Peptide Health Lab

Immune & defense

Glutathione

Also known as: GSH, Reduced glutathione, L-glutathione

Regulatory status
Rx via compounding
Evidence grade
Human RCT evidence

Last reviewed September 1, 2026 · 17 sources

What glutathione is and how it works

Glutathione is not a drug candidate that someone designed. It is a tripeptide of glutamate, cysteine and glycine that every cell in the reader's body is synthesising right now, and it is the central redox agent of most aerobic organisms. Its functions run well past antioxidant defence into detoxification, redox signalling, iron handling, DNA synthesis, gene expression, cysteine metabolism, and the decisions a cell makes about proliferation, apoptosis and ferroptosis.[1]

Two features of that biology govern everything else on this page. The first is where it is made. Glutathione is assembled inside the cytosol by two ATP-dependent enzymes, and the rate-limiting inputs are the enzyme glutamate cysteine ligase and the availability of cysteine — which is why the compound most often used clinically to raise glutathione is N-acetylcysteine, a cysteine precursor and a different molecule entirely.[1] The second is how it is destroyed. Once exported from the cell, glutathione is broken down extracellularly by a membrane-anchored enzyme, gamma-glutamyl transferase, as part of the gamma-glutamyl cycle.[1] That enzyme sits in the intestine and the liver, and it is the reason the systemic availability of a swallowed dose was ever in question.

The premise most readers arrive with is that glutathione falls with age and with illness, so it should be replaced. The first half of that is well described: a review of glutathione biochemistry and gerontology reports levels declining in aging and attributes the decline chiefly to impaired biosynthesis.[1] The second half does not follow from the first, and one of the studies most often used to build the chain breaks it. A stable-isotope study measured glutathione synthesis directly in 8 elderly and 8 younger subjects and found the elderly deficit was a reduced synthesis rate rather than a supply failure; two weeks of supplementation with the precursors cysteine and glycine restored synthesis rates, concentrations and oxidative stress markers to the younger group's level.[7] What was corrected there was made by the body from precursors, not delivered as glutathione.

This page carries a "Human RCT evidence" badge, and it is worth saying plainly what that badge means and does not mean. It means randomized controlled trials have administered glutathione to people and measured outcomes — eight of them are cited below, across five routes. It is a statement about the quality of the evidence that exists, not a verdict that the compound works: most of those trials missed their primary endpoints, and the use that brings most readers here has not been tested at all.

What the research actually shows

Swallowed glutathione: the two sides of a real disagreement. In 1992, seven volunteers were given a single large oral dose and their plasma glutathione, cysteine and glutamate did not rise significantly; the authors concluded that systemic availability is negligible in man, and attributed it to hydrolysis by intestinal and hepatic gamma-glutamyl transferase.[2] In 2015, a 6-month randomized, double-blind, placebo-controlled trial in 54 non-smoking healthy adults reported glutathione rising 30 to 35 percent in erythrocytes, plasma and lymphocytes and 260 percent in buccal cells at the high dose, returning to baseline after a one-month washout.[10] Both results stand. A single-dose absorption challenge and six months of daily dosing are different experiments, and reading either as the last word is how this literature is usually misreported.

Raising the pool is not the same as changing a marker. The randomized trial that set out to test that step gave 40 adults 500 mg twice daily for four weeks with urinary F2-isoprostanes and 8-OHdG as its primary outcomes. Both endpoints missed, at p=0.38 and p=0.27, and erythrocyte glutathione status measures were unchanged as well.[6] The 6-month trial reports the other direction on a different measure: alongside the rise in stores, it records decreases in the oxidized-to-reduced glutathione ratio in whole blood at six months in both dose groups, which its authors read as a reduction in oxidative stress.[10] So a within-blood redox ratio moved in the longer trial and the urinary damage markers did not move in the shorter one. Those are different measurements over different periods, and neither trial repeated the other's endpoint, which is why this page grades the marker question as unsettled rather than answered either way.

The immune claim the category name invites rests on one secondary outcome. The 6-month trial's immune battery was a secondary endpoint measured in a subset of participants, and within it natural killer cell cytotoxicity increased more than twofold versus placebo at three months in the high-dose group.[10] That is a laboratory measure of immune cell activity in a subset, at one timepoint, in a trial whose primary question was glutathione stores. No trial cited on this page counted an infection, a duration of illness, or any clinical immune outcome at all.

Formulation is its own variable, and the one trial addressing it is an industry trial. A 2026 randomized crossover study in 14 healthy adults compared a proprietary micellar preparation at 300 mg against an unformulated standard preparation at 500 mg and reported roughly 2.49-fold higher baseline-adjusted whole-blood glutathione exposure and roughly 2.43-fold higher peak response for the micellar arm at those unequal amounts, widening to as much as 4-fold when the authors normalised both to a 300 mg equivalent. A 30-day single-arm follow-up phase in the same participants reported no significant changes in ALT, AST, ALP or creatinine. The authors are employees of the organisations behind the tested product, a patent on the tested matrix is pending, and the comparison is between two named preparations rather than between formulated and unformulated glutathione as classes.[17] A bioavailability difference is also not an outcome: nothing in that study measured whether the higher exposure changed anything a person would notice.

Delivery is not effect, demonstrated as cleanly as this literature allows. A 6-month multicentre randomized trial nebulised glutathione to 73 people with cystic fibrosis against 80 on placebo. Both primary FEV1 endpoints missed, at P=0.180 and P=0.205. Sputum glutathione and its metabolites rose significantly, so the peptide demonstrably reached the airways; the authors nonetheless report no indication of diminished oxidative stress to proteins or lipids and no evidence of anti-inflammatory or antiproteolytic action.[9]

Parkinson's disease, at two routes, against placebo. A double-blind pilot gave 1,400 mg intravenously three times weekly for four weeks to 21 patients and found no significant difference in Unified Parkinson's Disease Rating Scale change scores.[5] A phase IIb trial randomized 45 patients to intranasal placebo or one of two active amounts for three months; all cohorts improved, including placebo, and the authors state that neither treatment group was superior to placebo.[12]

The clearest positive administered result in this file is an oncology supportive-care result. In 52 patients on a bimonthly oxaliplatin regimen, intravenous glutathione given before each infusion reduced grade 2 to 4 neurotoxicity to 2 patients against 11 on placebo at eight cycles, P=.003, without reducing oxaliplatin's response rate.[4] That is a prevention result for a specific chemotherapy toxicity under oncology supervision.

Skin pigmentation is where oral glutathione has its own trial base, and it is modest. Oral glutathione in 60 medical students lowered melanin indices at all six measured sites but significantly more than placebo at only two.[8] A 12-week trial in 124 women found the winning arm was L-cystine combined with reduced L-glutathione, beating not only placebo but each single ingredient — so the glutathione-alone arm did not carry the effect. Two of that trial's five authors give their affiliation as BCF Life Sciences, an amino-acid ingredient manufacturer, and the remaining three a contract testing laboratory, which this page states for the same reason it states the industry authorship of the 2026 formulation study.[13] A 2025 systematic review characterises oral and topical glutathione as moderately efficacious and unsustainable, notes that roughly equal numbers of the studies it assessed carried low and high risk of bias, and states that intravenous glutathione "is contraindicated due to lack of efficacy and side effects".[16]

Where the evidence is weak

The route that dominates real-world use has no outcome trial. A PubMed search on 1 September 2026 for intravenous glutathione or glutathione infusion together with wellness, anti-aging, energy or detoxification in healthy people or volunteers returned no records. What the literature holds for infused glutathione in healthy people is a pharmacokinetic study in 10 volunteers, in which plasma total glutathione rose from 17.5 to 823 micromoles per litre and then fell with an elimination half-life of 14.1 minutes while urinary excretion rose 300-fold.[3] A molecule that leaves the circulation in a quarter of an hour is a demanding thing to build a wellness claim on.

Near-neighbours are constantly read across, and four of them matter here. N-acetylcysteine is a cysteine precursor and a different molecule with its own approved products and its own literature. GlyNAC is glycine plus N-acetylcysteine, and the 2023 randomized trial reporting that it improves glutathione deficiency and multiple aging hallmarks in older adults administered those two precursors rather than glutathione — a paper whose title contains the word glutathione is not thereby a glutathione trial.[14][7] Glutathione monoethyl ester and S-acetyl-glutathione are separate molecules again; a PubMed search on 1 September 2026 for S-acetyl-glutathione restricted to human records returned one paper, an in-vitro study in cultured lymphoma cell lines, so no human claim about that form has support here. And a formulated preparation is not an unformulated one: the 2026 crossover study described above tested one named proprietary micellar matrix and does not license a claim about formulated glutathione as a class.[17] Glutathione S-transferase genotype studies, which make up a large share of what a naive database search returns, are genetic association papers and carry no information about administering anything.

Endogenous depletion is a marker, and it has repeatedly failed as a justification. The same review that documents the age-related decline also records the inverse observation that elderly people in excellent physical and mental health show heightened glutathione, which makes the level a candidate marker rather than an established lever.[1] The cystic fibrosis programme is the worked example: extracellular lung glutathione is depleted in that disease, inhaled glutathione measurably restored it in sputum, and the clinical endpoints did not move.[9]

Nothing here has been studied long. The randomized trials on this page ran four weeks to six months. A 2016 review that searched MEDLINE to 30 September 2015 across skin-lightening use and all medical indications reported finding no study of long-term intravenous glutathione use for any indication.[11] A PubMed search on 1 September 2026 for glutathione supplementation or administration in randomized controlled trials mentioning twelve months, one year or twenty-four months returned two records, neither of which administered glutathione for a year.

Immune support, the goal this compound is most often filed under, has almost no literature behind it. The one result, described above, is a secondary outcome in a subset of a single trial.[10] A PubMed search on 1 September 2026 for glutathione supplementation or administration with infection or immune endpoints in randomized controlled trials in healthy people returned two records: that trial and a trial of precursors rather than of glutathione. No trial cited here counted an infection.

Legal and regulatory status

Three distinct US regulatory facts sit on top of this one molecule, and most of the confusion about it comes from collapsing them into one.

There is no FDA-approved glutathione drug product for any systemic route. Drugs@FDA returns exactly one application whose active ingredient list contains a glutathione species: NDA 018469, BSS PLUS, held by Alcon — a prescription intraocular irrigating solution used in eye surgery, whose glutathione component is glutathione disulfide, the oxidised form, at 0.184 mg/mL. A second application carrying the same formulation is discontinued. Searches for glutathione, L-glutathione, reduced glutathione and GSH returned nothing else, run in the same session as positive controls for semaglutide and levocarnitine that both returned full prescription approval records. A reader who searches the national drug code directory will find 34 rows for glutathione, and it is worth saying in advance what they are: 16 are bulk active-ingredient registrations, 6 of those explicitly registered for human prescription compounding; 15 are unapproved homeopathic over-the-counter listings; 1 is an over-the-counter monograph topical; and the sole prescription rows in that set, retrieved on 1 September 2026, are the eye-surgery irrigant above. A bulk ingredient registration is a registration of a raw material. It is not an approval of anything.

The compounding position is the real story, and it is an evaluation in progress rather than a decision. Glutathione appears once in FDA's list of bulk drug substances nominated for use in compounding under section 503A, in Category 1, "Bulk Drug Substances Under Evaluation", in the version of that document dated 14 May 2026 and retrieved on 1 September 2026; it appears once in the equivalent section 503B document, again in Category 1. Under FDA's interim policy, a Category 1 listing means the agency does not intend to take action against a compounder using the substance while its evaluation continues, provided the conditions in the guidance are met. That is enforcement discretion pending evaluation. It is not an approval, it is not a compounding authorisation, and it is not a safety clearance. Glutathione does not appear on the final section 503A bulks list at 21 CFR 216.23, either among the six substances included or among the four that FDA determined would not be included, and it does not appear on the final 503B bulks list. It has been neither accepted nor rejected.

An advisory committee looked at it in 2022 and the outcome is easy to misread. At the Pharmacy Compounding Advisory Committee meeting of 8 June 2022, FDA proposed that glutathione not be included on the 503A bulks list. The committee voted 8 yes, 5 no, 1 abstain in favour of adding it — against FDA's own proposal. The recorded reasoning on the "no" side was a lack of scientific evidence of effectiveness for the conditions evaluated, and the abstaining member cited mixed evidence across the many indications under review. That vote is advisory and non-binding, and the outcome above is the proof: glutathione is still absent from 21 CFR 216.23. It is not an FDA endorsement of anything.

FDA has an open safety investigation into injected glutathione, and it is five days old at the time of this review. In a compounding alert published on 27 August 2026, FDA reported at least 30 patients with adverse events after intravenous glutathione compounded by several different pharmacies, all using powder drawn from one lot labelled as dietary supplement grade — which, in FDA's words, is not an appropriate ingredient to make injectable drugs. Reported events were fever, chills, pain, dizziness, signs of shock and sepsis-like symptoms, with some hospitalisations, consistent with excessive endotoxin exposure. Two Texas pharmacies conducted recalls over elevated endotoxin levels, and FDA states it continues to receive reports and is actively investigating. This is the second time: an alert dated 7 June 2019 describes seven patients at one outpatient clinic who developed symptoms within minutes of receiving 1,400 mg intravenous doses compounded from repackaged dietary-supplement-grade L-glutathione, one of whom was hospitalised. The failure mode in both is the same and it is the reason this page separates routes so insistently: the exact commodity sold on a shelf for swallowing is being infused intravenously. A published case report of systemic inflammatory response syndrome after an unregulated cosmetic glutathione infusion describes what that looks like at the bedside.[15]

Outside the US, one regulator's position was retrieved directly. The Philippine Food and Drug Administration's Advisory No. 2019-182 states that there are no published clinical trials evaluating injectable glutathione for skin lightening and no published guidelines for dosing or duration, that it has approved no injectable product for skin lightening, and that injectable glutathione is approved in the Philippines as an adjunct in cisplatin chemotherapy only. It names liver, kidney and nervous-system toxicity, possible Stevens-Johnson syndrome, and transmission of infectious agents where administration occurs outside a sterile facility. That is one jurisdiction's regulatory position, attributed to it and stated as such. It is not an FDA position, it is not an endorsement of the chemotherapy indication for anyone else, and it is not a route to obtaining anything. PHL does not sell anything and does not tell anyone where to obtain anything.

Being lawfully sold as a supplement is a statutory position, not a finding about the molecule. Nothing in that category requires a demonstration of effect, and nothing in it evaluates a product's suitability for any route other than swallowing. The two FDA alerts above are precisely what happens when that distinction collapses: material qualified for a shelf ends up in a vein.

Anti-doping. In the 2026 World Anti-Doping Code International Standard Prohibited List, in force from 1 January 2026 and retrieved from the World Anti-Doping Agency on 1 September 2026 via the United States Anti-Doping Agency's prohibited-list page, a full-text search for glutathione and GSH returned zero hits, and the same search of the 2026 Monitoring Program retrieved the same day also returned zero hits; positive controls for erythropoietin, insulin and testosterone all returned hits in the same document. Absence from the List is never a statement that a substance is permitted. What does reach this compound is written against a route instead of against a molecule: prohibited method M2.2 prohibits intravenous infusions or injections of more than a total of 100 mL per 12-hour period, except for those legitimately received in the course of hospital treatments, surgical procedures or clinical diagnostic investigations. M2.2 is prohibited at all times and is the one prohibited method classed as a Specified Method. It is about volume and route and applies whatever the bag contains, which makes it live for a compound whose dominant real-world delivery is an infusion. The List is reissued annually, so anyone competing under anti-doping rules should read the edition in force at first hand rather than relying on a static page.

Questions to bring to a provider

The compound splits so sharply by route that the first question is which one is actually being discussed. Questions worth raising:

  • Which route is under consideration, and what is the specific evidence for that route rather than for glutathione in general? Oral and intravenous glutathione have different evidence, different regulatory status and different risk.[3]
  • If an infusion is being considered, what is the pharmaceutical grade of the starting material and who assigned the beyond-use date? This is the exact question behind two FDA compounding alerts and a published case of systemic inflammatory response syndrome.[15]
  • What outcome would be expected, on what timescale, and how would anyone tell whether it happened? The trial that measured oxidative-stress markers directly found no change in them.[6]
  • Would supplying precursors answer the same question? The study that corrected the age-related glutathione deficit did it with cysteine and glycine.[7]
  • If skin lightening is the goal, what does the systematic-review evidence actually support at each route, and what is the reasoning behind that review's conclusion on the intravenous one?[16][11]
  • If cancer treatment is under way or planned, how does any antioxidant fit into that plan? The randomized trial cited here measured one specific chemotherapy toxicity under oncology supervision and does not generalise past it.[4]
  • Given that no trial has followed anyone on administered glutathione beyond six months, what would a stopping point or a reassessment look like?[11]

This compound is unusual in the library because it is easy to get and hard to grade. A clinician who separates the swallowed form from the infused one before answering any of the above is reading the literature the way it was actually produced.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Raising body glutathione stores by swallowing glutathione
Human RCT evidence human observational · human RCT

This is the best-supported administered-glutathione claim on the page and it is a biochemical one, and the literature genuinely disagrees with itself. A 1992 pharmacokinetic study in 7 volunteers found that plasma glutathione, cysteine and glutamate did not rise significantly after a single large oral dose and concluded that systemic availability is negligible in man. A 6-month randomized, double-blind, placebo-controlled trial in 54 healthy adults then found that daily oral glutathione raised glutathione by 30 to 35 percent in erythrocytes, plasma and lymphocytes and by 260 percent in buccal cells at the high dose, with levels returning to baseline after a one-month washout, and the authors framed that as a first demonstration. A 2026 randomized crossover study in 14 adults reported that a proprietary micellar formulation produced roughly 2.5-fold higher incremental whole-blood exposure than an unformulated preparation at the amounts given; its authors are employees of the organisations behind the tested product and a patent on that formulation is pending, and the result describes that one formulation rather than formulated glutathione as a class. Single dose and sustained daily dosing are answering different questions.

[2] [10] [17]

Reducing systemic oxidative stress in healthy adults
Human RCT evidence human RCT

A randomized, double-blind, placebo-controlled trial gave 40 adults without acute or chronic disease 500 mg of oral glutathione twice daily for four weeks and set urinary F2-isoprostanes and 8-hydroxy-2'- deoxyguanosine as its primary outcomes. Both missed: F2-isoprostanes at p=0.38 and 8-OHdG at p=0.27, and the authors record that erythrocyte total reduced, oxidized and ratio measures of glutathione status were also unchanged. The 6-month trial that did raise glutathione stores reported a fall in the oxidized-to-reduced ratio in whole blood at six months. Raising a pool and lowering a damage marker are separate results and the trials that looked directly for the second one did not find it.

[6] [10]

Immune function in healthy adults
Human RCT evidence human RCT

This is the claim the compound's category name invites and the evidence for it is one secondary outcome. In the 6-month randomized trial in 54 healthy adults, natural killer cell cytotoxicity increased more than twofold versus placebo at three months in the high-dose group, measured in a subset of participants as part of a secondary battery of immune markers. A PubMed search on 1 September 2026 for glutathione supplementation or administration together with infection or immune endpoints, restricted to randomized controlled trials in healthy people, returned two records: that trial and a separate trial of glutathione precursors rather than glutathione itself. A laboratory measure of immune cell activity moving in a subset is not the same result as fewer or shorter infections, and no trial on this page measured the latter.

[10]

Skin lightening and pigmentation
Human RCT evidence human RCT · review

Oral glutathione has real randomized evidence here and it is modest and route-specific. A 4-week trial in 60 healthy medical students given 500 mg daily found melanin indices fell at all six measured sites but significantly more than placebo at only two, the right side of the face and the sun-exposed left forearm, and the authors described the effect as lightening in a small number of subjects. A 12-week trial in 124 Asian women found that the combination of 500 mg L-cystine with 250 mg reduced L-glutathione beat placebo, L-cystine alone and reduced L-glutathione alone, so the winning arm was the combination and the glutathione-only arm did not carry the effect; two of that trial's five authors give their affiliation as BCF Life Sciences, an amino-acid ingredient manufacturer, and the other three a contract testing laboratory, which is worth knowing about a result whose winning arm is an ingredient combination. A 2025 systematic review concluded that topical and oral glutathione both provide moderately efficacious but unsustainable lightening, that roughly equal numbers of the studies it assessed carried low and high risk of bias, and, verbatim, that intravenous glutathione "is contraindicated due to lack of efficacy and side effects".

[8] [13] [16]

Preventing oxaliplatin-induced peripheral neuropathy
Human RCT evidence human RCT

This is the strongest positive result for administered glutathione in this file, and it is an oncology supportive-care result rather than a wellness one. A randomized, double-blind, placebo-controlled trial in 52 patients on a bimonthly oxaliplatin regimen gave 1,500 mg per square metre intravenously before each oxaliplatin infusion. After eight cycles, grade 2 to 4 neurotoxicity by National Cancer Institute criteria affected 2 patients in the glutathione arm against 11 on placebo, P=.003, with the separation holding at twelve cycles, P=.004, and sural sensory nerve conduction declining significantly in the placebo arm but not the glutathione arm. Response rates were 26.9 versus 23.1 percent, which the authors read as no loss of oxaliplatin activity. Their own word for the compound on this indication is "promising".

[4]

Parkinson's disease
Human RCT evidence human RCT

Randomized trials exist at two routes and neither beat placebo. A double-blind pilot gave 1,400 mg intravenously three times weekly for four weeks to 21 patients and found no significant differences in change in Unified Parkinson's Disease Rating Scale scores; the intravenous arm improved by a mean of 2.8 scale points more over the treatment period at P=0.32 and then worsened by a mean of 3.5 scale points more than placebo over the following eight weeks at P=0.54, and the authors described a possible mild symptomatic effect remaining to be evaluated. A 3-month phase IIb trial randomized 45 patients to intranasal placebo, 100 mg or 200 mg three times daily; every cohort improved including placebo, the high-dose group improved against its own baseline on total and motor scores, and the authors state that neither treatment group was superior to placebo. They also record that the placebo improvement was more robust than in previous Parkinson's studies.

[5] [12]

Cystic fibrosis lung disease
Human RCT evidence human RCT

This trial is the cleanest demonstration in the file that delivery is not effect. A 6-month randomized, double-blind, placebo-controlled multicentre trial nebulised 646 mg of glutathione in 4 mL every 12 hours to 73 people with cystic fibrosis against 80 on placebo. The primary efficacy endpoints, FEV1 as pre-post difference and as area under the curve, both missed at P=0.180 and P=0.205. Sputum glutathione and its metabolites rose significantly, demonstrating that the peptide reached the airways, and the authors report no indication of diminished oxidative stress to proteins or lipids and no evidence of anti-inflammatory or antiproteolytic action. Exacerbation frequency and quality-of-life scores did not improve either.

[9]

Intravenous glutathione for wellness, energy, detoxification or anti-aging in healthy adults
Anecdotal reports only human observational

This is the form most people mean when they say they are getting glutathione, and it is the form with no efficacy literature to grade. A PubMed search on 1 September 2026 for intravenous glutathione or glutathione infusion together with wellness, anti-aging, energy or detoxification in healthy people or volunteers returned no records. What the literature does contain for infused glutathione in healthy people is a pharmacokinetic study in 10 volunteers in which plasma total glutathione rose from 17.5 to 823 micromoles per litre after a 2 g per square metre infusion and then fell with an elimination half-life of 14.1 minutes, while urinary glutathione excretion rose 300-fold. That is a description of how quickly the molecule leaves, with no clinical endpoint attached.

[3]

Aging and healthspan
Anecdotal reports only review · human observational · human RCT

The premise here is real and it is a premise about the molecule the body makes rather than about swallowing or infusing it. A 2023 review of glutathione biochemistry and gerontology describes glutathione levels declining during aging, attributes that decline chiefly to impaired biosynthesis, and notes the opposite observation that elderly people in excellent physical and mental health show heightened glutathione, suggesting a marker and possibly a causative factor. A stable-isotope study in 8 elderly and 8 younger subjects located the deficit precisely: the elderly had markedly lower glutathione fractional and absolute synthesis rates, and two weeks of supplementation with the precursors cysteine and glycine restored synthesis, concentration and oxidative stress markers to the level of the younger group. A 16-week randomized trial of glycine plus N-acetylcysteine in 24 older adults reported the same direction of effect on glutathione deficiency and multiple aging measures. Every one of those interventions supplied precursors rather than glutathione, and a PubMed search on 1 September 2026 for glutathione supplementation or administration in randomized controlled trials mentioning twelve months, one year or twenty-four months returned two records, neither of which administered glutathione for a year.

[1] [7] [14]

Typical protocol range in the research

  • Oral daily amounts given as trial arms in a 6-month randomized, double-blind, placebo-controlled trial in 54 non-smoking healthy adults, and in a 4-week randomized, double-blind, placebo-controlled trial in 40 adults without acute or chronic disease

    250 or 1,000 mg daily for 6 months; 500 mg twice daily for 4 weeks [10] [6]

  • Oral daily amounts given as trial arms in two randomized skin pigmentation trials, the first in 60 healthy Thai medical students over 4 weeks and the second in 124 Asian women over 12 weeks, where the 250 mg figure is the reduced-glutathione-alone arm

    500 mg daily in two divided doses for 4 weeks; 250 mg daily for 12 weeks [8] [13]

  • A single oral pharmacokinetic challenge in 7 healthy volunteers, which is an absorption experiment rather than a treatment schedule; the published amount is a body-weight-scaled molar dose that the authors describe as a single 3 g dose

    0.15 mmol per kg as one oral dose [2]

  • Intravenous amounts given as the active arm of a randomized, double-blind, placebo-controlled pilot trial in 21 people with Parkinson's disease whose motor symptoms were not adequately controlled on their existing regimen

    1,400 mg intravenously three times a week for 4 weeks [5]

  • Intravenous amounts given before each chemotherapy cycle in the active arm of a randomized, double-blind, placebo-controlled trial in 52 adults with advanced colorectal cancer on a bimonthly oxaliplatin-based regimen

    1,500 mg per square metre of body surface area infused over 15 minutes before oxaliplatin [4]

  • A single intravenous pharmacokinetic study in 10 healthy volunteers, which measured disposal rather than any clinical outcome

    2 g per square metre of body surface area as one infusion [3]

  • Inhaled amounts given by nebuliser as the active arm of a 6-month randomized, double-blind, placebo-controlled multicentre trial in 153 people with cystic fibrosis aged 8 and over

    646 mg in 4 mL every 12 hours [9]

  • Intranasal amounts given as the two active arms of a 3-month randomized, double-blind, placebo-controlled phase IIb trial in 45 people with Hoehn and Yahr stage 1-3 Parkinson's disease

    100 mg or 200 mg three times daily [12]

Every entry above names its route, and the routes are not interchangeable. An oral amount and an intravenous amount are different interventions with different absorption, different regulatory status and different risk, and neither reads across to the other. Two kinds of number are deliberately absent. The first is the concentration and per-dose figures that appear in the nomination paperwork asking FDA to add glutathione to the section 503A bulk drug substances list; those describe what a party seeking listing proposed, not an amount any published study administered to anyone. The second is any intake ceiling, tolerable upper intake level or dietary intake estimate, none of which is a dose a trial gave a participant. For the use that brings most people to this compound, no amount is established at all: a PubMed search on 1 September 2026 for intravenous glutathione or glutathione infusion together with wellness, anti-aging, energy or detoxification in healthy people or volunteers returned no records.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

  • Oral supplementation was tolerated in the randomized trials that measured it, with one review dissenting

    No treatment-attributed serious adverse events were reported in the 6-month trial in 54 healthy adults or the 4-week trial in 40 adults · Both randomized trials of oral glutathione in adults without acute or chronic disease reported the compound as tolerated over their study periods. That is a statement about oral capsules over four weeks to six months in trial populations. It is not a statement about indefinite use, and it is not a statement about any other route. Two reviews qualify that picture rather than confirm it. The 2025 systematic review of skin-lightening use sets oral glutathione against topical glutathione, not against the intravenous route, and puts oral on the unfavourable side of its own comparison: topical versus oral, verbatim, "have minimal versus substantial adverse effects". The 2016 review that searched MEDLINE to 30 September 2015 reports that most trials it located described either no or minimal adverse effects, but that every one of them ran only a few intravenous doses or four to twelve weeks.

    [10] [6] [16] [11]

  • Acute systemic inflammatory reactions after intravenous administration of non-pharmaceutical-grade material

    Not quantified as a rate; described in a 2025 case report and in two FDA compounding alerts covering at least 37 patients between them · A published case report describes a previously healthy woman who collapsed with shock and a temperature above 41 degrees Celsius within an hour of receiving a high-dose unregulated intravenous glutathione-containing cosmetic infusion for skin lightening, with marked leucocytosis, acute liver injury and coagulopathy and no infectious source identified; she recovered fully with supportive care. The authors offer two hypotheses and do not choose between them. The syndrome resulted, in their words, from either endotoxin contamination of the unregulated product or a synergistic effect of supraphysiological glutathione in a nutritionally compromised host. The first attaches to the material and the setting, which is the risk the regulatory section describes; the second attaches to the molecule and the amount given, so this report cannot be read as being about contamination alone. The defining context of the case, named in the paper's own title, is that the patient had been self-administering tirzepatide for weight loss with prolonged low nutritional intake — reported here as the circumstance in which this single case occurred, not as a finding about tirzepatide, which the report did not set out to evaluate.

    [15]

  • A cardiomyopathy event in the high-dose arm of the intranasal trial

    One participant of 45 randomized, in the 200 mg three-times-daily group · The phase IIb intranasal trial in Parkinson's disease records that one participant in the high-dose cohort developed cardiomyopathy. A single event in a trial of this size establishes neither a rate nor a causal link, and the trial report does not attribute it. It is recorded here because a page that reports the efficacy result of that trial and omits its one serious event would be reporting the trial selectively.

    [12]

  • A theoretical pigment-related skin cancer concern that has not been studied

    Not established; raised as a mechanism-based concern rather than an observed rate · The proposed skin-lightening mechanism, as the authors of the 12-week combination trial state it, is a skewing of the melanin synthesis pathway toward the production of lighter pheomelanin instead of darker eumelanin. The 2016 review that searched MEDLINE to 30 September 2015 flagged that this switch from brown to red melanin production may increase the risk of sun-induced skin cancers in previously protected individuals, and reported finding no study of long-term use for any indication that could answer the question. Sun-exposure history is a reason to raise this with a clinician rather than a verdict.

    [11] [13]

  • Long-term safety of administered glutathione is uncharacterised at every route

    Not established at any route · The randomized trials on this page ran from four weeks to six months. A 2016 review that searched MEDLINE to 30 September 2015 for glutathione use in skin lightening and across all medical indications reported that it found no study of long-term intravenous glutathione use for any indication, and a PubMed search on 1 September 2026 for glutathione supplementation or administration in randomized controlled trials mentioning twelve months, one year or twenty-four months returned two records, neither of which administered glutathione for a year. Absence of reported harm from a literature that has not looked past six months is not a safety finding.

    [11]

  • Concurrent use with chemotherapy is a clinician's decision, not a self-directed one

    Studied in one randomized trial of 52 patients on an oxaliplatin regimen · The randomized trial cited on this page that gave intravenous glutathione alongside chemotherapy reported response rates of 26.9 percent in the glutathione arm and 23.1 percent in the placebo arm, which the authors read as no reduction in oxaliplatin activity. That is a specific finding about one infusion schedule given immediately before one drug under oncology supervision. Any antioxidant taken during cancer treatment is a provider-discussion flag, and this result does not generalise to other agents, other schedules or unsupervised use.

    [4]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage
Glutathione is supplied as a dry powder, as capsules and tablets for oral use, and as a bulk active ingredient registered for compounding. The dry forms are conventionally kept cool, dry, and protected from light and air, because the reduced tripeptide oxidises to glutathione disulfide on exposure. None of the studies cited on this page was a stability study, so no shelf-life window is established here; where a dry form carries a manufacturer expiry, that document governs rather than a reference page.
Reconstituted storage
A compounded sterile glutathione solution is dispensed by a pharmacy that assigns its own storage conditions and beyond-use date on its own label. That label is the authoritative document. In solution the reduced form is conventionally refrigerated, protected from light, and treated as short-dated.
Reconstitution diluent
Oral capsules, tablets and powders are swallowed and are never reconstituted. Where glutathione reaches a patient as an injection it is a compounded sterile preparation, and the diluent, concentration and beyond-use date are specified on the compounding pharmacy's own label rather than by any general convention. The grade of the starting powder is the load-bearing question here rather than the choice of diluent: FDA has twice warned compounders that dietary-supplement-grade glutathione is not an appropriate ingredient for an injectable drug.
Reconstitution & handling
PHL publishes no volume, unit or concentration arithmetic for this compound, because those are dosing and preparation decisions and, for a prescription-only compounded sterile preparation, they belong to the prescribing clinician and the dispensing pharmacy. General handling conventions for a dispensed sterile solution are to keep the stopper sanitized, protect the solution from light, and discard anything cloudy, discolored or carrying visible particulate.
Handling notes
There is no FDA-approved glutathione drug product for oral, intravenous, inhaled or intranasal use, so there is no manufacturer label, no approved stability programme and no lot-level release testing standing behind any general storage claim about those forms. The single approved US product containing a glutathione species is an intraocular surgical irrigating solution, and its labeling describes that product only.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

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Citations

17 sources · every identifier checked against PubMed

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