Also Known As: GSH, Reduced Glutathione, γ-L-Glutamyl-L-cysteinyl-glycine, L-Glutathione
Glutathione (GSH) is an endogenous tripeptide of γ-glutamate, cysteine and glycine, joined by an atypical γ-peptide bond through the side-chain carboxyl of glutamate. It is the dominant intracellular thiol antioxidant and a co-substrate for glutathione peroxidases, glutathione S-transferases and glutaredoxins. Small human studies of intravenous GSH have been published in early Parkinson's disease and chemotherapy-induced peripheral neuropathy. Limited human data — research use only.
Studies report that glutathione detoxifies reactive oxygen species by direct thiol chemistry and as a co-substrate of glutathione peroxidases. Observed in research settings.
Intracellular GSH concentration ranges from 1 to 10 mM and exceeds GSSG by approximately 100-fold under physiological conditions. In hepatocytes, glutathione is the principal Phase II conjugate for detoxifying reactive metabolites such as N-acetyl-p-benzoquinone imine (NAPQI, the hepatotoxic acetaminophen metabolite). Oral bioavailability of free GSH is poor — most oral preparations are hydrolysed in the gut to amino acids. Intravenous or inhaled administration bypasses this first-pass loss.
The published evidence base consists of numerous mechanistic animal and cell studies, plus small, predominantly open-label human pilots in neurology, oncology and pulmonology; large controlled trials are sparse.
Sechi 1996: intravenous GSH 600 mg twice daily for 30 days in 9 untreated Parkinson's patients reported symptomatic improvement; not controlled, not randomized.
— Sechi G et al. 1996, Prog Neuropsychopharmacol Biol Psychiatry 20(7):1159-1170
Observed in research settings
Limited human data. Oral GSH is generally well tolerated; intravenous use has been described as tolerable in small pilots, but systematic pharmacovigilance data do not exist. Observed in research settings.
Forman HJ, Zhang H, Rinna A Glutathione: overview of its protective roles, measurement, and biosynthesis Molecular Aspects of Medicine 2009;30(1-2):1-12. 2009 .
Lu SC Glutathione synthesis Biochimica et Biophysica Acta 2013;1830(5):3143-3153. 2013 .
Sechi G, Deledda MG, Bua G, Satta WM, Deiana GA, Pes GM, Rosati G Reduced intravenous glutathione in the treatment of early Parkinson's disease Progress in Neuro-Psychopharmacology & Biological Psychiatry 1996;20(7):1159-1170. 1996 .
Mitochondrial coenzyme (pyridine nucleotide)
Pyridine-nucleotide coenzyme central to mitochondrial energetics and sirtuin/PARP activity. Not a peptide — research compound. Limited human data.
View DetailsMitochondrial-derived peptide (MDP) — Mitochondrial / Longevity Research
Mitochondrial-derived peptide (MDP) — natural 16-amino-acid peptide (MRWQEMGYIFYPRKLR) encoded by a small open reading frame within human MT-RNR1 (12S mt-rRNA) on mitochondrial DNA (mtDNA); not nuclear DNA. First MDP with a defined systemic metabolic role (AMPK activation). Not approved by FDA or EMA. On the WADA Prohibited List as of 2024 (Class S4, AMPK activators). Research use only.
View DetailsMitochondria-targeting synthetic tetrapeptide (Szeto–Schiller / MTP class) — mitochondrial / longevity research; FDA-approved 2025 for Barth syndrome (FORZINITY)
Synthetic mitochondria-targeting tetrapeptide (Szeto–Schiller / SS-31 / MTP-131 / Bendavia / Forzinity class) — H-D-Arg-Tmt-Lys-Phe-NH₂. FDA-approved on 19 September 2025 as FORZINITY (NDA 215244) under accelerated approval for Barth syndrome (≥30 kg) — the first FDA-approved therapy for Barth syndrome and the first FDA-approved mitochondria-targeted peptide therapeutic. EMA: not approved. All other indications remain investigational; for research use only outside the Barth indication.
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