfonates, ascorbates, glycerophosphates, ketoglutarates and the like. [0047] Described herein are prodrugs of the compound of Formula (I), which on administration undergo chemical conversion by metabolic processes before becoming active pharmacological substances. In general, such prodrugs will be functional derivatives of a compound of the invention, which are readily convertible in vivo into a compound of the invention. [0048] The compounds described herein may also exhibit polymorphism. This invention further includes different polymorphs of the compounds of the present invention. The term polymorph refers to a particular crystalline state of a substance, having particular physical properties such as X-ray diffraction, IR spectra, melting point and the like. [0049] The compounds described herein can also be prepared in any solid or liquid physical form, for example, the compound can be in a crystalline form, in amorphous form and have any particle size. Furthermore, the compound particles may be micronized or nanosized, or may be agglomerated, particulate granules, powders, oils, oily suspensions or any other form of solid or liquid physical forms. [0050] The term “protecting agent” refers to a chemical compound which provides a temporary group added during organic synthesis to prevent a portion of a molecule from reacting thereby assists chemoselectivity; the term “deprotecting agent” refers to a chemical compound which assists in removing the protecting group from the compound during organic synthesis. [0051] The term “antagonist” refers to a substance that acts against and block a molecular action. The term “antagonist” refers to an inhibitor of a natural ligand i.e., hormone or neurotransmitter. The term “agonist” refers to a substance that mimics the natural ligand and produces the same effects as that of the natural ligand. [0052] The term “EphA2 receptor” refers to ephrin type-A receptor 2, a protein that in humans is encoded by the EphA2 gene; the term “Vitamin D receptor (VDR) ” refers to a nuclear, ligand-dependent transcription factor that in complex with hormonally active vitamin D. [0053] The term “receptor” refers to a region of tissue, or a molecule in a cell membrane, which responds specifically to a particular neurotransmitter, hormone, antigen, or other substance. [0054] The term “solvate” refers to a compound formed by the interaction of a solvent and a solute. In the present disclosure, the term solvate refers to a compound formed by the interaction of solvent and the compounds of Formula I of the present disclosure. [0055] The term “ metabolite” refers to any substance involved in metabolism. [0056] Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood to one of ordinary skill in the art to which this disclosure belongs. Although methods and materials similar or equivalent to those described herein can be used in the practice or testing of the disclosure, the preferred methods, and materials are now described. All publications mentioned herein are incorporated herein by reference. [0057] The present disclosure is not to be limited in scope by the specific embodiments described herein, which are intended for exemplification only. Functionally equivalent products, compositions, and methods are clearly within the scope of the disclosure, as described herein. A term once described, the same meaning applies for it, throughout the patent. [0058] In an embodiment of the present disclosure, there is provided a compound of Formula I Formula I and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein R _a is selected from hydrogen, SiR ₂ R ₃ R ₄ , C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or COR ₂ , wherein C _1-18 alkyl, C2-18 alkenyl, C _2-18 alkynyl, C6-10 aryl, C _1-18 heteroalkyl is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R _2, R ₃ , R ₄ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or -OC _1-18 alkyl, wherein C1-18 alkyl, C _2-18 alkenyl, C2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -OC _1-18 alkyl is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₁ is NR ₅ R ₆ or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , or -CONHR8, wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , -CONHR ₈ is optionally substituted with one or more substituents selected from -OC1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C5-10 heteroaryl; R8 is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl; and n is 1 to 18. [0059] In an embodiment of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein R _a is selected from hydrogen, SiR ₂ R ₃ R ₄ , C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1- 18 heteroalkyl, or COR ₂ ; R ₂ , R ₃ , R ₄ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or -OC _1-18 alkyl, wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or -OC _1-18 alkyl is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C1-6 haloalkyl, C3-6 cycloalkyl, C6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₁ is selected from NR ₅ R ₆ or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C2-18 alkynyl, C6-10 aryl, C1-18 heteroalkyl, -COR ₈ , -COOR ₈ , or - CONHR8 wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, - COR ₈ , -COOR ₈ , -CONHR ₈ is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R8 is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, or C _1-18 heteroalkyl; and n is 1 to 18. [0060] In an embodiment of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein R _a is selected from hydrogen, SiR ₂ R ₃ R ₄ , C _1-18 alkyl or C _2-18 alkenyl; R _2, R _3, R ₄ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or -OC _1-18 alkyl wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -OC1-18 alkyl is optionally substituted with one or more substituents selected from -OC1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₁ is NR ₅ R ₆ or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , or -CONHR8 wherein C _1-18 alkyl, C2-18 alkenyl, C2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , -CONHR ₈ is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₈ is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl; and n is 1 to 18. [0061] In an embodiment of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein R _a is hydrogen or SiR ₂ R ₃ R ₄ ; R ₂ , R ₃ , R ₄ is independently selected from hydrogen, C1-18 alkyl, C _2- 18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or -OC _1-18 alkyl; wherein C1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -OC _1-18 alkyl is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C1-6 haloalkyl, C3-6 cycloalkyl, C6-10 aryl, C _3-10 heterocyclyl, or C5-10 heteroaryl; R ₁ is NR5R6 or N ⁺ R5R6R7; R5, R6, R7 is independently selected from hydrogen, C _1-18 alkyl, C _{2- 18} alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , or -CONHR ₈ wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C1-18 heteroalkyl, -COR8, - COOR ₈ , - -CONHR8 is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₈ is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C1-18 heteroalkyl; and n is 1 to 18. [0062] In an embodiment of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein Ra is hydrogen or SiR ₂ R ₃ R ₄ ; R _2, R _3, R ₄ is independently selected from C _1-18 alkyl, C _2-18 alkenyl, C2-18 alkynyl, C6-10 aryl or C1-18 heteroalkyl; R1 is selected from NR5R6 or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , or -CONHR ₈ wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C6-10 aryl, C1-18 heteroalkyl, -COR8, -COOR ₈ , -CONHR8 is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₈ is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl; and n is 1 to 10. [0063] In an embodiment of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein Ra is hydrogen or SiR2R3R4; R2, R3, R4 is independently selected from C _1-18 alkyl; R1 is NR5R6 or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, and C _1-18 alkyl, wherein C _1-18 alkyl is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _{5- 10} heteroaryl; R ₈ is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl; and n is 1 to 8. [0064] In an embodiment of the present disclosure, there is provided a compound of Formula I, and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof, wherein R _a is hydrogen or SiR ₂ R ₃ R ₄ ; R ₂ , R ₃ , R ₄ is independently selected from C _1-18 alkyl; R1 is NR5R6 or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from C _1-18 alkyl; and n is 1 to 6. [0065] In an embodiment of the present disclosure, there is provided the compound of Formula (I) wherein the compound of Formula (I) is selected from the group consisting of and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof. [0066] In an embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula (I) as disclosed herein, the process comprising: a) protecting a compound of Formula X with at least one protecting agent to obtain a compound of Formula XI; b) reacting the compound of Formula XI with a compound of Formula XII to obtain a compound of Formula XIII, and c) deprotecting the compound of Formula XIII to obtain the compound of Formula (I) Ra is selected from hydrogen, SiR ₂ R ₃ R ₄ , C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, or COR ₂ , wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _{1- 18} heteroalkyl is optionally substituted with one or more substituents selected from -OC _1- 18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C5-10 heteroaryl; R ₂ , R ₃ , R ₄ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -OC _1-18 alkyl, wherein C _1-18 alkyl, C _{2- 18} alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -OC _1-18 alkyl is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₁ is NR ₅ R ₆ or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C6-10 aryl, C1-18 heteroalkyl, -COR ₈ , -COOR ₈ , -CONHR ₈ , wherein C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl, -COR ₈ , -COOR ₈ , -CONHR ₈ is optionally substituted with one or more substituents selected from -OC _1-18 alkyl, hydroxyl, cyano, C _1-6 haloalkyl, C _3-6 cycloalkyl, C _6-10 aryl, C _3-10 heterocyclyl, or C _5-10 heteroaryl; R ₈ is selected from hydrogen, C _1-18 alkyl, C _2-18 alkenyl, C _2-18 alkynyl, C _6-10 aryl, C _1-18 heteroalkyl; and n is 1 to 18. [0067] In an embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula (I) as disclosed herein, the process comprising: a) protecting a compound of Formula X with at least one protecting agent to obtain a compound of Formula XI; b) reacting the compound of Formula XI with a compound of Formula XII to obtain a compound of Formula XIII, and c) deprotecting the compound of Formula XIII to obtain the compound of Formula (I), wherein Ra is hydrogen or SiR ₂ R ₃ R ₄ ; R ₂ , R ₃ , R ₄ is independently selected from C _1-18 alkyl; R1 is NR5R6 or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from C _1-18 alkyl, and n is 1 to 6. [0068] In an embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula(I), wherein the at least one protecting agent is selected from tert-butyldimethylsilylchloride, tert-butyldiphenylsilylchloride, methoxymethyl chloride, dihydropyran, allyl bromide or benzyl chloride; and the at least one protecting agent is selected from tert-butyldimethylsilylchloride or tert- butyldiphenylsilylchloride, methoxymethyl chloride, dihydropyran, allyl bromide or benzyl chloride. In yet another embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula(I), wherein the at least one protecting agent is tert-butyldimethylsilylchloride. [0069] In an embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula(I), wherein the reacting the compound of Formula XI with a compound of Formula XII to obtain a compound of Formula XIII is carried out in the presence of at least one base selected from di-isopropyl ethylamine, di- isopropyl phenylethylamine, triethylamine, hexafluorophosphate azabenzotriazole tetramethyl uronium (HATU) or hexafluorophosphate benzotriazole tetramethyl uronium (HBTU). In another embodiment of the present disclosure, wherein the at least one base is selected from di-isopropyl ethylamine, di-isopropyl phenylethylamine or triethylamine. In yet another embodiment of the present disclosure, wherein the at least one base selected from di-isopropyl ethylamine or di-isopropyl phenylethylamine. [0070] In an embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula (I), deprotecting the compound of Formula XIII to obtain the compound of Formula (I) is carried out in the presence of at least one deprotecting agent selected from tetrabutylammonium fluoride, hafnium triflate, Sodium tetrachloroaurate(III) dehydrate, acetyl chloride or N-iodosuccinimide. In another embodiment of the present disclosure, wherein the at least one deprotecting agent selected from tetrabutylammonium fluoride, hafnium triflate or sodium tetrachloroaurate(III) dehydrate. In yet another embodiment of the present disclosure, wherein at least one deprotecting agent is tetrabutylammonium fluoride. [0071] In an embodiment of the present disclosure, there is provided a process for the preparation of the compound of Formula (I) as disclosed herein, the process comprising: a) protecting a compound of Formula X with the protecting tert- butyldimethylsilylchloride to obtain a compound of Formula XI; b) reacting the compound of Formula XI with a compound of Formula XII in the presence of the base di- isopropyl ethylamine to obtain a compound of Formula XIII, and c) deprotecting the compound of Formula XIII in the presence of deprotecting agent tetrabutylammonium fluoride to obtain the compound of Formula (I), wherein R _a is hydrogen or SiR ₂ R ₃ R ₄ ; R _2, R ₃ , R ₄ is independently selected from C _1-18 alkyl; R1 is NR5R6 or N ⁺ R ₅ R ₆ R ₇ ; R ₅ , R ₆ , R ₇ is independently selected from C _1-18 alkyl; and n is 1 to 6. [0072] In an embodiment of the present disclosure, there is provided the compound of Formula (I) and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof as disclosed herein, wherein the compound of Formula (I) acts as an antagonist for EphA2 receptor and as an agonist for Vitamin D receptor. [0073] In an embodiment of the present disclosure, there is provided the compound of Formula (I) and its polymorphs, stereoisomers, prodrugs, solvates, co-crystals, intermediates, pharmaceutically acceptable salts, and metabolites thereof as disclosed herein, wherein the compound of Formula (I) for use as a medicament for treating a skin disease, wherein the skin disease is psoriasis, skin inflammations, acne, sunburns, eczema, dermatitis, alopecia, vitiligo, melanoma. [0074] In an embodiment of the present disclosure, there is provided a pharmaceutical composition comprising the compound of Formula (I) or a pharmaceutically acceptable salt thereof with a pharmaceutically acceptable carrier, optionally in combination with one or more other pharmaceutical compositions or in combination with at least one active ingredient and at least one excipient. In another embodiment of the present disclosure, wherein the pharmaceutical composition is a nano formulation. [0075] In an embodiment of the present disclosure, there is provided a pharmaceutical composition comprising the compound of Formula (I) or a pharmaceutically acceptable salt thereof with a pharmaceutically acceptable carrier, in combination with at least one active ingredient selected from a group consisting vitamin D receptor agonists, glucocorticoid receptor agonists, mTOR inhibitors, HDAC inhibitors, non-steroidal inflammatory drugs, microtubule inhibitors, PKR inhibitors, AKT inhibitors and combinations thereof; and the at least one excipient is selected from a group consisting of carbohydrates, fatty acids, fatty acid esters, polyethylene glycols, polycaprolactones, poly(lactic-co-glycolic acid) long carbon chain alcohols. [0076] In an embodiment of the present disclosure, there is provided the pharmaceutical composition, wherein the composition is in a form selected from solution, aerosol, suspension, gel, lotion, powder, or cream. [0077] In an embodiment of the present disclosure, there is provided a method for the treatment of a condition mediated by a skin disease, said method comprising administering to a subject an effective amount of the compound of Formula (I) or the pharmaceutical composition as disclosed herein optionally with other clinically relevant immune modulator agents to a subject in need of thereof and wherein the skin disease is psoriasis, skin inflammations, acne, sunburns, eczema, dermatitis, alopecia, vitiligo, melanoma. EXAMPLES [0078] The following examples provide the details about the synthesis, activities, and applications of the compounds of the present disclosure. It should be understood the following is representative only, and that the invention is not limited by the details outlined in these examples. [0079] There is provided a process as shown in the following schemes 1 and 2 for the preparation of compounds of the Formula (I), wherein all the groups are as defined earlier. The process for the preparation of the compounds of Formula (I) comprises of the following: [0080] All compounds were characterized by using ¹ H-NMR, ESI-MS (Electrospray Ionization Mass Spectrometry), and all final compounds were characterized by using ¹ H- NMR, ¹³ C-NMR, ESI-MS and HRMS (High-Resolution Mass Spectrometry). The purities of all the final compounds were examined by HPLC (High-Performance Liquid Chromatography) and they are consistently found to be ̴ 98% pure. I. Synthesis of tertiary amine intermediates- Formula XII by Scheme 1 [0081] A representative synthetic procedure for the intermediate has been described below for all the tertiary amine intermediates i.e. Formula XII, Scheme 1. Step 1A. Synthesis of tert-butyl (2-aminoethyl) carbamate (Intermediate 1A, Scheme 1) [0082] 10 g of ethylenediamine (166 mmol) in 30 mL of dioxane was stirred in a 2-neck round bottom flask at 0 °C.45 g of Di-tert-butyl dicarbonate (BOC-anhydride, 20.8 mmol) was dissolved in 50 mL of dioxane and added slowly to the stirring diamine solution for a time period of 2.5 h. After completion of BOC-anhydride addition, the reaction mixture was further stirred for another 22 h at room temperature. After 22 h of stirring, the reaction mixture is concentrated to dryness (dioxane solvent removal) followed by the addition of water (100 mL). The residue containing aqueous solution was filtered to remove Di-BOC protected ethylene diamine (as white solid). Mono-BOC protected ethylene diamine was extracted from the aqueous filtrate using dichloromethane (4 x 50 mL). Combined organic layers were collected, dried over anhydrous sodium sulfate, concentrated and evaporated to dryness to give Intermediate 1A as yellow liquid. No purification was performed as the product obtained pure. Yield: 2.1 g (62%). Step 1B. Synthesis of tert-butyl (2-(dihexylamino)ethyl)carbamate (Intermediate 1B, Scheme 1) [0083] 1 g of Intermediate 1A (6.2 mmol) prepared in step a was dissolved in 15 mL of ethyl acetate and stirred in 50 mL round bottom flask.2.61 mL of 1-bromohexane (18.6 mmol) and 3.4 g of oven-dried potassium carbonate (24.8 mmol) was added to the stirring solution and the mixture was refluxed for 24 h. After completion of the reaction, the reaction mixture was filtered over celite pad and washed with ethyl acetate. Resulting ethyl acetate filtrate was collected, concentrated and vacuum dried to yield crude BOC protected C6-tertiary amine intermediate 1B. Crude intermediate 1B was subjected for column chromatographic purification using 60-120 mesh silica gel with hexane and ethyl acetate solvent system as eluent. After chromatographic purification pure Intermediate 1B was obtained as yellowish liquid (solidifies to white solid at 4 °C). Yield: 1.6 g (78%). Step 1C- Synthesis of N ¹ , N ¹ -dihexylethane-1,2-diamine (Formula XII, Scheme 1) [0084] To the ice-cold solution of intermediate 1C (1.5 g, 4.56 mmol) in 50 mL round bottom flask, 5 mL of dry dichloromethane was added and kept for stirring. To the stirring solution, 5 mL of trifluoroacetic acid was added slowly at 0 °C and stirring continued for another 4 h at r.t. After completion of the reaction, the reaction mixture was diluted with 15 mL of dichloromethane an excess trifluoroacetic acid was neutralized slowly with saturated sodium bicarbonate (NaHCO3) solution at 0 °C. The pH of the solution was checked to ensure complete neutralization. The resulting solution was further washed with water (2 x 10 mL) followed by brine wash (1 x 10 mL). Combined organic layers were dried over anhydrous sodium sulfate, concentrated and evaporated to dryness to yield free amine Formula XII as white solid. No further purification step was employed as the product obtained was pure. Yield: 1 g (96%). II Synthesis of Formula I – Substituted Lithocholic Acid (Scheme 2) [0085] A representative synthetic procedure for the target compound, lithocholic acid derivate with C6 alkyl chain (LC6) has been described for all the tertiary amine intermediates i.e. LC6 to LC12, Scheme 2. Step 2A. Synthesis of O-TBDMS protected Lithocholic acid (Formula XI from Formula X, Scheme 2) [0086] 1 g of lithocholic acid (Formula X) (2.65 mmol) was taken in 100 mL round bottom flask and dissolved in 30 mL of dry dichloromethane. To the lithocholic acid solution, 0.63 g of imidazole (9.3 mmol), a catalytic amount of dimethyl aminopyridine (DMAP) was added and stirred for 20-30 min at r.t. To the stirring reaction mixture, 1.39 g of tetrabutyldimethylsilyl chloride (TBDMS-Cl, 9.3 mmol) was added and stirring continued for overnight. After completion of the reaction, the reaction mixture was diluted with 30 mL of dichloromethane and washed with water (3 x 30 mL) followed by brine solution (1 x 30 mL). Organic layers were collected, dried over anhydrous sodium sulfate and evaporated to dryness to yield crude TBDMS-protected lithocholic acid, intermediate Formula XI. Crude product upon column chromatographic purification with 60-120 mesh silica gel and chloroform:methanol as eluent solvent system yielded pure Formula XI as transparent semi-solid. Yield: 1.1 g (84%). (4R)-4-((3R,8R,9S,10S,13R,14S,17R)-3-((tert-butyldimethylsil yl)oxy)-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pent anoic acid (TLCA): ¹ H NMR (400MHz, CDCl3):δ0.20 (s, 6H, g,g’ H), 0.58 (s, 3H, C21H), 0.86-0.93 (m, 15H, h,h’,h’’,f, f’H), 0.98-2.29 (m, 29H), 3.47 m, 1H, C3H ) ppm. Step 2B. Synthesis of C6-Tert-Amine Conjugated (O-TBDMS) Lithocholic acid (FormulaVI, Scheme 2) [0087] Solid HOBt (Hydroxybenzotriazole) (0.405 g, 3 mmol) and EDCI (1-Ethyl-3-(3- dimethylaminopropyl)carbodiimide) (0.573 g, 3 mmol) were added sequentially to an ice- cold and stirred solution of O-TBDMS protected lithocholic acid, Formula XI (1.0 g, 2.0 mmol) in 5 mL dry DCM under nitrogen atmosphere. After half an hour, N ¹ , N ¹ -dihexyl- 1, 2-ethylenediamine (Formula XII, Scheme 1, 0.475 g, 2.0 mmol) dissolved in dryDCM (2 mL) was added to the reaction mixture.0.52 mL of Di-isopropyl ethylamine (DIPEA, 3.0 mmol) was added dropwise to the reaction mixture until it became alkaline to litmus. The resulting solution was left stirred at r.t. overnight, diluted with excess DCM and washed sequentially with saturated sodium bicarbonate (3x50 mL) and water (3x50 mL). The organic layer was dried over anhydrous sodium sulfate, filtered and the solvent from the filtrate removed by rotary evaporation. The residue upon column chromatographic purification with 60-120 mesh silica gel using 1-2% methanol in dichloromethane (v/v) as eluent afforded 0.9 g of the pure Formula XIII, C6-Tert-Amine Conjugated (O-TBDMS) lithocholic acid (63% yield, Rf= 0.5,9:1 chloroform:methanol, v/v) as yellowish liquid which solidified upon storage at 4 ºC. (4R)-4-((3R,8R,9S,10S,13R,14S,17R)-3-((tert-butyldimethylsil yl)oxy)- 10,13dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl )-N- (2(dihexylamino)ethyl)pentanamide (Formula VI): ¹ H NMR (400MHz, CDCl3):δ 0.07 (s,6H, g,g’ H), 0.63 (s, 3H, C21H), 0.86-0.93 (m, 15H, h,h’,h’’,f, f’H), 0.98-2.29 (m, 51H), 2.52 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 3.34 (t, 2H, a H), 3.58 (m, 1H, C3H ) ppm. ESI-MS: calculated mass 700.25 (for C44H84N2O2Si) found [M] ⁺ :701 (4R)-4-((3R,8R,9S,10S,13R,14S,17R)-3-((tert-butyldimethylsil yl)oxy)- 10,13dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl )-N- (2(dioctylamino)ethyl)pentanamide (Formula VII) ¹ H NMR (400MHz, CDCl3):δ 0.07 (s,6H, g,g’ H), 0.63 (s, 3H, C21H), 0.86-0.93 (m, 15H, h,h’,h’’,f, f’H), 0.98-2.29 (m, 59H), 2.52 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 3.34 (t, 2H, a H), 3.58 (m, 1H, C3H ) ppm. ESI-MS: calculated mass 757.36 (for C48H92N2O2Si) found [M+H] ⁺ : 758 (4R)-4-((3R,8R,9S,10S,13R,14S,17R)-3-((tert-butyldimethylsil yl)oxy)-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)-N-( 2- (didecylamino)ethyl)pentanamide (Formula VIII): ¹ H NMR (400MHz, CDCl3):δ0.07 (s,6H, g,g’ H), 0.63 (s, 3H, C21H), 0.86-0.93 (m, 15H, h,h’,h’’,f, f’H), 0.98-2.29 (m, 67H), 2.52 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 3.34 (t, 2H, a H), 3.58 (m, 1H, C3H ) ppm. ESI-MS: calculated mass 813.47 (for C52H100N2O2Si) found [M+H] ⁺ : 814 (4R)-4-((3R,8R,9S,10S,13R,14S,17R)-3-((tert-butyldimethylsil yl)oxy)-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)-N-( 2- (didodecylamino)ethyl)pentanamide (Formula IX): ¹ H NMR (400MHz, CDCl3):δ0.07 (s,6H, g,g’ H), 0.63 (s, 3H, C21H), 0.86-0.93 (m, 15H, h,h’,h’’,f, f’H), 0.98-2.29 (m, 75H), 2.52 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 3.34 (t, 2H, a H), 3.58 (m, 1H, C3H ) ppm. ESI-MS: calculated mass 869.58 (for C56H108N2O2Si) found [M] ⁺ : 870 Step 2C. Synthesis of Formula I ( Scheme 2) [0088] The compound of Formula XIII prepared in step 2B (0.3 g, 0.42 mmol) was dissolved in 1 mL of dry THF and added with 0.25 mL of tetrabutylammonium fluoride (TBAF, 0.84 mmol). The resulting solution was left under stirring at r.t for 6 h. After completion of the reaction, reactionmixturewas added with a saturated NH4Cl solution (5 mL) and the aqueous layer was extracted with chloroform (3x5 mL). Combined organic layers were washed with brine solution, dried over anhydrous sodium sulfate, filtered and concentrated to dryness on a rotary evaporator to afford crude iodide salt of C6-Q-Amine lithocholic acid as gummy solid. The residue upon column chromatographic purification with silica gel (60-120 mesh size) using 5-6% methanol/ chloroform (v/v) as eluent followed by chloride ion-exchange chromatography (using amberlite IRA 400 chloride ion exchange resin) obtained 0.12 g (48% yield) of the pure target lipid Formula I C6-T- Amine lithocholic acid chloride salt (Litho-T-C6). (Rf = 0.25, 9:1 chloroform: methanol, v/v). All the substituted lithocholic acid were characterized by ¹ H NMR, ¹³ C NMR, ESI- MS,and HRMS and are found to be pure by HPLC. Spectral Data: (4R)-N-(2-(dihexylamino)ethyl)-4-((3R,8R,9S,10S,13R,14S,17R) -3-hydroxy-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pent anamide (Formula II): ¹ H NMR (400 MHz, CDCl3):δ 0.64 (s, 3H, C21H), 0.84-0.93 (m, 12H, C18, C19, f, f’H), 0.96-2.28 (m, 45H), 2.49 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 2.78, (m, 1H, C20 H), 3.33 (t, 2H, a H), 3.62 (m, 1H, C3H ) ppm. ¹³ C NMR (101 MHz, CDCl3):δ 173.96, 71.87, 56.50, 56.08, 53.75, 52.76, 42.77, 42.14, 40.46, 40.20, 36.51, 36.30, 35.89, 35.58, 35.38, 34.61, 33.65, 31.93, 31.86, 30.59, 29.69, 29.63, 29.53, 29.36, 28.27, 27.39, 27.24, 26.45, 26.04, 24.25, 23.41, 22.72, 20.85, 18.40, 14.15, 12.09 ppm. ESI-MS: calculated mass 587.0 (for C38H70N2O2) found: 587 (M ⁺⁾ HRMS:587.5467 (4R)-N-(2-(dioctylamino)ethyl)-4-((3R,8R,9S,10S,13R,14S,17R) -3-hydroxy-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pent anamide (Formula III): ¹ H NMR (400MHz, CDCl3):δ 0.63 (s, 3H, C21H), 0.88-0.93 (m, 12H, C18, C19, f, f’ H), 0.96-2.28 (m, 45H), 2.49 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 2.77, (m, 1H, C20 H), 3.32 (t, 2H, a H), 3.62 (m, 1H, C3H) ppm. ¹³ C NMR (101 MHz, CDCl3):δ 173.80, 71.87, 56.50, 56.08, 53.82, 52.72, 42.77, 42.14, 40.46, 40.21, 36.52, 35.89, 35.57, 35.38, 34.61, 33.70, 31.96, 31.88, 30.59, 29.70, 29.60, 29.40, 28.27, 27.48, 27.23, 26.52, 26.46, 24.26, 23.40, 22.73, 20.85, 18.41, 14.15, 12.09 ppm. ESI-MS: calculated mass 643.1 (for C ₄₂ H ₇₈ N ₂ O ₂ ) found: 644 (M+H) ⁺ HRMS: 643.6153 (4R)-N-(2-(didecylamino)ethyl)-4-((3R,8R,9S,10S,13R,14S,17R) -3-hydroxy-10,13- dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pent anamide (Formula IV ): ¹ H NMR (400MHz, CDCl3): δ 0.64 (s, 3H, C21H), 0.84-0.93 (m, 12H, C18, C19, f, f’ H), 0.96-2.28 (m, 45H), 2.49 (t, 4H, e, e’ H), 2.62 (t, 2H, b H), 2.78, (m, 1H, C20H), 3.32 (t, 2H, a H), 3.69 (m, 1H, C3H) ppm. ¹³ C NMR (101 MHz, CDCl3): δ 173.95, 71.87, 56.50, 56.08, 53.74, 52.75, 42.77, 42.14, 40.46, 40.20, 36.51, 36.31, 35.89, 35.58, 35.38, 34.61, 33.65, 31.93, 31.86, 30.59, 29.69, 29.63, 29.54, 29.37, 28.27, 27.40, 27.23, 26.45, 26.06, 24.25, 23.41, 22.72, 20.85, 18.40, 14.15, 12.09 ppm. ESI-MS: calculated mass 699.2 (for C46H86N2O2) found: 699.68 (M+) HRMS: 699.67986 (4R)-N-(2-(didodecylamino)ethyl)-4-((3R,8R,9S,10S,13R,14S,17 R)-3-hydroxy- 10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-y l)pentanamide (Formula V) ¹ H NMR (400MHz, CDCl3): δ0.64 (s, 3H, C21H), 0.88-0.93 (m, 12H, C18, C19, f, f’ H), 0.97-2.28 (m, 45H), 2.48 (t, 4H, e, e’ H), 2.60 (t, 2H, b H), 2.78, (m, 1H, C20H), 3.32 (t, 2H, a H), 3.62 (m, 1H, C3H) ppm. ¹³ C NMR (101 MHz, CDCl3): δ 173.93, 71.87, 56.50, 56.08, 53.82, 52.72, 42.77, 42.14, 40.46, 40.21, 36.52, 35.89, 35.57, 35.39, 34.61, 33.71, 31.96, 31.88, 30.59, 29.73, 29.70, 29.60, 29.40, 28.27, 27.48, 27.23, 26.54, 26.46, 24.26, 23.40, 22.73, 20.85, 18.41, 14.15, 12 ppm. ESI-MS: calculated mass 755.3 (for C ₅₀ H ₉₄ N ₂ O ₂ ) found: 756 (M+) HRMS: 755.74360 Example 2 Materials and Methods Preparation of substituted lithocholic acid: [0089] A stock of substituted lithocholic acid of Formula II-LC6, Formula III-LC8, Formula IV-LC10 and Formula V-LC12 (1 mM) in ethanol was prepared and aliquots (5 μL) of the stock solution were added to the deionized water (1 mL) with constant vortex followed by sonication in an ice bath until clarity using a Branson 450 sonifier at 100% duty cycle & 25W output power to furnish the 1 mM self-assembled nano-formulations. For N-(lissamine rhodamine B sulfonyl) phosphatidylethanolamine Rh-PE labeled nano- formulation preparation, the first ethanol stock of Rh-PE (at 5 mol%) and LC12 ethanol were mixed and then added to the deionized water. For in vivo experiments, 10 mg of LC10 compound were dissolved in 200uL of ethanol. This 200uL LC10 compound containing ethanol was dispersed in 4.8 mL glycerol. Characterization techniques for substituted lithocholic acid nano-formulations: Zeta potential (ξ) and size measurements: [0090] Hydrodynamic diameter and the surface charges (zeta potentials) of the nano- formulations were measured on a Lite Sizer ^TM 500Particle Analyzer, manufactured by Anton Paar. The sizes were measured in deionized water for stability study sizes were measured in 10% FBS. The system was calibrated by using the 200 nm + 5 nm polystyrene polymer (Duke Scientific Corps.Palo Alto, CA). The zeta potential was measured using the following parameters:viscosity, 0.89 cP; dielectric constant, 79; temperature, 25 °C; F(Ka), 1.50(Smoluchowski); maximum voltage of the current, V. Measurements were done 10 times with the zero-field correction. The potentials were calculated by using the Smoluchowski approximation. TEM analysis of nano-formulations: [0091] TEM images of the nano-formulations were captured using a high-resolution transmission electron microscope (JEOL-JEM 2100). Briefly, 5μL of 1 mMnano- formulations solution was placed on a 200-meshcarbon-coated copper grid (glow discharged for 45 s using TolaronHivac Evaporator) and kept for 10 min. Excess sample was removed by soaking with Whatman filter paper.5 μL of 2% uranyl acetate solution was added to the above grid, kept for 2 min, air-dried and analyzed at 120 KV. In vitro cytokine analysis: Tumor Necrosis Factor- TNF-αexpression study in RAW.264.7 cell lines: [0092] The level of TNF- α cytokine was estimated in substituted LC treated RAW.264.7 cells were used according to the manufactures protocol. Briefly, 30,000 cells / well was seeded in 48 well plate, incubate the cells for overnight. After incubation cells were treated with 1µg of LPS (Positive control) to promote the secretion of pro-inflammatory cytokines. After 24 hrs of LPS pre-treatment cells were treated with substituted LC at 100nM concentration. After 24h, supernatants were collected. Pre-coated ELISA plates were incubated with 50 μl culture supernatants for 2 h at room temperature. Subsequently 50 μl aliquots of antibody were added and the plates were incubated at 37°C for 90 min. The plates were washed thoroughly using the washing solution from the kit and 100 μl streptavidin-horseradish peroxidase (HRP) was added, followed by a further 30 min incubation at 37°C. The plates were washed thoroughly and 50μl substrate solution (freshly prepared tetramethylbenzidine with H ₂ O ₂ ) was added. The plates were then incubated at 37°C for 20 min in a dark chamber, and the optical density was measured at 450 nm. Recombinant murine TNF-α were diluted and used as standards. All of the experiments were performed in triplicate. Psoriatic markers in hPBMCs: [0093] Immune response of substituted lithocholic acid were evaluated using human peripheral blood mononuclear cells (PBMCs), they were isolated from blood using Ficoll- paque method. Briefly, blood were collected from three individual volunteer donors into CPTs (Cell preparation tubes) containing sodium heparin tubes. The blood was diluted with phosphate-buffered saline, pH 7.4 (1X PBS), containing 0.05 M ethylenediaminetetraacetic acid (EDTA).25 mL of the Ficoll-Paque PLUS was added to 12.5 mL of diluted blood. This ficoll gradient were centrifuged at 300g for 40 minutes and set the acceleration and deceleration “0” at room temperature. Discard the upper layer (plasma), The PBMC interface was carefully collected by pipette and washed with PBS- EDTA and centrifuged at 1000 rpm for 10 min. PBMC pellets were suspended in ammonium-chloride-potassium (ACK) lysing buffer (Invitrogen) and incubated for 10 min at room temperature with gentle mixing to lyse contaminating red blood cells (RBC). This was followed by a wash with PBS-EDTA and cells were counted. [0094] To examine the TNF-α, Interleukin IL-17 and IL-23 cytokines 30,000 cells/well was seeded in 48 well plate, incubate the cells for 24hours. After incubation cells were pre-treated with 1µg of LPS, after 24 hrs cells were treated with LC10 nanoparticles at 50,100 and 200nM concentration. Adherent macrophages were collected by using trypsin EDTA and cell count were approximately 10 lacks per mL and to make cytokines to come out we were performed the repeated freeze-thaw cycles and collected the supernatant by using centrifugation (2000-3000rpm for 20min). Pre-coated ELISA plates were incubated with 50 μl culture supernatants for 2 h at room temperature. Subsequently, 50 μl aliquots of antibody were added and the plates were incubated at 37°C for 90 min. The plates were washed thoroughly using the washing solution from the kit and 100 μl streptavidin- horseradish peroxidase (HRP) was added, followed by a further 30 min incubation at 37°C. The plates were washed thoroughly and 50 μl substrate solution (freshly prepared tetramethylbenzidine with H ₂ O ₂ ) was added. The plates were then incubated at 37°C for 20 min in a dark chamber, and the optical density was measured at 450 nm. Recombinant murine TNF-α, IL17 and IL23 were diluted and used as standards. All of the experiments were performed in triplicate. Skin permeation studies: Skin permeation potential of substituted LC using Franz diffusion method: [0095] The rat skin was collected from Sprague-dawly rats, which were sacrificed by an overdose of halothane anesthesia. The skin from the dorsal region was excised with subsequent removal of the subcutaneous fat and connective tissues(Ref). Briefly, the collected skin was rinsed with physiological saline and then soaked in 10% v/v glycerol in saline solution for 30 min and then rat skin was mounted on Franz diffusion cells (Permegear Inc., Riegelsville, PA, USA) between the donor and receiver compartments (recv comp) with the epidermis facing the donor compartment. The recv comp comprised of distilled water, stirred at 300 rpm and maintained at 32 ⁰ C ± 0.5 ⁰ C using a circulating water bath. The mounted skin was equilibrated with the recv comp for 1 hr prior to the application of the respective formulations. The skin permeation studies were performed for 24 h under un-occlusive conditions. [0096] For the permeation studies carried out with the dermatomed human skin, 100 µl of each of the test formulation was applied on the diffusional surface of the skin in the donor compartment.300 μl samples were collected from the recv comp at different time points from 1-24 h. For the skin collection, after pre-determined time period, the donor cell was removed, and the excess formulation was removed from the surface of the skin using a cotton swab. The skin was then washed with 50% v/v ethanolic solution in water and blotted dry with lint-free absorbent wipes. The entire dosing area (0.636 cm ² ) was collected with a biopsy punch. The drug amounts permeated into the recv comp collected were analyzed with HPLC (Waters Corp, Milford, MA). The in vitro human skin permeation was performed for caffeine containing formulations of substituted lithocholic acid (LC6-LC12). Skin extraction of the drug: [0097] To determine the drug amounts retained in rat skin samples, extraction of the respective drugs from skin was carried out. The epidermis was separated from the dermis using sharp forceps. Then the collected layers were minced with subsequent addition of 250 µl of PBS (pH 7.4) to all samples and boiled in a water bath for 10 min. The samples were cooled down to room temperature and then 250 µl of acetonitrile was added. The vials were sonicated in a bath sonicator for 30 sec and then vortexed for 2 min. Finally, all the tissue samples were centrifuged at 13,000 rpm for 15 min. The supernatant was collected and analyzed for drug content using HPLC. HPLC method for caffeine: [0098] The mobile phases used for analysis of caffeine were methanol (solvent A) and 0.1% v/v TFA in water (solvent B) and they were run at a gradient of 20:80 to 85:15 (solvent A:B, respectively) for 10 min, with a flow rate of 1 ml/min. Caffeine content in the samples was determined at 272 nm. Skin permeation potential of LC10 formulations using confocal microscopy [0099] In order to, know the skin permeation ability of Rhodamine labelled LC10 formulations, the skin permeation studies were performed in BALB/c mice. Rhodamine- labeled LC10 nanoparticles was applied topically on the dorsal region of the shaved mice. After 6 hours the skin was collected and stored in 10% neutral phosphate buffered formalin. The skin was frozen in freezing medium (Leica Microsystem, Germany), followed by cryo-sectioning of 5μm thin sections with a cryotome (Leica CM1850 cryostat, Germany). Then the tissue section was mounted with 4-6-diamidino-2- phenylidone (DAPI)-containing mounting medium and images were captured in Nikon confocal microscope at 10X magnification. Rhodamine PE were used as a control. Development of mouse psoriatic model [0100] The psoriatic plaque like model was developed as described earlier by Marepally S et al. Topical administration of dual siRNAs using fusogenic lipid nanoparticles for treating psoriatic-like plaques. Nanomedicine. 2014;9:2157-74. Briefly, 62.5 μg of Imiquimod (IMQ) suspension (Glenmark Pharmaceuticals Ltd) was applied topically on the dorsal region of the BALB/c mice. Variations in mice body weight were continuously monitored. After six continuous days of applications, we observed prominent psoriatic plaques on the skin. Treatment regimen: [0101] Psoriatic mice were randomly grouped (5 mice for each group) and treatments was started. The treatment groups included a negative control group (healthy mice), a placebo group (vehicle control), a positive control group (Sorvate C Ointment (Glenmark Pharmaceutical)) and LC10 formulations (10mg/kg body weight) group. To the inflamed skin area, test formulations were applied topically every day for 5 days. Variations in mice body weight were continuously monitored. Psoriasis area and severity index (PASI) evaluation: [0102] The objective scoring system was developed on the clinical PASI to score the severity of inflammation. Erythema, scaling and thickening were scored independently on a scale from 0 to 4:0, none; slight; 2, moderate; 3, marked; 4 very marked. The scoring was performed every 24 h for 5 days. Biochemical and immunological evaluation: Serum parameters: [0103] The blood sample (~500 μL) from each mouse was collected into eppendroff by retro orbitalplexus puncture and sacrificed. The samples were further processed for serum separation by centrifugation at 4000 rpm, 15 mins, 4ºC. The supernatant serum thus obtained was employed for determination of following biochemical parameters: AST(aspartate aminotransferase), ALT (alanine transaminase), Alkaline Phosphatase, Bilirubin and Protein content. All the biochemical parameters were estimated using auto analyzer (Siemens Dimension XpandPlus Integrated Chemistry System). Cytokine analysis by multiplex cytokine assay: [0104] The level of inflammatory cytokines, including IL-1α, IL1β, IL-6, IL-10, IL- 12p70, IL-17A, IL-23, IL-27, CCL2(MCP-1), IFN-β, IFN-γ, TNF-α, and GM-CSF in mouse serum from Healthy, IMQ, LCA and Sorvate C treated mouse groups, were determined by multiplex cytometric bead-based LEGENDplex immunoassay (Mouse Inflammation Panel; BioLegend, London, UK) according to the manufacturer’s protocol. Briefly, the serum samples were 2-fold diluted using dilution buffer and the equal volume diluted serum samples, cytokine standards were incubated with specific capture antibodies beads (25 µl each) for 2 hours with shaking at approx.800 rpm. The capture bead-analyte complexes were spin down at 250 x g and washed using 1x wash buffer. 25 µl of biotinylated detection antibody cocktail was added to beads and incubated for 1 hour with shaking to forming capture bead-analyte-detection antibody sandwiches. 25 µl of Streptavidin-phycoerythrin (SA-PE) subsequently was added to bind to the biotinylated detection antibodies complex. After washing and spin down, the beads were diluted in 150 µl of 1x wash buffer. Then, fluorescent signal intensities of each bead were analyzed using a BD Aria (BD Biosciences, San José, USA). The concentration of serum cytokines was calculated in LEGENDplex analysis software (BioLegend, San Diego, USA) using FCS file generated on BD Aria. Real-time RT-PCR (qRT-PCR) [0105] Total RNA was purified using TRIzolreagent (Invitrogen, USA) from skin tissue of different treatment groups and one μg of RNA was converted into cDNA using Reverse Transcription System kit (Takara, Japan) as per manufacturing instructions. The qRT- PCR analyses of the samples were performed in a QuantStudio 6 system (Applied Biosystems, USA) with SYBR Green-Rox master mix (Takara, Japan) using gene-specific primers, as given in Table. The fold change of gene expression was calculated using 2 ^ΔΔCt method. Therapeutic and Toxicological evaluation [0106] For therapeutic studies psoriatic models of BALB/c mice were used. For toxicological evaluations, healthy rats were used for chronic toxicity analysis. Isolation of skin and organs for tissue analysis [0107] The inflamed skin and organs were collected at the end of experiment and we have measured the spleen weights, followed by stored in 10% neutral phosphate buffered formalin. Following fixation, samples were dehydrated and embedded in paraffin. Five micrometer microtome sections of the inflamed skin were then stained with hematoxylin and eosin. The Olympus BX43 light microscope equipped with computer-controlled digital camera was used to visualize the images on the slides. [0108] To understand tolerated dose of LC10 formulations for long term applications, we have taken 20 Wistar rats and, divided into 4 groups, each group (n=5) was treated topically on dorsal region with Placebo, LC10 10mg/kg B.W(Body Weight), LC10 20mg/kg B.W and LC1050mg/kg B.W. After six continuous days of applications, sacrificed the rats and collected all major organs along with skin. We have measured the spleen weights and all organs were fixed in formalin at rt for 24 h. Following fixation, samples were dehydrated and embedded in paraffin. Five micrometer microtome sections of the organs were then stained with hematoxylin and eosin and Masson’s tricome. The Olympus BX43 light microscope equipped with computer-controlled digital camera was used to visualize the images on the slides. Immunohistochemistry [0109] Immunohistochemistry (IHC) study was performed for TNFα, IL-17 and IL-23. In brief, formalin-fixed, paraffin-embedded skin sections were used for IHC studies according to the protocol specified in the ImmunoCruzTM mouse ABC staining kit. The section slides were washed in xylene and hydrated in different concentrations of alcohol. The slides were incubated with the primary antibody against TNFα, IL-17 and IL-23 separately overnight at 4 °C. Horseradish peroxidase-conjugated secondary antibody was applied to locate the primary antibody. The specimens were stained with DAB chromogen and counterstained with hematoxylin. The presence of brown staining was considered a positive identification for activated TNFα, IL-17 and IL-23. Olympus BX43 light microscope equipped with computer-controlled digital camera was used to visualize the images on the slides. In Vivo bone marrow cell cycle study [0110] The cellular DNA content was measured by cell cycle assay. In vivo bone marrow cell cycle analysis was carried out following previous literature. In brief, on final day of experiment mice were sacrificed, and then bone marrow cells from tibia and femur was collected using ice cold PBS. Bone morrow cells were washed twice to remove the excess tissues by centrifugation at 200 rpm for 5 min and fixed with 70 % ethanol at -20 ^o Cfor overnight. [0111] Bone marrow cells were processed using following procedure before running FACS, ethanol was removed and washed with 1X PBS. The cells were then suspended in 500 μL of PI staining solution (50 μg/mL propidium iodide, 0.1 mg/mLRNAse, 0.05% Triton X-100) and incubate in dark for 40 min at 37 °C. After incubation cells were collected by centrifugation, washed with 1X PBS, re-suspended in 500 μL 1X PBS, and data was recorded using flow cytometer (FACS Canto II, Becton-Dickinson, San Jose, CA, USA) and were analyzed with FACS Diva software. A minimum of 10,000 events were gated per sample. Statistical analysis [0112] The statistical analysis was performed by comparing each experimental value with the corresponding control groups. The results are expressed as mean ± standard error mean(SEM). While assessment between two individual groups was performed employing student’s unpaired t-test, comparison between multiple groups was done by one-way analysis of variance (ANOVA) test, followed by Dunnett’s test post-hoc analysis. P < 0.05 was considered to be statistical significance for all tests. Example 3 Results Characterization of substituted Lithocholic acid [0113] Substituted lithocholic acid of Formula II-LC6, Formula III-LC8, Formula IV- LC10, Formula V- LC12 prepared from above example 1 were dispersed in ethanol to result in ethanolic solutions of LC6, LC8, LC-10 and LC-12. Figure 1 Tabular form represent the diameter, surface charge and polydispersity of self-assembled nanoparticles in water and 10% serum-containing medium of LC6, LC8, LC10 and LC12 using DLS(Differential Light scattering). Their particle sizes were in the range of 110-190 nm (Figure 1A&B), surface potentials were found to be neutral (Figure 1A&C), and PDI found in between 22 to 25% (Figure 1A). TEM analysis show the shape and particle size distribution of nanoparticles (Scale bar 0.5µm). TEM (Transmission Electron Microscopic) images of these dispersions visualized that they were below 200nm (Figure 1D) Screening nano-LC formulations for their keratinocyte growth inhibitory properties [0114] Nano-assemblies of substituted lithocholic acid (LC6, LC8, LC10 and LC12) were evaluated for their cytotoxic effects against Normal Human Epidermal Keratinocytes (NHEK) at varying concentrations including 10, 50 and 100nM at different time points including 24, 48, 72 and 96 hours (Figure 2). All the analogues from LC6 to LC12 showed no effect of keratinocyte proliferation at 10nM. While LC6 (Figure 2A) and LC8 (Figure 2B) exhibited growth arrest at 50nM and high cytotoxicity at 100nM, LC10 (Figure2) and LC12 (Figure 2D) showed no significant growth arrest at 50nM, but effectively arrested cells at 100nM. Based on preliminary cytotoxicity studies and after considering the balance between cytotoxicity and efficacy, it was considered that LC10 would be potential drug for further evaluations. Screening nano-LC formulations for their anti-inflammatory properties [0115] Anti-inflammatory properties LC analogues were evaluated as described below. RAW264.7 cells were pre-treated with lipopolysaccharides (LPS), which can bind to toll- like receptor 4 (TLR4) on macrophages and stimulate the secretion of pro-inflammatory cytokines. LPS was used as a positive control and 4.54-fold up-regulated TNF-α levels as compared to untreated. At 100nM concentration, all the LC analogues showed significant (p<0.0001) reduction in levels of TNF-α, (Figure 3A) when compared to LPS treated macrophages. Among them, LC10 showed better down-regulation when compared with LC6 (0.64-fold), LC8 (0.73-fold) and LC12 (0.83 -fold). Then the effect of LC10 on other cytokines involved in psoriatic progression was tested. The effect of LC10 on expression of Tumor necrosis factor-TNF-α(Figure 3B), IL-17(Interleukin-17) (Figure 3C) and IL- 23(Figure 3D) in human PBMCs (Peripheral blood mononuclear cell) at 50nM,100nM and 200nM concentrations. LPS treatment significantly (p<0.0001) upregulated TNF-α (16.2-fold), IL-17 (21.42-fold) and IL-23 (0.51-fold) levels as compared to untreated. It was observed that the gradual reduction of cytokines resulted from a gradual increase in concentrations of LC10 nanoparticles. At 200nM concentration of LC10 significantly (P<0.0001) down-regulated the expression levels of TNF-α (1.99-fold) (Figure 4B), IL- 17 (0.66-fold) (Figure 3C) and IL-23 (1.95-fold) (Figure 3D) pro-inflammatory cytokines as compared to LPS treatment group. These results indicated that, among all nano-LC analogues, LC10 demonstrated superior anti-inflammatory effect. Skin permeation studies [0116] To evaluate the skin permeation properties of nano-LCs, skin permeation experiments were performed with rat skin in Franz-diffusion cells using caffeine as a model drug and oleic acid (OA) as a standard skin permeating agent. The analysis of the skin permeation studies showed that all the nano-LC analogues showed better skin- permeation properties compared to the permeation enhancer standard, OA. Among all, LC10 lipid showed the highest skin retention of caffeine in both the epidermal and dermal layers, compared to the other LC-analogues (Figure 4A). In comparison, LC10 showed about 3.26 and 1.91-fold increase in drug retention more than OA at the epidermal and dermal layers, respectively. The skin retention of caffeine at the epidermal layer for LC8 lipid was comparable to LC10 lipid. However, the amount of drug retained in the dermis was about 1.5-fold less than LC10 lipid. Overall, LC10 demonstrated better skin permeation properties compared to its analogues LC6, LC8 and LC12. [0117] Towards visualizing the intra-dermal distribution of nano-LC10 in the skin layers, the skin permeation studies of nano-LC10 labeled with Rh-PE on mouse skin were performed. Skin sections clearly showed that there was red fluorescence throughout the skin, indicating that LC10 has penetrated into each cell of the skin (Figure 4B). Screening of nano-LC formulations for their skin permeation and inti-inflammatory properties revealed that LC10 has a superior efficiency than other LC analogues. Further its therapeutic efficacy in imiquimod induced psoriasis model was evaluated. Therapeutic evaluation of LC10 formulation in IMQ induced psoriatic plaque model [0118] To evaluate the therapeutic efficacy of LC10, psoriasis was induced by topical application of imiquimod on the shaved dorsal region of BALB/c mice (Figure 5B) daily for five days. After 6 days of IMQ applications, erythema, scaling, and thickening were observed on the skin. The mice significantly lost approximately 20% of body weight within 6 days (Figure 5C). From 7 ^th day onwards, treatment was started. The treatment groups included a negative control group (Normal), a placebo group (IMQ), a positive control group (Sorvate) and LC10 formulations (10mg/kg body weight) group. To the inflamed skin area, test formulations were applied topically every day for 5 days. After 5 days of treatments, it was seen that the prevalence of erythema and plaques on the skin were in the order IMQ>Sorvate>LC10>Normal. LC10 treated mice regained the body weights (1.17-fold, p< 0.05) towards normalcy as compared to IMQ (Figure 5C). The dermatological scoring of the psoriatic skin lesions was documented on 0, 4, 8, 12 and 15 days. On 15 ^th day, healthy mice, IMQ control, Sorvate treated mice and LC10 treated mice PASI (Psoriasis Area and Severity Index) score were observed as a 0.00, 3.27, 0.94 and 0.66, respectively (Figure 5A). Collectively these results suggested that topical application of LC10 reduced PASI scores, made inflamed skin comparable with normal skin and also rescued the animal from severe weight loss. More importantly, the therapeutic efficacy found to be superior when compared with the commercial standard, Sorvate, a calcitriol formulation. Histological analysis [0119] The analysis of H&E stained sections of skin (Figure 6, upper panel) from the IMQ-treated skin showed increased epidermal thickening with elongation of epidermal rete ridges, a disturbed epidermal differentiation and infiltration of leukocytes into both, dermis and epidermis compared to normal skin. Further, the skin from the LC10 treatment has very similar characteristics to that of the normal skin. The analysis of H&E stained sections of the spleen (Figure 6, lower panel) from the IMQ-treated spleen showed higher infiltration of leukocytes, LC10 treated spleen is similar to that of the normal spleen (indicated by yellow arrows). These results convincingly demonstrated that LC10 could alleviate the skin inflammation efficiently compared to the best topical standard formulation sorvate. Immunohistochemistry analysis [0120] The treated skin sections were examined for the changes in their levels of pro- inflammatory cytokines TNF-α, IL-17, and IL-23 by IHC. The presence of brown staining was considered an identification for activated TNF-α, IL-17, and IL-23. The results indicated that the skin from the LC10 treatment showed similar TNF-α (Figure 7, Upper panel), IL-17 (Figure 7, Middle panel) and IL-23 (Figure 7, Lower panel) brown staining to that of the normal skin. Additionally, these results demonstrated that LC10 formulation also has anti-inflammatory potential and can be used for the treatment of inflammation caused by psoriasis. Serum biochemical analysis [0121] Furthermore, serum biochemical parameters including Serum glutamic pyruvic transaminase (SGPT), Serum glutamic oxaloacetic transaminase (SGOT) and Alkaline phosphatase (ALP) were analyzed to know the systemic effect on the treatment of LC10. At the end of the experiment, serum was collected, and the biochemical analysis was performed to understand the physiological metabolism and functioning of the liver and spleen in different treatment groups. In the case of healthy mice, SGPT, SCOT, and ALP were present in the serum within a normal range. When mice were treated with IMQ, SGPT significantly (p< 0.01) increased by 1.65-fold, SGOP significantly (p <0.0001) increased by 7.80-fold, and ALP was significantly (p <0.0001) reduced by 0.44-fold as compared to control. Liver enzymes were elevated in a chronic inflammatory condition. Hence, upon IMQ induced systemic inflammation, the levels of the transaminases in the liver were elevated, indicating liver damage (Figure 8). Upon treatment with LC10, there was an improvement in liver function as indicated by the significant (p<0.01) change in SGPT which decreased by 0.65-fold, SGOT which decreased by 1.81-fold, and ALP which had small but significant (p< 0.0001) increase (0.25-fold) (Figure 8). The same trend was observed when animals were treated with Sorvate. A further measure of liver function, bilirubin, was analyzed. While there was no significant change in direct bilirubin level (soluble form of bilirubin) compared to control, the level of indirect bilirubin (an insoluble form of bilirubin) increased by 1.33-fold when treated with IMQ. When LC10 treatment was done, the indirect bilirubin level dropped by 0.33-fold compared to IMQ. The protein content levels remained unchanged across all the treatment groups. [0122] The spleens were excised from the mice in different treatment groups on the final day of the experiment. Upon analyzing the spleen weights, it was observed that there was a 0.82-fold increase upon IMQ treatment, indicating the high infiltration of lymphocytes. LC10 treatment caused a decrease in spleen weight by 0.21-fold as compared to that of IMQ. These findings indicated that topical treatment with LC10 reduced systemic inflammation in turn rescued liver from damage. Serum cytokine analysis [0123] Serum cytokine levels upon the treatment with LC10 was evaluated to know which pro-inflammatory cytokines were regulated. Basal expression of all the cytokines was observed even in healthy mice, while in IMQ up-regulated the expression of pro- inflammatory cytokines and down-regulated the expression of anti-inflammatory cytokines. Then, fold change of cytokine expression relative to untreated psoriatic mice (IMQ) was analyzed. Upon LC10 treatment, significant (p<0.0001) up-regulation of anti- inflammatory cytokines such as IL-10 (2.03-fold) (Figure 9D) and GM-CSF (3.60-fold) (Figure 9M) was seen as compared to IMQ group. Whereas, LC10 treated group showed̴ 0.5 fold down-regulation of IL-12, IL-23, IL-27, TNF-α and MCP-1 (Figure 10E,G,H,I and L), ̴ 0.7 fold down-regulation of IL-6 (non-significant), IL-17 and IFN-β (Figure 9C,F and J), approximately one fold down-regulation of IL-1β (Figure 9B) and ̴1.5 fold down- regulation of IL-1α and IFN-γ (Figure 9A and K)pro-inflammatory cytokines as compared to IMQ. These results suggested that the topical application of LC10 not only reduced the skin inflammation, but also reduced systemic inflammation and restored to normal condition. Real-time PCR analysis [0124] The fold changes of mRNA expression levels with respect to that with IMQ treatment for VDR, EphA2, IL-10, IL-17, IL-23, TNF-α and GM-CSF in Normal, LC10 and Sorvate treatment groups were presented in Figure 10. The mRNA expression was stated in relation to the GAPDH mRNA level. Then the relative expression of each mRNA was normalized with that of IMQ to get the fold change in mRNA expression level. It was seen that VDR mRNA was up-regulated in the LC10 treated group by 0.7-fold, 2.57-fold and 2.83-fold compared to normal, IMQ and Sorvate treatment groups respectively (Figure 10 A), indicating that LC10 is more effective in reducing the inflammatory response in psoriatic skin areas through the up-regulation of VDR. Upon LC10 treatment, the EphA2 mRNA was observed to down-regulated by 0.52-fold compared to that in IMQ treatment group, the mRNA level is nearly similar to that of the normal treatment group and 0.69-fold lower to that Sorvate treated group (Figure 10 B). As the reason behind psoriasis is EphA2 overexpression, the reduction of EphA2 through LC10 treatment normalizes keratinocyte maturation, thereby reducing psoriasis. [0125] TNF-α, IL-17, and IL-23 of fold change mRNA expression levels were same as observed for the IHC analysis (Figure 7). Compared to normal mouse skin, IMQ treated mouse skin mRNA expressions were 0.75, 0.77 and 1.32-fold increased, respectively. Upon LC10 treatment, Pro-inflammatory cytokines such as TNF-α (0.40) (Figure 10F) IL-17 (1.20-fold) (Figure 10 D) and IL-23 (2.31-fold) (Figure 10E) genes were down- regulated as compared to IMQ group. [0126] Anti-inflammatory cytokines such as IL-10 (0.21-fold) and GM-CSF (0.48-fold) mRNAs were down-regulated in IMQ treated mouse skin as compared to normal mouse skin. IL-10 mRNA was 1.06-fold (Figure 10 C) up-regulated in LC10 treated mouse skins. Cell cycle analysis of bone marrow [0127] After 24h of last day treatment, bone marrow cells of mice from femur and tibia was collected and was assessed for the effect of formulations over different phases of cell cycle. The results (Figure 11) clearly revealed that IMQ induced cell cycle arrest in G2/M phase and Sorvate group also showed similar pattern as that of IMQ treated groups. However, LC10 treated bone marrow cells showed similar cell cycle phase pattern as that of healthy mice. Indicating that the application of LC10 has normalized the hematopoietic system. Toxicological evaluation [0128] In order to evaluate the maximum tolerated dose of LC10, healthy Wistar rats were administered with 10mg/kg, 20mg/kg and 50mg/kg body weight doses, topically. Figure 12 depicts (A) H&E and Masson trichrome stained skin sections of Wistar rats were dissected at the 6 ^th day after 5 continuous applications of LC10 nanoparticles at 10, 20 and 50mg/Kg body weight. (B) Variation of rat’s spleen weights by five continuous applications of LC10 nanoparticles at 10, 20 and 50mg/Kg body weight compared to untreated rats. ns indicates nonsignificant. The toxicity to the skin and other vital organs and spleen weights were evaluated. Skin (Figure 12A) and vital organ (Figure 12B) histopathologies were evaluated using H&E and Mason trichome staining. It was observed that up to 50mg/kg body weight dose, LC10 did not show any significant toxicological effects or alter the histological morphology in any of the vital organs and also on the skin, where it was directly administered. Splenomegaly, due to the infiltration of neutrophils, is a common phenomenon in IMQ-induced psoriatic models. As LC10 significantly reduced the neutrophil inflammation and subsequent splenomegaly in psoriatic models, its effect was evaluated on the spleen weights (Figure 12) of healthy animals. It was observed that up to 50mg/kg body weight dose, LC10 did not show any significant change in spleen weights, indicating that it is non-toxic to any of the vital organs. Figure 13, shows the H&E (A) and Masson trichrome (B) stained organ sections (Heart, Lung, Kidney, Spleen and Liver) of Wistar rats that were excised on the 6 ^th day after 5 continuous applications of LC10 nanoparticles at 10, 20 and 50mg/Kg body weight along with control. Advantages of the present disclosure [0129] The novel compounds of Formula I of the present disclosure was formed self- assembled nanoparticles in water and permeated through the skin without using a permeation enhancer. The formulations showed enhanced growth inhibition in human keratinocytes as well as specifically reduced the expression of pro-inflammatory cytokine in mouse and human macrophages. The formulations showed enhanced skin permeation property and therapeutic anti-psoriatic property as elucidated by reduction of psoriatic plaques and reduced expression of pro-inflammatory cytokines, and increased expression of anti-inflammatory cytokines. mRNA profiles in the treated skin revealed that VDR up- regulation and EphA2 down-regulation could be playing a major role in reducing skin inflammations. Further analysis of cytokines convincingly demonstrated that Th-2 and Th-17 pathways, which are significantly elevated in psoriatic condition, were restored to normal when compared to vitamin D derivative Calcitriol formulation Sorvate. Toxicological studies of LC10 demonstrated that the drug is safe to be administered even at concentrations as high as 50mg/kg bw, which is five time more than the therapeutic dose. Nano formulations convincingly demonstrated a self-assembled nanoparticular drug and could be a promising class of therapeutic molecule for treating psoriasis.