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Glutathione

Also identified as γ-L-glutamyl-L-cysteinyl-glycine, GSH

Tripeptide thiol

Sequence: γ-Glu-Cys-Gly

Molecular weight
307.3
Molecular formula
C10H17N3O6S
CAS
70-18-8
Published studies reviewed
4

FOR RESEARCH USE ONLY. NOT FOR HUMAN OR VETERINARY USE. NOT FOR HUMAN CONSUMPTION.

Compounds described on this site are supplied solely for laboratory research. They are not offered for human or veterinary use or for clinical use, and they are not intended to diagnose, mitigate, cure or prevent any disease.

Glutathione (GSH) is the tripeptide γ-Glu-Cys-Gly, in which glutamate is linked through its side-chain carboxyl group and cysteine carries a free thiol. The four publications reviewed are all human studies: a single-amount pharmacokinetic study and three randomised, double-blind, placebo-controlled trials. Their results do not agree with one another, and studies of cysteine precursors such as N-acetylcysteine are excluded as different compounds.

At a glance

Also identified as
γ-L-glutamyl-L-cysteinyl-glycine, GSH
Class
Tripeptide thiol
Target or mechanism
None of the publications recorded here identifies a receptor or a target.
Evidence types represented
human
Published studies reviewed
4
Regulatory and registry records
4
Last reviewed
2026-09-21

Overview

Glutathione is a tripeptide of glutamate, cysteine and glycine. Its glutamate is joined through the side-chain (γ) carboxyl group rather than the usual backbone linkage, and its cysteine carries a free thiol group. The thiol form is abbreviated GSH and the disulfide-linked form GSSG; the ratio between them is what the studies below mean by "glutathione status".

⚠️ Only studies of this material are recorded here. N-acetylcysteine and the other cysteine precursors are different compounds, and a study of one of them is not a study of this one. Observational work measuring how much glutathione people already carry is a measurement of endogenous biochemistry, not a study of giving anyone this material, and is not recorded either.

The publications on this page are four human studies: one single-amount pharmacokinetic study, two randomised, double-blind, placebo-controlled trials in healthy adults, and one randomised, double-blind, placebo-controlled trial in Parkinson's disease.

They do not all point the same way, and the page prints them as they are. The 1992 pharmacokinetic study found no measurable rise in plasma glutathione after a single amount and concluded systemic availability is negligible. The 4-week trial found no change in either of its primary biomarkers, or in glutathione status. The 6-month trial reports increases in measured glutathione in several body compartments. The Parkinson's disease trial reports no statistically significant difference on its rating-scale outcome.

Mechanism under investigation

None of the publications recorded here identifies a receptor or a target. What they measured is where the molecule goes and what happens to measured concentrations: the 1992 study reports that hydrolysis by intestinal and hepatic gamma-glutamyltransferase is the authors' explanation for the absence of a rise in plasma, and the two trials in healthy adults measured concentrations in blood compartments rather than mechanism.

Scope of the published work

Areas investigated
  • Systemic availability
  • Urinary biomarkers of oxidative stress
  • Glutathione concentrations in blood compartments
  • Rating-scale outcomes in Parkinson's disease
  • Tolerability
Models used
  • Single-amount study in healthy volunteers
  • Randomised human studies

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Limitations

Evidence represented on this page: human. No in vitro or animal research is represented. The page reviews 4 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Common questions

What is Glutathione?

Glutathione is a tripeptide of glutamate, cysteine and glycine.

How does Glutathione work, according to the published research?

None of the publications recorded here identifies a receptor or a target. What they measured is where the molecule goes and what happens to measured concentrations: the 1992 study reports that hydrolysis by intestinal and hepatic gamma-glutamyltransferase is the authors' explanation for the absence of a rise in plasma, and the two trials in healthy adults measured concentrations in blood compartments rather than mechanism.

What has published research on Glutathione found, and what are its limits?

This page records 4 publications, reporting human work in 4. Each is listed with its identifier under References.

Human studies represented: Richie et al., 2015, PMID 24791752; Allen et al., 2011, PMID 21875351; Hauser et al., 2009, PMID 19230029; Witschi et al., 1992, PMID 1362956.

Evidence represented on this page: human.

No in vitro or animal research is represented.

The page reviews 4 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Is Glutathione approved by the U.S. FDA?

This page cites no FDA approval record for Glutathione; PepGenex Science states a U.S. regulatory status only where a sourced record exists.

PepGenex research materials are not FDA approved and are not for human or veterinary use.

What risks have published studies of Glutathione reported?

1 published human study on this page reports adverse events or safety measurements. Each is listed with its publication in the adverse-events section of this page.

Trial events do not establish a complete safety profile.

What adverse events have been reported in published studies of Glutathione?

Adverse events and safety measurements as reported by the published human studies on this page. Each entry is attributed to its publication.

Hauser et al., 2009, PMID 19230029

Design and population
Randomised, double-blind, placebo-controlled pilot trial. Subjects received glutathione or placebo over 4 weeks, with 8 further weeks of follow-up. Twenty-one subjects were randomly assigned, 11 to glutathione and 10 to placebo; one assigned to glutathione withdrew for personal reasons before any post-randomisation assessment. The stated objectives were safety, tolerability and preliminary efficacy.
Events reported
Glutathione was well tolerated. There were no withdrawals because of adverse events in either group, reported adverse events were similar in the two groups, and the authors state that no safety concerns were identified.

Trial events do not establish a complete safety profile.

Published research

Grouped by the kind of study. Select one to narrow what is shown below.

Human study (phase not stated)(4)

Human study (phase not stated)n = 54

Randomized controlled trial of oral glutathione supplementation on body stores of glutathione.

Richie JP Jr, Nichenametla S, Neidig W, Calcagnotto A, Haley JS, Schell TD, Muscat JE., European Journal of Nutrition, 2015;54(2):251-263

published

Six-month randomised, double-blinded, placebo-controlled trial in 54 non-smoking adults. Glutathione was given in one of two study arms, and glutathione was measured in blood, erythrocytes, plasma, lymphocytes and exfoliated buccal mucosal cells. A one-month washout period followed. Secondary outcomes in a subset of participants were a battery of immune markers.

  • Glutathione concentrations in blood were higher than baseline at 1, 3 and 6 months at both amounts. At 6 months, mean glutathione was 30-35 % higher in erythrocytes, plasma and lymphocytes and 260 % higher in buccal cells in the higher-amount group (P < 0.05), and 17 % and 29 % higher in blood and erythrocytes respectively in the lower-amount group (P < 0.05). The increases were in most cases dependent on the amount given and on time, and concentrations returned to baseline after the one-month washout. The authors state that these findings show, for the first time, that consumption of glutathione supplements increased body-compartment stores of glutathione.
  • The ratio of oxidised to reduced glutathione in whole blood decreased in both glutathione groups after 6 months.
  • Natural-killer cell cytotoxicity was more than twofold higher in the higher-amount group than in the placebo group at 3 months (P < 0.05). The abstract describes the immune markers as secondary outcomes measured in a subset of participants, and gives neither the size of that subset nor a figure for the lower-amount group.
Context

The three studies in healthy volunteers on this page were not asking the same question, and their answers cannot simply be added up. The 1992 study followed plasma for 270 minutes after one amount and found nothing measurable. The 4-week trial measured two urinary biomarkers of oxidative stress and erythrocyte glutathione status, and found no change in any of them. The 6-month trial measured glutathione itself in five compartments and reports higher concentrations. Longer, larger amounts and different things measured — so what the page establishes is that the question of what an amount of glutathione does depends on which measurement and which timescale, not that one study is right and another is wrong.

View publication →
Human study (phase not stated)n = 40

Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers.

Allen J, Bradley RD., Journal of Alternative and Complementary Medicine, 2011;17(9):827-833

published

Randomised, double-blind, placebo-controlled trial in 40 adult volunteers without acute or chronic disease, run at Bastyr University Research Institute and the Bastyr Center for Natural Health. Participants took glutathione or placebo for 4 weeks. The primary outcome measures were change in creatinine-standardised urinary F2-isoprostanes and urinary 8-hydroxy-2'-deoxyguanosine; erythrocyte reduced glutathione, oxidised glutathione and their ratio were also measured, by tandem liquid chromatography / mass spectrometry. Thirty-nine participants completed the study per protocol.

  • At week 4 the change in creatinine-standardised F2-isoprostanes (ng/mg creatinine) was 0.0±0.1 versus 0.0±0.1, p=0.38, and the change in 8-hydroxy-2'-deoxyguanosine (µg/g creatinine) was -0.2±3.3 versus 1.0±3.2, p=0.27. The abstract prints each comparison as a pair and does not say which value belongs to which group, so the pair is reproduced as printed. Total reduced glutathione, oxidised glutathione and their ratio were also unchanged. The authors report that no significant changes were observed in any biomarker of oxidative stress, glutathione status included.
View publication →
Human study (phase not stated)n = 21

Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson's disease.

Hauser RA, Lyons KE, McClain T, Carter S, Perlmutter D., Movement Disorders, 2009;24(7):979-983

published

Randomised, double-blind, placebo-controlled pilot trial. Subjects received glutathione or placebo over 4 weeks, with 8 further weeks of follow-up. Twenty-one subjects were randomly assigned, 11 to glutathione and 10 to placebo; one assigned to glutathione withdrew for personal reasons before any post-randomisation assessment. The stated objectives were safety, tolerability and preliminary efficacy.

  • There were no significant differences between the groups in change in Unified Parkinson's Disease Rating Scale (UPDRS) scores. Over the 4 weeks, UPDRS activities-of-daily-living plus motor scores improved by a mean of 2.8 units more in the glutathione group (P = 0.32), and over the subsequent 8 weeks worsened by a mean of 3.5 units more in the glutathione group (P = 0.54). The authors describe the data as suggesting the possibility of a mild symptomatic effect that remains to be evaluated in a larger study.
  • Glutathione was well tolerated. There were no withdrawals because of adverse events in either group, reported adverse events were similar in the two groups, and the authors state that no safety concerns were identified.
Limitations

Twenty-one people were randomised in the Parkinson's disease trial, and the authors call it a pilot. Neither rating-scale difference reached statistical significance, and at that size neither the absence of a difference nor the direction of either figure establishes anything — which is why the safety and tolerability record, the trial's stated first objective, is the part of it worth reading.

View publication →
Human study (phase not stated)n = 7

The systemic availability of oral glutathione.

Witschi A, Reddy S, Stofer B, Lauterburg BH., European Journal of Clinical Pharmacology, 1992;43(6):667-669

published

Seven healthy volunteers were given a single amount of glutathione, and plasma glutathione, cysteine and glutamate were measured over the following 270 minutes. There was no placebo group.

  • Basal plasma concentrations were 6.2 µmol/L for glutathione, 8.3 µmol/L for cysteine and 54 µmol/L for glutamate. Over the 270 minutes that followed, none of the three rose significantly. The authors conclude that the systemic availability of glutathione given this way is negligible in man, attribute it to hydrolysis of glutathione by intestinal and hepatic gamma-glutamyltransferase, and state that a single amount of that size cannot raise circulating glutathione to a clinically meaningful extent.
Limitations

The availability study had seven volunteers, no placebo group and a single observation window of 270 minutes. It is a strong result about that window and a weak one about anything else: it does not address repeated amounts over weeks, which is what the two later trials measured.

View publication →

Registered clinical trials

A ClinicalTrials.gov search returned 55 interventional records naming Glutathione as an intervention on 2026-09-24. The 4 listed here were selected to show how the registered research is organised, by phase.

Each entry shows registry fields only, as ClinicalTrials.gov listed them when fetched. None of them reports a result here. Published findings are under Published research, each with its publication.

Phase 2

NCT00266331

Official title
Prospective Blinded Randomized Study; RayGel Versus Placebo-an Alternative for Skin Care During External Beam Radiation.
Sponsor
Nathalie Johnson
Phase
Phase 2
Design
Randomized, parallel assignment, triple-blind
Enrollment
150 (actual)
Status
Completed
Start
2004-10
Primary completion
2011-05
Study completion
2011-05
Last update posted
2013-08-28
Last verified
2026-09-24

Phase 3

NCT02311907

Official title
The Use of Glutathione (GSH) for Prevention of Paclitaxel/Carboplatin (TAXOL/CBDCA) Induced Peripheral Neuropathy: A Phase III Randomized, Double-Blind Placebo Controlled Study
Sponsor
Alliance for Clinical Trials in Oncology
Phase
Phase 3
Design
Randomized, parallel assignment, triple-blind
Enrollment
195 (actual)
Status
Completed
Start
2009-12
Primary completion
2012-08
Study completion
2012-08
Last update posted
2017-02-23
Last verified
2026-09-24

Not applicable

NCT01967667

Official title
Biological Evaluation of Dietary Supplement Liposomal Glutathione
Sponsor
University of Maryland, Baltimore
Phase
Not applicable
Design
Randomized, crossover assignment, quadruple-blind
Enrollment
11 (actual)
Status
Completed
Start
2014-04
Primary completion
2021-02
Study completion
2021-02
Last update posted
2021-04-28
Last verified
2026-09-24

NCT02948673 (DIMITOS)

Brief title
The Production of Reactive Oxygen Species in Response to Glutathione Supplementation and Acute Exercise
Sponsor
University of Copenhagen
Phase
Not applicable
Design
Randomized, parallel assignment, double-blind
Enrollment
20 (actual)
Status
Completed
Start
2016-05
Primary completion
2017-12
Study completion
2017-12
Last update posted
2018-05-02
Last verified
2026-09-24

References

Published studies reviewed (4)

  1. The systemic availability of oral glutathione. — Witschi A, Reddy S, Stofer B, Lauterburg BH., European Journal of Clinical Pharmacology, 1992;43(6):667-669
    DOI 10.1007/BF02284971 · PMID 1362956
  2. Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers. — Allen J, Bradley RD., Journal of Alternative and Complementary Medicine, 2011;17(9):827-833
    DOI 10.1089/acm.2010.0716 · PMID 21875351 · PMC3162377
  3. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. — Richie JP Jr, Nichenametla S, Neidig W, Calcagnotto A, Haley JS, Schell TD, Muscat JE., European Journal of Nutrition, 2015;54(2):251-263
    DOI 10.1007/s00394-014-0706-z · PMID 24791752
  4. Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson's disease. — Hauser RA, Lyons KE, McClain T, Carter S, Perlmutter D., Movement Disorders, 2009;24(7):979-983
    DOI 10.1002/mds.22401 · PMID 19230029

Regulatory and registry records (4)

  1. ClinicalTrials.gov, NCT00266331
    Registry record, phase 2. Registry fields only. Retrieved 2026-09-24.
  2. ClinicalTrials.gov, NCT02311907
    Registry record, phase 3. Registry fields only. Retrieved 2026-09-24.
  3. ClinicalTrials.gov, NCT01967667
    Registry record, not applicable. Registry fields only. Retrieved 2026-09-24.
  4. ClinicalTrials.gov, NCT02948673 (DIMITOS)
    Registry record, not applicable. Registry fields only. Retrieved 2026-09-24.

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