Investigational Drug Details
Drug ID: | D158 |
Drug Name: | Glutathione |
Synonyms: | 5-L-Glutamyl-L-cysteinylglycine; gamma-L-Glutamyl-L-cysteinyl-glycine; Glutathion; Glutathione; Glutathione-SH; GSH; N-(N-gamma-L-Glutamyl-L-cysteinyl)glycine; Reduced glutathione |
Type: | Chemical drug |
DrugBank ID: | DB00143 |
DrugBank Description: | A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides. |
PubChem ID: | 124886 |
CasNo: | 70-18-8 |
Repositioning for NAFLD: | Yes |
SMILES: | [C@H](C(=O)NCC(=O)O)(NC(=O)CC[C@@H](C(=O)O)N)CS |
Structure: |
|
InChiKey: | RWSXRVCMGQZWBV-WDSKDSINSA-N |
Molecular Weight: | 307.328 |
DrugBank Targets: | Microsomal glutathione S-transferase 3; Hematopoietic prostaglandin D synthase; Glutathione S-transferase A1; Glutathione S-transferase A2; Microsomal glutathione S-transferase 1; S-formylglutathione hydrolase; Gamma-glutamyltranspeptidase 1; Glutathione |
DrugBank MoA: | Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion. It participates in the detoxification of methylglyoxal, a toxic by-product of metabolism, mediated by glyoxalase enzymes. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. GSH is a cofactor of conjugation and reduction reactions that are catalyzed by glutathione S-transferase enzymes expressed in the cytosol, microsomes, and mitochondria. However, it is capable of participating in non-enzymatic conjugation with some chemicals, as it is hypothesized to do to a significant extent with n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450 reactive metabolite formed by toxic overdose of acetaminophen. Glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein sulfhydryl groups which would otherwise be toxically adducted. The preferred medical treatment to an overdose of this nature, whose efficacy has been consistently supported in literature, is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and allow a usable GSH pool. |
DrugBank Pharmacology: | -- |
DrugBank Indication: | For nutritional supplementation, also for treating dietary shortage or imbalance |
Targets: | MGST3; HPGDS; GSTM2; GSTM5; GPX7 cofactor; MGST2; GSS; GSTM1; GSTK1; GSTM3; GSTM4; GPX1 cofactor; GPX2 cofactor; GPX3 cofactor |
Therapeutic Category: | -- |
Clinical Trial Progress: | Phase 3 on-going (CTRI/2010/091/000087) |
Latest Progress: | Under clinical trials |

Trial ID | Source ID | Phases | Status | Study Results | Start Date | Last Update Posted | |
---|---|---|---|---|---|---|---|
L0004 | NCT04475276 | Phase 4 | Recruiting | No Results Available | February 23, 2021 | July 7, 2021 | Details |
L0388 | ChiCTR2100044996 | Not applicable | Recruiting | No Results Available | 03/04/2021 | 2 November 2021 | Details |
L0405 | IRCT20200531047614N2 | Phase 3 | Recruiting | No Results Available | 13/11/2020 | 30 November 2020 | Details |
L0425 | IRCT20200531047614N1 | Phase 3 | Not Recruiting | No Results Available | 19/06/2020 | 7 September 2020 | Details |
L0462 | IRCT20190714044196N1 | Phase 3 | Not Recruiting | No Results Available | 31/07/2019 | 7 October 2019 | Details |
L0548 | DRKS00005767 | Phase 3 | Not Recruiting | No Results Available | 10/05/2017 | 7 February 2022 | Details |
L0552 | IRCT201701172709N44 | Phase 3 | Not Recruiting | No Results Available | 10/04/2017 | 13 July 2020 | Details |
L0642 | JPRN-UMIN000011118 | Not applicable | Not Recruiting | No Results Available | 10/07/2013 | 2 April 2019 | Details |
L0714 | IRCT20150205020965N5 | Phase 3 | Not Recruiting | No Results Available | 13/12/2019 | 17 August 2020 | Details |
L0833 | NCT02992470 | Not applicable | Not recruiting | No Results Available | 12/12/2016 | 9 January 2017 | Details |
L0961 | CTRI/2010/091/000087 | Phase 3 | Not Recruiting | No Results Available | 04/02/2010 | 24 November 2021 | Details |
Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs |
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Article ID | PMID | Source | Title | |
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A01096 | 34870139 | Metabol Open | Protective effects of cerium oxide nanoparticles in non-alcoholic fatty liver disease (NAFLD) and carbon tetrachloride-induced liver damage in rats: Study on intestine and liver. | Details |
A01379 | 34768813 | Int J Mol Sci | The Ameliorative Effects of Saikosaponin in Thioacetamide-Induced Liver Injury and Non-Alcoholic Fatty Liver Disease in Mice. | Details |
A01411 | 34757160 | Toxicology | The combined impact of decabromodiphenyl ether and high fat exposure on non-alcoholic fatty liver disease in vivo and in vitro. | Details |
A01484 | 34729306 | Acta Pharm Sin B | 3D disorganization and rearrangement of genome provide insights into pathogenesis of NAFLD by integrated Hi-C, Nanopore, and RNA sequencing. | Details |
A01587 | 34684533 | Nutrients | Supplementation with a Specific Combination of Metabolic Cofactors Ameliorates Non-Alcoholic Fatty Liver Disease, Hepatic Fibrosis, and Insulin Resistance in Mice. | Details |
A01594 | 34684335 | Nutrients | Pathway Preferential Estrogens Prevent Hepatosteatosis Due to Ovariectomy and High-Fat Diets. | Details |
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