Glutathione Vial

Glutathione ( -L-glutamyl-L-cysteinyl-glycine, GSH) is an endogenous tripeptide synthesized intracellularly in two ATP-dependent steps and present in millimolar concentrations in nearly every mammalian cell.

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Description

Glutathione (γ-L-glutamyl-L-cysteinyl-glycine, GSH) is an endogenous tripeptide synthesized intracellularly in two ATP-dependent steps and present in millimolar concentrations in nearly every mammalian cell. It is the principal cellular antioxidant and a substrate for glutathione peroxidase, glutathione S-transferase, and the glutaredoxin system, with central roles in detoxification (Phase II conjugation in the liver), redox signaling, and protein S-glutathionylation. Glutathione has been used clinically by intravenous administration for decades in chronic liver disease, acute poisoning, and as an investigational therapy in Parkinson’s disease and other neurodegenerative conditions.

The original positive human signal for IV glutathione comes from Sechi et al.’s open-label trial in newly diagnosed, untreated Parkinson’s disease: 9 patients received intravenous reduced glutathione 600 mg twice daily for 30 days, with all patients improving and a mean 42% reduction in disability scores, the therapeutic effect persisting two to four months after treatment was discontinued (Sechi et al., Progress in Neuro-Psychopharmacology & Biological Psychiatry 1996).1

Important Note on the Evidence Base

Glutathione has an unusually large body of human research compared with most research peptides — including multiple randomized controlled trials, pharmacokinetic studies, and decades of clinical use in Japan and parts of Europe for hepatic indications. However, the human efficacy data in Parkinson’s disease are mixed: an early open-label study by Sechi et al. reported significant disability improvement, while the Hauser et al. RCT found tolerability and safety but no significant efficacy signal versus placebo. Oral glutathione bioavailability is low because of GI peptide hydrolysis; the strongest human efficacy evidence is for intravenous and intranasal routes. This product is sold as a vial intended for laboratory research; it is not approved by the FDA or EMA as a therapeutic agent.

Published Research on Glutathione

Original IV Glutathione in Early Parkinson’s Disease — Sechi et al., Progress in Neuro-Psychopharmacology & Biological Psychiatry (1996)

This open-label study administered intravenous reduced glutathione (600 mg twice daily) for 30 days to nine patients with newly diagnosed, untreated Parkinson’s disease. All patients improved, with a mean 42% reduction in disability scores by the end of the treatment period. The therapeutic effect persisted for two to four months after treatment was discontinued. Although uncontrolled, this was the original positive human signal that prompted the larger Hauser RCT a decade later, and it remains the single most-cited human study supporting IV glutathione for Parkinson’s disease.1

Randomized Double-Blind Pilot in Parkinson’s Disease — Hauser et al., Movement Disorders (2009)

This randomized, placebo-controlled, double-blind pilot trial enrolled 21 PD patients whose motor symptoms were not adequately controlled with their existing medication, randomizing them to intravenous glutathione 1,400 mg or placebo three times weekly for 4 weeks. The study’s primary aim was safety, tolerability, and preliminary efficacy. Glutathione was well tolerated with no withdrawals from adverse events and an adverse event profile similar to placebo. There were no statistically significant differences in UPDRS scores between groups, and the authors emphasized the trial was not powered to detect efficacy. The study established IV glutathione’s safety profile in PD and informed the design of subsequent intranasal glutathione trials by Mischley et al.2

Glutathione Deficiency in Aging — Sekhar et al., American Journal of Clinical Nutrition (2011)

Using stable-isotope infusions of [2H2]glycine in 8 elderly and 8 younger subjects, this Baylor College of Medicine study quantified red blood cell glutathione synthesis rate, intracellular concentration, and plasma markers of oxidative stress. Elderly subjects had 46% lower erythrocyte glutathione than younger controls, a deficit driven by reduced synthesis rather than increased turnover. Two weeks of dietary supplementation with the precursors cysteine (as N-acetylcysteine) and glycine fully restored glutathione synthesis and concentrations and reduced markers of oxidative stress to levels indistinguishable from younger subjects, demonstrating that age-related glutathione decline is reversible at the precursor level.3

Oral Glutathione in Nonalcoholic Fatty Liver Disease — Honda et al., BMC Gastroenterology (2017)

This open-label, single-arm, multicenter pilot trial enrolled 34 Japanese patients with ultrasonography-confirmed NAFLD. After a 3-month run-in of diet and exercise intervention, patients received oral glutathione 300 mg/day for 4 months. The 29 patients who completed the trial showed reductions in alanine aminotransferase (the primary endpoint) as well as triglycerides, non-esterified fatty acids, and ferritin levels. ALT responders (those whose ALT decreased below the median change) were younger and lacked severe diabetes. The study was the first prospective trial of oral glutathione in NAFLD and supports the hypothesized link between hepatic glutathione status and steatosis.4

About the Compound

Glutathione is a tripeptide composed of glutamic acid, cysteine, and glycine, with the unusual feature that the γ-carboxyl group of glutamate (rather than the α-carboxyl) forms the peptide bond with cysteine, protecting the peptide from cleavage by typical aminopeptidases. The cysteine sulfhydryl is the redox-active site: in its reduced form (GSH) the peptide donates an electron to neutralize reactive oxygen species, generating glutathione disulfide (GSSG), which is recycled back to GSH by glutathione reductase using NADPH. Cellular GSH:GSSG ratio is one of the most widely used biomarkers of intracellular redox state. Glutathione’s primary research applications include redox biology, hepatic phase II conjugation studies, oxidative stress in neurodegeneration models, and antioxidant supplementation studies.

  • Compound class: endogenous tripeptide; principal cellular antioxidant
  • Sequence: γ-L-Glu-L-Cys-Gly (γ-glutamyl bond between Glu and Cys)
  • Synonyms: GSH, reduced glutathione, L-glutathione
  • CAS Number: 70-18-8 (reduced form)
  • Molecular Formula: C10H17N3O6S
  • Molecular Weight: 307.32 g/mol
  • Solubility: water-soluble (lyophilized; reconstitute with bacteriostatic water or saline)
  • Mechanism: cysteine-mediated electron donation to neutralize reactive oxygen species; substrate for glutathione peroxidases, S-transferases, and glutaredoxins
  • Regulatory status: not approved by the FDA or EMA as a therapeutic agent. Used clinically in Japan and parts of Europe for hepatic indications by IV administration

Product Specifications

  • Format: lyophilized peptide in vial (reconstitute with bacteriostatic water or saline for IV/IM research administration)
  • Strength: 1500 mg per vial
  • Purity: ≥99% (HPLC verified)
  • Container: sealed glass vial (lyophilized powder)
  • Certificate of Analysis: lot-specific COA available

See the FDA Disclosure, Storage Instructions, and RUO tabs for handling, storage, and regulatory information.

References

  1. Sechi G, Deledda MG, Bua G, et al. Reduced intravenous glutathione in the treatment of early Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 1996;20(7):1159-1170. doi:10.1016/S0278-5846(96)00103-0
  2. Hauser RA, Lyons KE, McClain T, Carter S, Perlmutter D. Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson’s disease. Mov Disord. 2009;24(7):979-983. doi:10.1002/mds.22401
  3. Sekhar RV, Patel SG, Guthikonda AP, et al. Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation. Am J Clin Nutr. 2011;94(3):847-853. doi:10.3945/ajcn.110.003483
  4. Honda Y, Kessoku T, Sumida Y, et al. Efficacy of glutathione for the treatment of nonalcoholic fatty liver disease: an open-label, single-arm, multicenter, pilot study. BMC Gastroenterol. 2017;17(1):96. doi:10.1186/s12876-017-0652-3
For research use only. Not for human consumption.