CYSTEAMINE AND ITS ANALOGUES ARE USED FOR THE TREATMENT OF CYSTINOSIS, NASH AND LEIGH SYNDROME FIELD OF INVENTION This disclosure generally relates to compounds and compositions for the treatment of Cystinosis, metabolic conditions, non-alcoholic steatohepatitis, hypertriglyceridemia and neurodegenerative diseases. More particularly, this invention relates to treating subjects with a pharmaceutically acceptable dose of compounds, crystals, esters, amides, salts, hydrates, prodrugs, or mixtures thereof. INTRODUCTION Nephropathic cystinosis is a rare autosomal recessive disease characterized by raised intracellular levels of cystine. Symptoms include renal Fanconi syndrome and growth retardation. If untreated, cystinosis results in death from renal failure by the second decade of life. The only treatment for cystinosis is administration of Cysteamine, an aminothiol with an offensive taste and smell, which is excreted in breath and sweat causing halitosis and body odor as well as .gastric irritation. As a result, patient compliance may be poor. The purpose of this research was to synthesize and develop a new molecule having odorless and tasteless pro-drug forms of cysteamine. It is envisaged that these compounds will improve compliance among cystinotic patients and lead to an increase in patient treatment success and quality of life. Excess cystine forms crystals that can build up and damage cells. These crystals negatively affect various systems in the body, especially the eyes, spleen, liver, bone marrow and kidneys. Cystinosis is an autosomal recessive disorder, caused by mutations of the lysosomal cystine carrier cystinosin, encoded by the CTNS gene (17pl3). The concomitant intralysosomal cystine accumulation leads to multi-organ damage, with kidneys being the first affected and later spleen, eyes, liver and bone marrow, Altered mitochondrial oxidative phosphorylation has been demonstrated in animal proximal tubules loaded with cystine dimethyl ester, mimicking cystine accumulation in cystinosis, but has not been confirmed in cells of patients with cystinosis. BACKGROUND Metabolism is the process, the body uses to get or make energy from proteins, carbohydrates and fats. Cystinosis is a disorder in which the body accumulates the amino acid cystine (a building block of proteins) within cells. Excess cystine forms crystals that can build up and damage cells. These crystals negatively affect various systems in the body, especially the eyes, spleen, liver, bone marrow and kidneys. Cystinosis is an autosomal recessive disorder, caused by mutations of the lysosomal cystine carrier cystinosin, encoded by the CTNS gene (17pl3). The concomitant intralysosomal cystine accumulation leads to multi-organ damage, with kidneys being the first affected and later spleen, eyes, liver and bone marrow, altered mitochondrial oxidative phosphorylation has been demonstrated in animal proximal tubules loaded with cystine dimethyl ester, mimicking cystine accumulation in cystinosis, but has not been confirmed in cells of patients with cystinosis. Non-alcoholic steatohepatitis (NASH) is a liver disease characterized by macrovesicular steatosis, hepatocyte necrosis, inflammation, Mallory bodies, and fibrosis. NASH is closely associated with the metabolic or insulin resistance syndrome. Oxidative stress is believed to play an important role in pathogenesis of NASH. It is likely involved in the progression of disease from steatosis to NASH and potentially cirrhosis. It has been shown that chronic oxidative stress, generated through the oxidation of cytotoxic free fatty acids, can lead to upregulation of cytokines, induction of the liver cytochrome P450 enzyme 2E1, and depletion of hepatic antioxidant concentration. Neurodegenerative disorders are a heterogeneous group of diseases of the nervous system, including the brain, spinal i cord, and peripheral nerves that have much different aetiology. Many are hereditary; some are secondary to toxic or i metabolic processes. Free radicals are highly reactive molecules or chemical species capable of independent existence. Generation of highly Reactive Oxygen Species (ROS) is an integral feature of normal cellular function like mitochondrial respiratory chain, phagocytosis and arachidonic acid metabolism. The release of oxygen free radicals has also been reported during the recovery phases from many pathological noxious stimuli to the cerebral tissues. Some of the neurodegenerative disorders include Alzheimer's disease, Huntington's disease, Parkinson's disease and Lateral sclerosis. Hypertriglyceridemia is a commonly encountered lipid abnormality frequently associated with other lipid and metabolic derangements. The National Cholesterol Education Program recommends obtaining a fasting lipid panel in adults over the age of 20. The discovery of hypertriglyceridemia should prompt an investigation for secondary causes such as high fat diet, excessive alcohol intake, certain medications, and medical conditions (eg, diabetes mellitus, i hypothyroidism). In addition, patients should be evaluated for other components of the metabolic syndrome. These | include abdominal obesity, insulin resistance, low high-density lipoprotein (HDL), high triglyceride, and hypertension. ! Hypertriglyceridemia is classified as primary hypertriglyceridemia when there are no secondary causes identified. | Hypertriglyceridemia is a risk factor for pancreatitis and it accounts for 1 to 4% of cases of acute pancreatitis. Although a few patients can develop pancreatitis with triglyceride levels >500 mg/dL, the risk for pancreatitis does not become clinically significant until levels are >1000 mg/dL. More importantly however, hypertriglyceridemia is typically not an isolated abnormality. It is frequently associated with other lipid abnormalities and the metabolic syndrome (abdominal obesity, insulin resistance, low high-density lipoprotein (HDL), high triglyceride, and hypertension), which are linked to coronary artery disease. Managing acute pathology of often relies on the addressing underlying pathology and symptoms of the disease. There is currently a need in the art for new compositions to treatment of metabolic conditions such as cystinosis, non¬alcoholic Steatohepatitis, hypertriglyceridemia and neurodegenerative disorders. SUMMARY OF INVENTION The present invention provides compounds, compositions containing these compounds and methods of synthesizing and for using the same to treat, prevent and/or ameliorate the effects of the conditions such as cystinosis, NASH, hypertriglyceridemia, metabolic conditions and neurodegenerative diseases. The invention herein provides composition comprising of formula I and their pharmaceutical acceptable salts thereof. The invention also provides pharmaceutical compositions comprising one or more compounds of formula I and their intermediates thereof and one or more of pharmaceutically acceptable carriers, vehicles or diluents. These compositions may be used in the treatment of metabolic conditions and neurodegenerative disorders and its associated complications. In certain embodiments, the present invention relates to the compounds and compositions of formula I, or pharmaceutically acceptable salts thereof, Formula 1 wherein, Ri, R2, and R3 each independently represent hydrogen, thiol, alkyl, alkyl thiol, Triphenyl thiol, acetyl thiol, disulfide, acyl, acylalkyl, alkenyl, alkylthioalkyl, alkynyl, alkoxyaryl, alkoxyalkyl, aryl, aralkyl, aryloxyalkyl, arylthioalkyl, cycloalkyl, ether, ester, heteroaryl, heterocyclyl, lower alkyl, sulfone, sulfoxide, or hydroxyalkyl; substituted alkyl thiol, substituted aryl thiol, null, etc. Whereas "S" and "N" were combined with protection groups represented as follows. R.2 and R3 either individually or both represent at least one of a residue of guanidine, a residue of hydrazine, an acid, a residue of pyruvic acid, a residue of oxaloacetic acid, a residue of tocopherol, a residue of ascorbic acid, a residue of thiamine, thioctic acid, a residue of thioctic acid, a residue of acetyl cysteine, a residue of alpha-keto glutaric acid, a residue of dimercaprol, a residue of an NO donor, a residue of glutathione, (RS)-2, 3-disulfanylpropan-l-ol, (R)-2-acetamido-3-sulfanylpropanoic acid, Ecosapentanoic acid, different amino acids and an analog of any one of the foregoing and in general represented by the following structures. In certain embodiments, the present invention relates to the compounds and compositions of formula (1,2 and 3) or pharmaceutically acceptable salts thereof, Wherein, Ri, R2 and R3 each independently represents at least one of the following: null, hydrogen, methyl, amine, cycohexyl methyl ether, butoxy, propoxy, thiol, alkyl, alkyl thiol, acetyl thiol, acetyl, disulfide, acyl, acylalkyl, alkenyl, alkylthioalkyl, alkynyl, alkoxyaryl, alkoxyalkyl, arylj aralkyl, aryloxyalkyl, arylthioalkyl, cycloalkyl, ether, ester, amide, heteroaryl, heterocyclyl, lower alkyl, sulfone, sulfoxide, or hydroxyalkyl; R also independently represents at least one of hydrogen, carboxyl, amine, -NH-CO-NH-, -NH-CO-CH2-NH-, -NH-CO-, R-COO-R1, thiol, disulfide, In certain embodiments, the present invention relates to the compounds and compositions of formula (1,2 and 3) or pharmaceutically acceptable salts thereof are represented by: In one embodiment, steps of synthesizing the compounds of formula 1, 2 and 3 are described. Herein the application also provides a kit comprising any of the pharmaceutical compounds, salts, solvates, hydrates, polymorphs, or compositions disclosed herein. The kit may comprise instructions for use in the treatment of metabolic conditions, non-alcoholic steatohepatitis, neurodegenerative disorder or its related complications. The application also discloses a pharmaceutical composition comprising a pharmaceutically acceptable carrier and any of the compositions herein. In some aspects, the pharmaceutical composition is formulated for systemic administration, oral administration, sustained release, parenteral administration, injection, subdermal administration, or transdermal administration. The compositions described herein have several uses. The present application provides, for example, methods of treating a patient suffering from metabolic conditions, non-alcoholic steatohepatitis, neurodegenerative disorders or its related complications manifested from metabolic conditions, chronic diseases or disorders; Hepatology, Hematological, Orthopedic, Cardiovascular, Renal, Skin, Neurological or Ocular complications. Example embodiments are illustrated by way of example and not limitation in the figures of the accompanying drawings, in which like references indicate similar elements and in which: Synthesis of the compounds according to General Formula 1: Reaction Scheme for synthesis of compound 6: Approach 1 Step-1: Synthesis of compound 2 Procedure: To a solution of 2-aminoethanethiol HC1 (21.0 g, 0.18 mol; 1.0 eq) in TFA (63 mL; LR grade), trityl alcohol (51 g, 0.19 mol; 1.05 eq) was added at 0 °C and the reaction mixture was stirred for 3 h at room temperature. On completion of the reaction (monitored by TLC), the reaction mixture was quenched with saturated aqueous NaHC03 solution. The separated solid was filtered and dried in vacuo to get 55g of compound 2 (Trityl protected) as a white solid. Yield%: 55 g (92.7%) Analytical Data: ^-NMR (DMSO-d6): 5 2.29 - 2.33 (t, 2H), 2.47 -, 2.50 (t, 2H), 5.99 (bs, 2H), 7.18 -7.36 (m, 15H). Step-2: Synthesis of compound 4 , Procedure: To a solution of compound-3 (50 g, 0.151 mpl, 1 eq) in EtOH (500 mL) and H20 (200 mL) was added NaOH (14.5 g, 0.362 niol, 2.4 eq) at 0°C. The reaction mixture was stirred for 4 h at room temperature. On completion of the reaction (monitored by TLC), the reaction mixture was concentrated in vacuo to remove the ethanol. The aqueous layer was acidified with 3N HC1 (pH ~4) and extracted with dichloromethane. The organic layer was dried over anhydrous sodium sulphate and evaporated in vacuo to yield 45 g of compound 4 as oil. Yield%: 45 g (98.3%) Analytical Data: ^-NMR (DMSO-d6): 8 0.88 - 0.92 (t, 3H), 1.49 - 1.56 (m, 2H), 1.82 (s, 6H), 2.0 - 2.05 (m, 4H), 2.15 - 2.19 (t, 2H), 2.72 - 2.84 (m, 8H), 5.23 - 5.73 (m, 10H). Step-3: Synthesis of compound 5: Procedure: To a solution of compound 4 (30 g, 0.099 mol; 1.0 eq), HATU (52.84 g, 0.139 mol; 1.4 eq) and DiPEA (38.44 g, 0.29 mol, 3.0 eq) in dichloromethane (300 mL) was added compound 2 (38 g, 0.119 mol, 1.2 eq) at 0°C. The reaction mixture was stirred for 4 h at room temperature & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was diluted with dichloromethane (500 mL), washed with ice-water (2x 500 mL), dried over anhydrous Na2S04 and evaporated in vacuo. The crude compound (114 g) was purified by column chromatography over 100-200 mesh silica gel by using 15 -20% ethyl acetate-hexane to yield 57 g of compound 5 as oil. Yield%: 57g (90%) Analytical Data: ^-NMR (DMSO-dg): 8 0.87 - 0.91 (t, 3H), 1.47 - 1.50 (m, 2H), 2.01 - 2.18 (m, 6H), 2.48 - 2.49(t, 2H), 2.72 - 2.79 (m, 8H), 2.93 - 2.98 (m, 2H), 5.25 - 5.35 (m, 10H), 7.21 - 7.33 (m, 10H), 7.83 (t, 1H). Step-4: Synthesis of compound 6 Procedure: To a solution of Compound 5 (57.2 g, 0.094 mol; 1.0 eq) in TFA/DCM (48.6 mL/572 mL), triethylsilane (13.2 g, 0.113 mol, 1.2 eq) was added drop wise at 0 °C and the reaction mixture was stirred for 2 h at 0°C. Reaction was monitored by TLC. On completion of the reaction, the reaction mixture was diluted with dichloromethane (100 mL), washed with water (1 x 500 mL). The organic layer was dried over anhydrous Na2S04 and evaporated in vacuo. The crude compound (72 g) was purified by column chromatography over neutral alumina using 13 -15% ethyl acetate-hexane as eluent to get 13.7 g (yield - 40%)of final target as colorless liquid. HPLC Purity: 94% Mass: 360.5 (M+ - H) Analytical Data: 'H-NMR (CDC13): 8 0.95 - 0.99 (t, 3H), 1.41 - 1.42 (m, 2H), 1.69 - 1.76 (m, 2H), 2.04 - 2.18 (m, 4H), 2.20 - 2.28(t, 2H), 2.64 - 2.69 (m, 2H), 2.81 - 2.84 (m, 8H), 3.40 - 3.45 (m, 2H), 5.28 - 5.43 (m, 10H), 5.82 (bs, 1H) and its proton NMR spectrum attached below. Step-1: Synthesis of compound 2 Procedure: 2-aminoethanethiol HCl (15 g, 0.132 mol; 1.0 eq) and acetone (300 mL; LR grade), was reflux for 5 h. On completion of the reaction (monitored by TLC), the reaction mixture was cooled to room temperature and obtained solid was filtered dried in vacuo to get 18.8 g of compound 2 as a white solid. Yield%: 18.8 g (92.5%) Analytical Data: !H-NMR (DMSO-d6): 8 1.70 (s, 6H), 3.23 - 3.27 (t, 2H), 3.57 - 3.60 (t, 2H), 10.2 (bs, 1H). Step-2: Synthesis of compound 4 Procedure: To a solution of compound 3 (4.6 g, 15.23 mmol; 1.0 eq), HATU(7.9 g, 20.78 mmol; 1.4 eq) and DiPEA (7.85 g, 60.85 mmol, 4.0 eq) in DMF (20 mL) was added compound 2 (2.57 g, 16.74 mmol, 1.1 eq) at 0°C. The reaction mixture was stirred for 5 h at room temperature & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was quenched onto ice cold water and extracted with ethyl acetate (2 x 100 mL), dried organic layer over anhydrous Na2S04 and evaporated in vacuo. The crude compound (8.72 g) was purified by column chromatography over neutral alumina by using 5% ethyl acetate-hexane yielded 3.5 g (yield - 57%)of compound as oil. Analytical Data: ^-NMR (CDC13): 8 0.95 - 0.99 (t, 3H), 1.69 - 1.73 (t, 2H), 1.82 (s, 6H), 2.0 - 2.15 (m, 4H), 2.24 - 2.28 (t, 2H), 2.81 - 2.84 (m, 8H), 2.96 - 2.99 (t, 2H), 3.84,3.87 (t, 2H), 5.32 - 5.39 (m, 10H). Mass: 402.49 [M + H] + Step-3: Synthesis of compound 5: Procedure: To a solution of Compound 4 (2.2 g, 0.094 mol; 1.0 eq) in methanol (25 mL) was charged cone. HCl (44 ML) and stirred mass at room temperature for overnight. On completion of the reaction mass was extracted with ethyl acetate (2 x 75 mL) and washed with brine solution (1 x 50 mL). The organic layer was dried over anhydrous Na2SC>4 and evaporated in vacuo. The crude compound (2 g) was purified by column chromatography over basic alumina using 13- 15% ethyl acetate-hexane as eluent to get 0.89 g of compound 4 as colorless liquid. Analytical Data: ^-NMR (CDCb): 8 0.95 - 0.99 (t, 3H), 1.41 - 1.42 (m, 2H), 1.69 - 1.76 (m, 2H), 2.04 - 2.18 (m, 4H), 2.20 - 2.28(t, 2H), 2.64 - 2.69 (m, 2H), 2.81 - 2.84 (m, 8H), 3.40 - 3.45 (m, 2H), 5.28 - 5.43 (m, 10H), 5.82 (bs, 1H). Mass: 360.1 [M-H]" Reaction Scheme for synthesis of compound 4: Approach 3 (cyclic Amide Target) Step-1: Synthesis of compound 2 Procedure: To 2-aminoethanethiol HC1 (6.8 g, 0.06mol; 1.0 eq) was charged water (100 mL) and PH of the solution was adjusted to 6.2 with 2N NaOH solution. Formaldehyde solution (7.5 mL, 35 % wt/wt, 0.087mol) was added and mass was stirred for overnight at RT. On completion of the reaction (monitored by TLC), the reaction mixture was extracted with dichloromethane (3 x 50 mL). Collective organic layer was dried over Na2S04 and evaporated in vacuo to get compound 2 as oily mass. Yield%: 1.5 g (28%) Analytical Data: ^-NMR(DMSO-A;): 8 2.74-2.77 (t, 2H), 2.83 (bs, 1H), 3.07 - 3.10 (t, 2H), 4.11 (s, 2H). Step-2: Synthesis of compound 4 Procedure: To a solution of compound 3 (1.0 g, 3.31 mmol; 1.0 eq), HATU (1.92 g, 5.05 mmol; 1.5 eq) and DiPEA (0.86 g, 6.66 mmol, 2.0 eq) in DCM (30 mL) was added compound 2 (0.3 g, 3.31 mmol, 1.0 eq) at 0°C. The reaction mixture was stirred for overnight at room temperature & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was washed with water (1 x 50 mL), dried over anhydrous Na2S04 and evaporated in vacuo. The crude compound (2.4 g) was purified twice by column chromatography over neutral alumina followed by basic alumina by using 10 -15 % ethyl acetate-hexane to yield 550 mg of compound. Analytical Data: 'H-NMR (CDC13): 5 0.95 - 0.99 (t, 3H), 1.71 - 1.78 (m, 2H), 2.03 - 2.16 (m, 4H), 2.29- 2.34 (m, 2H), 2.79 - 2.84 (m, 8H), 2.96 - 2.99 (t, 1H), 3.06 - 3.09 (t, 1H), 3.69 - 3.72 (t, 1H), 3.83 - 3.86 (t, 1H), 5.28 - 5.41 (m, 1 OH). HPLC purity: 96.95% ? Reaetion Scheme for synthesis of Ester Target Step-1: Synthesis of compound 2 To a solution of 2-aminoethanethiol HC1 (21.0 g, 0.18 mol; 1.0 eq) in TFA (63 mL; LR grade), trityl alcohol (51 g, 0.19 mol; 1.05 eq) was added at 0 °C and the reaction mixture was stirred for 3 h at room temperature. On completion of the reaction (monitored by TLC), the reaction mixture was quenched with saturated aqueous NaHCC>3 solution. The separated solid was filtered and dried in vacuo to get 55g of compound 2 (Trityl protected) as a white solid. Yield%: 55 g (92.7%) Analytical Data; ^-NMR (DMSO-d6): 5 2.29 - 2.33 (t, 2H), 2.47 - 2.50 (t, 2H), 5.99 (bs, 2H), 7.18 - 7.36 (m, 15H). Step-2: Synthesis of compound 3 To the solution of compound 2 (36.8 g, 0.115 mol; 1.0 eq), TEA (35 g, 0.346 mol; 3.0 eq) in dichloromethane (368 mL, 10 V) was added bromo acetyl bromide 3 (35 g, 0.173 mol; 1.5 eq) drop wise for 30 min, at room temperature. The reaction mixture was stirred for additional 2 h. On completion of the reaction (monitored by TLC), the reaction mixture was diluted with dichloromethane, washed with water, dried over anhydrous sodium sulphate and evaporated in vacuo. The crude compound (52.4 g) was purified by column chromatography over 100-200 mesh silica gel by using 30% ethyl acetate-hexane as eluent to yield 25.5 g of compound 3 as a solid. Yield%: 25.5 g (50.23%) Analytical Data: !H-NMR (DMSO-d6): 8 2.19 - 2.22 (t, 2H), 2.96 - 3.01 (m, 2H), 3.78 (s, 2H), 7.22 - 7.35 (m, 15H), 8.31- 8.34 (t,lH). ; Step-3: Synthesis of compound 5 To a solution of compound-5 (50 g, 0.151 mol, 1 eq) in EtOH (500 mL) and H20 (200 mL) was added NaOH (14.5 g, ; 0.362 mol, 2.4 eq) at 0°C. The reaction mixture was stirred for 4 h at room temperature. On completion of the reaction ! (monitored by TLC), the reaction mixture was concentrated in vacuo to remove the ethanol. The aqueous layer was acidified with 3N HC1 (pH ~4) and extracted with dichloromethane. The organic layer was dried over anhydrous i sodium sulphate and evaporated in vacuo to yield 45 g of compound 5 as oil. ' Yield%: 45 g (98.3%) Analytical Data; *H-NMR (DMSO-d*): 8 0.88 - 0.92 (t, 3H), 1.49 - 1.56 (m, 2H), 1.82 (s, 6H), 2.0 - 2.05 (m, 4H), 2.15 - 2.19 (t, 2H), 2.72 - 2.84 (m, 8H), 5.23 - 5.73 (m, 10H). ; Step-4: Synthesis of compound 6 To a solution of compound 5 (37.0 g, 0.122 mol; 1.0 eq), K2CO3 (26 g, 0.188 mol; 1.5 eq) and in dimethylformamide ! (230 mL) was added compound 3 (64 g, 0.145 mol, 1.18 eq) at room temperature. The reaction mixture was stirred for 3 h at room temperature & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was diluted with diethyl ether (1500 mL), washed with ice-water (2x 1000 mL), dried over anhydrous Na2S04 and evaporated in vacuo. The crude compound (96 g) was purified by column chromatography over 100-200 mesh silica gel by using 20% ethyl acetate-hexane to yield 63 g of compound 6 as a pale yellow gum. Yield%: 63 g (77.6%) Analytical Data; ^-NMR (DMSO-d*): 8 0.88 - 0.91 (t, 3H), 1.55 -1.59 (m, 2H), 1.99 - 2.08 (m, 4H), 2.33 - 2.37 (t, 2H), 2.48 - 2.49 (t, 2H), 2.76 - 2.81 (m, 8H), 2.97 - 3.02 (m, 2H), 4.37 (s, 2H), 5.27 - 5.34 (m, 10H), 7.21 - 7.34 (m, 15H), 8.02- 8.04 (t, 1H). Step-5: Synthesis of compound 7 (Ester Target) To a solution of Compound 6 (63 g, 0.095 mol; 1.0 eq) in TFA/DCM (53/630 mL), triethylsilane (13.5 g, 0.116 mol, 1.2 eq) was added drop wise at 0 °C and the reaction mixture was stirred for 2 h at 0°C. Reaction was monitored by TLC. On completion of the reaction, the reaction mixture was diluted with dichloromethanej washed with water. The organic layer was dried over anhydrous Na2S04 and evaporated in vacuo. The crude (77 g) compound was purified by column chromatography over neutral alumina using 90% DCM-hexane as eluent to yield 11.2 g of final target as colorless liquid. Yield%: 11.2 g (28 %) LS-MS purity: 95 % Analytical Data: ^-NMR (CDC13): 8 0.95 - 0.99 (t, 3H), 1.74 - 1.80 (m, 2H), 1.99 - 2.46 (m, 4H), 2.42 - 2.46 (m, 2H), 2.64 - 2.84 (m, 10H), 3.47 - 3.52 (m, 2H), 4.56 (s, 2H), 5.11 - 5.37 (m, 10H), 6.53 (bs, 1H). 1 Reaction Scheme for synthesis of cyclic Ester Target Step-1: Synthesis of compound 2 Procedure; To 2-aminoethanethiol HC1 (6.8 g, 0.06 mol; 1.0 eq) was charged water (100 mL) and PH of the solution was adjusted to 6.2 with 2N NaOH solution. Formaldehyde solution (7.5 mL, 35 % wt/wt, 0.087 mol) was added and mass was stirred for overnight at RT. On completion of the reaction (monitored by TLC), the reaction mixture was extracted with dichloromethane (3 x 50 mL). Collective organic layer was dried over Na2SC>4 and evaporated in vacuo to get compound 2 as oily mass, 1.5 g (Yield = 28%). Analytical Data: *H-NMR (DMSO-d6): 8 2.74 - 2.77 (t, 2H), 2.83 (bs, 1H), 3.07 - 3.10 (t, 2H), 4.11 (s, 2H). Step-2: Synthesis of compound 4 Procedure: To a solution of compound 3 (2.0 g, 6.62 mrnol; 1.0 eq) in DMF (12 mL) was charged K2C03 (1.82 g, 13.18 mmol; 2 eq) and t-Butyl chloroacetate (1.19 g, 7.93 mmol; 1.2 eq) at room temperature. The reaction mixture was stirred for overnight & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was quenched onto water (200 mL) and mass was extracted with ethyl acetate (3x 100 mL). Collective organic layer was dried over anhydrous NaiSC^and evaporated in vacuo. The crude compound (4.5 g) was purified by column chromatography over silica 100-200 mesh using 10 % ethyl acetate in pet ether to yield 2.7 gm of the title compound as oil (Yield = 98%). Analytical Data: 'H-NMR (CDC13): 8 0.96 - L00 (t, 3H), 1.48 (s, 9H), 1.72 -1.80 (m, 2H), 2.05 - 2.18 (m, 4H), 2.41 -2.45 (m, 2H), 2.81 - 2.85 (m, 8H), 4.50 (s, 2H), 5.31- 5.44 (m, 10 H). Step-3: Synthesis of compound 5 Procedure: To a solution of compound 4 (2.7 g, 6.49 mmol; 1.0 eq) in DCM (15 mL) was slowly added trifluoroacetic acid (4.43 g, 38.85 mmol; 6 eq) at room temperature. The reaction mixture was stirred for overnight & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was dilute with DCM (200 mL) and washed with water (2 x 100 mL). Combined organic layer was dried over anhydrous Na2S04 and evaporated in vacuo. The crude compound (3.3 g) was purified by column chromatography over 100-200 mesh silica using 7 % methanol in DCM to yield 2 gm of desire compound (Yield = 85%). Analytical Data: ^-NMR (CDC13): 8 0.95 - 0.99 (t, 3H), 1.71 - 1.78 (m, 2H), 2.04 - 2.16 (m, 4H), 2.41 - 2.45 (m, 2H), 2.81 - 2.84 (m, 8H), 4.66 (s, 2H), 5.30- 5.42 (m, 10 H). Step-4: Synthesis of compound 6 Procedure: To a solution of compound 5 (3.0 g, 8.33 mmol; 1.0 eq), HATU(3.2 g, 8.42 mmol; 1.5 eq) and DiPEA (1.44 g, 11.16 mmol, 2.0 eq) in DCM (45 mL) was added compound 2 (0.5 g, 5.61 mmol, 1.0 eq) at <10°C. The reaction mixture was stirred for overnight at room temperature & reaction was monitored by TLC. On completion of the reaction, the reaction mixture was dilute with DCM (200 mL) and washed with water (1 x 100 mL). Dried over anhydrous Na2S04 and evaporated in vacuo. The crude compound (4.5 g) was purified by column chromatography over 100 - 200 mesh silica using 25 % ethyl acetate in pet ether yielded 1.55 gm (HPLC purity = 96%) Analytical Data: ^-NMR (CDCI3): 5 0.95 - 0.99 (t, 3H), 1.72 - 1.80 (m, 2H), 2.04 - 2.17 (m, 4H), 2.44 - 2.48 (m, 2H), 2.80 - 2,84 (m, 8H), 8 2.98 - 3.01 (t, IH), 8 3.10 - 3.13 (t, IH), 3.67 - 3.70 (t, IH), 3.86 - 3.89 (t, IH), 4.44 - 4.60 (m, 2H), 4.66 - 4.69 (m, 2H), 5.30-5.43 (m, 10 H). HPLC Purity: 96 %, Mass: 432 [M + H]+ Stag -1 Synthesis: To a stirred solution of Cysteamine.HCl (5:0 g, 0.044 mole; 1.0 eq) in THF (20 mL) was added 4N NaOH solution (1.76 gm in 10.9 mL water^ 0.044 mole; 1.0 eq). Stirred reaction mass for 2 hrs at room temperature. Evaporated THF undelr reduced pressure and ethanol (50 mL) was added to the residue. Separated solid was filtered and mother liquor was evaporated to dryness to get 3.5 gm of solid mass as a basified product. Analytical Data; *H-NMR (CDC13): 8 2.43 - 2.46 (t, 2H), 2.62 - 2.65 (t, 2H), 2.69 - 2.71 (bs, 1H), 2.78 - 2.87 (bs, 2H), Stag -2 Synthesis: To a clear solution of cysteamine base (0.24 g, 3.11 mmoles; 1.0 eq) in dichlorornethane (10 mL) and methanol (5 mL) was added R-Lipoic acid (0.64 g, 3.11 mmoles; 1.0 eq) in mixture of dichlorornethane (15 mL) and methanol (5 mL) drop wise at room temperature over 15-20 min and the reaction mixture was stirred over night. Evaporate organic layer under reduced pressure to get solid mass, which was triturated with ether (20 mL) and filtered to get 0.645 g of compound as a yellow solid. Analytical Data: Melting point of R-Lipoic Acid: 50 - 52 ° C and Melting point of Salt: 100 -102 ° C Synthetic scheme Cvstamirie Di-Lipoate salt Stag -1 Synthesis: To a stirred solution of Cystamine.diHCl (1.0 g, 0.044 mole; 1.0 eq) in THF (10 mL) was added 4N NaOH solution (0.35 gm in 2.18 mL water, 0.088 mole; 2.0 eq). Stirred reaction mass for 3 hrs at room temperature. Extracted mass with ethyl acetate (20 mL) and washed with water (15 mL). Collective organic layer was dried over Na2SC«4 and evaporated under reduced pressure to obtain 163 mg oily mass. Stag -2 Synthesis: To a clear solution of cystamine base (0.08 g, 0.52 mmoles; 1.0 eq) in dichloromethane (5 mL) and methanol (2 mL) was added R-Lipoic acid (0.216 g, 1.05 mmoles; 2.0 eq) in mixture of dichloromethane (20 mL) and methanol (3mL) drop wise at room temperature over 15-20 min and the reaction mixture was stirred over night. Evaporate organic layer under reduced pressure to get solid mass, which was triturated with ether (20 mL) and filtered to get 0.366 g of compound as a yellow solid. Analytical Data: Melting point of R-Lipoic Acid: 50 - 52 ° C and Melting point of Salt: 100 -104 ° C. Few of the examples mentioned below. DETAILED DESCRIPTION Definitions As used herein, the following terms and phrases shall have the meanings set forth below. 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. The term "alkyl" refers to the radical of saturated aliphatic groups, including straight-chain alkyl groups, branched-chain alkyl groups, cycloalkyl (alicyclic) groups, alkyl-substituted cycloalkyl groups, and cycloalkyl-substituted alkyl groups. In preferred embodiments, a straight chain or branched chain alkyl has 30 or fewer carbon atoms in its backbone (e.g., C1-C30 for straight chains, C3-C30 for branched chains), and more preferably 20 or fewer. Likewise, preferred cycloalkyls have from 3-10 carbon atoms in their ring structure, and more preferably have 5, 6 or 7 carbons in the ring structure. The term "alkyl" as Used herein refers to a saturated linear or branched-chain monovalent hydrocarbon radical of one to twelve carbon atoms. Examples of alkyl groups include, but are not limited to, methyl (Me, -CH3), ethyl (Et, -CH2CH3), 1 - propyl (n-Pr, n- propyl, -CH2CH2CH3), 2-propyl (i-Pr, i-propyl, -CH(CH3)2), 1 -butyl (n-Bu, n-butyl, -CH2CH2CH2CH3), 2-methyl-l -propyl (i-Bu, i-butyl, -CH2CH(CH3)2), 2-butyl (s-Bu, s*butyl, - CH(CH3)CH2CH3), 2-methyl-2-propyl (t-Bu, t-butyl, - C(CH3)3), 1-pentyl (n-pentyl,-CH2CH2CH2CH2CH3), 2-pentyl (-CH(CH3)CH2CH2CH3), 3-pentyl (-CH(CH2CH3)2), 2- methyl-2-butyl (- C(CH3)2CH2CH3), 3-methyl-2-butyl (-CH(CH3)CH(CH3)2), 3 -methyl-1 -butyl (- CH2CH2CH(CH3)2), 2-methyl-l -butyl (-CH2CH(CH3)CH2CH3), 1-hexyl (- CH2CH2CH2CH2CH2CH3), 2*hexyl (-CH(CH3)CH2CH2CH2 CH3), 3-hexyl (-CH(CH2CH3)(CH2CH2CH3)), 2-methyl-2-pentyl (-C(CH3)2CH2CH2CH3), 3-methyl- 2- pentyl (-CH(CH3)CH(CH3)CH2CH3), 4-methyl-2-pentyl (-CH(CH3)CH2CH(CH3)2)> 3- methyl-3-peiityl (-C(CH3)(CH2CH3)2), 2-methyl-3-pentyl (CH(CH2CH3)CH(CH3)2), 2,3-dimethyl-2-butyl (-C(CH3)2CH(CH3)2), 3,3-dimethyl-2-butyl (-CH(CH3)C(CH3)3,1 -heptyl, 1 -octyl, and the like. The term "alkenyl" refers to linear or branched-chain monovalent hydrocarbon radical of two to twelve carbon atoms with at least one site of unsaturation, i.e., a carbon- carbon, sp double bond, wherein the alkenyl radical includes radicals having "cis" and "trans" orientations, or alternatively, "E" and "Z" orientations. Examples include, but are not limited to, ethylenyl or vinyl (-CH=CH2), allyl (-CH2CH=CH2), and the like. The term "alkynyl" refers to a linear or branched monovalent hydrocarbon radical of two to twelve carbon atoms with at least one site of unsaturation, i.e., a carbon- carbon, sp triple bond. Examples include, but are not limited to, ethynyl (-C=CH), propynyl (propargyl, -CH2C