Research summary

Glutathione research

The body's master antioxidant tripeptide — central to cellular redox balance, Phase II detoxification, immune function, and mitochondrial protection.

Antioxidant & Detoxification PeptideTripeptide (γ-Glu-Cys-Gly)MW307.32 g/molCAS70-18-8StatusFDA-approved (oral/IV forms)NCAAPermitted

Evidence at a glance

What the research says about Glutathione

The Glutathione evidence base cited here is 8 sources — 2 clinical, 4 review. Its strongest evidence is human — 2 clinical studies, most recently 2009 ("Randomized, Double-Blind, Pilot Evaluation of Intravenous Glutathione in…"). Regulatory status: FDA-approved (oral/IV forms).

Summary

Key takeaways

  • Glutathione (GSH) is the body's 'master antioxidant' — a tripeptide (glutamate-cysteine-glycine) present in virtually every cell, central to neutralizing free radicals, detoxification, and recycling vitamins C and E.

Overview

It is a prescription product, and everything below is research context rather than medical guidance.

What Is Glutathione?

Glutathione is a tripeptide of glutamate, cysteine, and glycine (~307 Da). Its defining chemistry is the cysteine sulfhydryl (-SH) group, which does the antioxidant work, and an unusual gamma peptide bond between glutamate and cysteine that protects it from most peptidases (ordinary peptide bonds would be cleaved faster).

It exists in a reduced (active, GSH) form and an oxidized (GSSG) form; the ratio of the two — typically >100:1 in healthy cells — is a core marker of cellular redox balance.

How It Works

Pharmacokinetics

  • Plasma half-life ~14 minutes — very short; rapidly converted to cysteine and other metabolites
  • Intracellular half-life is longer than plasma

Side Effects & Safety

Key Studies

  • Parkinson's / substantia nigra (human post-mortem): ~40% GSH reduction in the substantia nigra of PD patients, linking glutathione depletion to oxidative stress in the disease.

Citations

8 peer-reviewed sources

All citations link to the original source (PubMed, journal site, or regulatory filing). Independent research database — no vendor influence on what's cited.

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