Peptide Decoding
Understanding compounds

Glutathione by Mouth, IV, IM or Nebulized: What Has Actually Been Studied?

By the Peptide Decoding Editorial Team
Published October 21, 2026
White capsules, an injection vial, a nasal spray and a topical cream jar arranged on a counter — the delivery routes compared on this page
The short version

The two routes people inject have no human trial behind them. The best trial ever run used a nebulizer, and it failed.

Glutathione, written GSH on most labels and certificates, gets sold for seven delivery routes, and a result for one is routinely treated as a result for the rest. They do not share an evidence base, and they are not even close. Two routes have a six-month randomized trial behind them, and the larger of the two failed. Two more were tested against placebo and came out null. One has an uncontrolled pilot in 12 people. Two have nothing at all, and those two are the ones sold in vials.

What does the glutathione evidence look like route by route?

Set side by side, the gap between the routes people study and the routes people buy is the whole story. Figures below were checked on October 20, 2026.

Route Best human evidence Size Result
By mouth Richie et al. 2014, Eur J Nutr, randomized, double-blind, placebo-controlled, 6 months1 54 adults Blood glutathione rose 30 to 35% at 1,000 mg/day
By mouth, liposomal Sinha et al. 2018, Eur J Clin Nutr, uncontrolled pilot, 1 month2 12 adults Whole blood up to 40%, no placebo arm
Nebulized Griese et al. 2013, Am J Respir Crit Care Med, randomized, double-blind, placebo-controlled, 6 months3 153 people with cystic fibrosis Primary endpoint not met (p = 0.180 and p = 0.205)
Intranasal Mischley et al. 2017, J Parkinsons Dis, randomized, double-blind, placebo-controlled, 3 months4 45 people with Parkinson's Not superior to placebo (p = 0.5581 and p = 0.3817)
Intravenous Hauser et al. 2009, Mov Disord, randomized, double-blind pilot, 4 weeks5 21 people with Parkinson's No significant difference (p = 0.32)
Intravenous, cosmetic Zubair et al. 2016, J Pak Assoc Dermatol, placebo-controlled, 12 injections over 6 weeks6 50 enrolled, 32 analyzed Not significant against placebo (p = 0.054); every treated subject had an adverse effect
Topical Watanabe et al. 2014, Clin Cosmet Investig Dermatol, randomized, double-blind, placebo-controlled split-face, 10 weeks7 30 women Melanin index fell to 243.5 against 265.5 on placebo (P < 0.001)
Intramuscular None found None Nothing published
Subcutaneous None found None Nothing published

Three things in that table deserve a second look. Both of the properly placebo-controlled trials, nebulized and intranasal, failed against placebo. The liposomal form is sold specifically as the fix for poor oral absorption, and it rests on a 12-person study with no control group. That is weaker evidence than the plain oral capsule has. The two routes with an empty column, meanwhile, are the two that a person reading about glutathione on a peptide site is most likely to be considering.

Does oral glutathione actually raise glutathione in your body?

Yes. That was a real question until fairly recently.

For years the standard objection ran that swallowed glutathione gets broken down in the gut before it reaches circulation. If true, oral dosing would be pointless. Richie and colleagues tested it directly. Fifty-four non-smoking adults, six months, blinded, with a placebo arm, taking either 250 or 1,000 mg a day.1

Glutathione rose in every compartment they measured. At six months on the higher dose, mean levels were up 30 to 35% in red blood cells, plasma and lymphocytes, and up 260% in cheek cells. The lower dose raised whole blood by 17% and red cells by 29%. The ratio of oxidized to reduced glutathione fell in both dose groups, the direction you would want. Natural killer cell activity was more than twice as high as placebo at three months in the high-dose group. Levels returned to baseline after a month off.1

Two caveats belong with that. The supplement was provided by a manufacturer and the lead author reports research support from them.1 That does not make the result wrong. That is not a disqualification. It does mean the result wants independent replication. The participants were also 76% female, and the authors say the findings should not be generalized to men without caution.1

What the trial establishes is that oral dosing moves a blood marker. Whether a higher blood marker produces anything a person would notice is a separate question, and this trial was not built to answer it.

Is liposomal glutathione better absorbed than regular capsules?

The evidence for it is weaker than the evidence for the plain version, and it is sold on the opposite claim.

Liposomal glutathione wraps the molecule in a fat bubble, and the pitch is that this carries it past the gut breakdown that the plain form is accused of. Sinha and colleagues gave 500 or 1,000 mg a day of a liposomal form to 12 healthy adults for a month.2 Whole blood glutathione rose up to 40%, red cells 25%, plasma 28%, and mononuclear cells 100%, all at p<0.05. Plasma 8-isoprostane, a marker of oxidative damage, fell 35%. Natural killer cell activity was up to 400% higher by week two.2

Those percentages look larger than the oral trial's while resting on a much weaker design: twelve people, one month, no placebo group stated anywhere in the abstract, and no measurable difference between the two doses despite one being double the other. The authors call the findings preliminary and say "statistical power was limited due to the small sample size in this study."2 One of the authors is also the lead author of the 54-person oral trial, so the two results come from the same lab.12

Set the two side by side and the comparison does not favor the liposomal form, because the plain capsule brings six months, 54 participants, blinding and a placebo arm, where the liposomal product brings one month, twelve participants and nothing to compare them against. Bigger numbers from a weaker design are not evidence of better absorption. That is where the comparison lands, and no study has given the same people both forms.

What happened in the best-designed glutathione trial?

It delivered the drug, confirmed it arrived, and changed nothing that mattered.

Griese and colleagues gave 646 mg of nebulized glutathione or placebo every 12 hours to 153 people with cystic fibrosis aged 8 and up, for six months, with neither patients nor investigators knowing who got which.3 Cystic fibrosis is a reasonable place to test this, because glutathione is the main antioxidant in the fluid lining the lung and it is depleted in that disease.

The primary endpoint was lung function, measured as FEV1, the volume of air a person can force out in one second. It did not differ between groups, at p = 0.180 analyzed one way and p = 0.205 analyzed the other. An exploratory look found a 100 mL advantage at three months that did not hold later. Glutathione did not reduce flare-ups or improve quality-of-life scores.3

The part that matters for every other route is what they measured in the sputum. Glutathione and its metabolites rose, so the drug reached the airway. There was also no sign of reduced oxidative damage to proteins or lipids, and no anti-inflammatory or antiprotease effect.3

Getting glutathione into the target tissue and getting a result are two different things. The only trial large enough and well-controlled enough to separate them is this one, and it separated them in the unwelcome direction.

Did intranasal glutathione work for Parkinson's?

No, and the placebo group is the reason the result is interesting.

Mischley and colleagues randomized 45 people with Parkinson's to intranasal saline, 300 mg a day of glutathione or 600 mg a day, three times daily for three months, blinded throughout.4 Every group improved, including placebo. The high-dose group improved on total symptom score by 4.6 points from baseline at p = 0.0025. That looks like a result until you compare arms. Against placebo at week 12 the p values were 0.5581 for the lower dose and 0.3817 for the higher one.4

The placebo group fell by 3.4 points on the same scale. The authors call that a more robust placebo response than previous Parkinson's studies had recorded, and it is the number doing the real work in this trial.4 One high-dose participant developed cardiomyopathy and withdrew.4

This trial is the clearest illustration on the page of why within-group improvement means little. A page reporting only that glutathione improved Parkinson's symptoms by 4.6 points at p = 0.0025 would be quoting this trial accurately, citing a real controlled study, and describing the finding entirely wrongly.

What has IV glutathione, including the drip, been tested for?

The published trial record is small. The use people actually buy it for is not in it.

Hauser and colleagues randomized 21 people with Parkinson's disease to 1,400 mg of intravenous glutathione three times a week or placebo, for four weeks, with eight weeks of follow-up.5 Symptom scores improved by 2.8 units more on glutathione during treatment, at p = 0.32, then worsened by 3.5 units more afterward, at p = 0.54. Neither is significant. The authors describe it as well tolerated with no safety concerns identified, and as suggesting a possible mild effect needing a larger study.5

A trial of 21 people over four weeks is a pilot. It neither establishes nor rules out anything, and the authors say as much themselves.

Skin lightening is the use that drives most of the cosmetic market, and one trial with a saline control has tested it.

Zubair and colleagues enrolled 50 women aged 25 to 47 at a hospital dermatology department in Pakistan. One group got 1,200 mg of glutathione with vitamin C intravenously twice a week for six weeks, twelve injections in all, and the other got intravenous saline.6 Skin tone was read off standardized shade cards at two sun-protected sites by two independent observers, at baseline, after the course, and again at two, four and six months.6

Nine participants were removed before analysis, eight of them for deranged liver function and one for anaphylactic shock, along with their matched controls, leaving 16 per group.6

At the end of treatment 37.5% of the glutathione group had improved against 18.7% on saline, at p = 0.054.6 By six months it was one woman out of sixteen, against none on saline.6 The authors conclude that glutathione "is not very effective for skin tone lightening," that it "loses its efficacy with time," and that "our study does not recommend glutathione for skin lightening."6

The safety table is the part that travels. Every one of the 25 originally treated subjects reported at least one adverse effect and none of the controls did: warmth during injection in 44%, abdominal cramps in 40%, deranged liver function in 32%, a sinking feeling in the heart in 28%, diarrhea and paresthesia in 16% each, dizziness in 12%, and anaphylactic shock in one person.6

One trial with 32 analyzed participants does not close a question. It is the only controlled test of the use that sells the most vials, it found no significant benefit, and a third of the treated group developed abnormal liver function.

Does topical glutathione lighten skin?

On one measure, in one trial, yes. This is the clearest positive result on the page. It belongs to the route nobody injects.

Watanabe and colleagues applied a 2% oxidized glutathione lotion to one side of the face and an identical lotion without it to the other side, in 30 Filipino women aged 30 to 50, twice daily for ten weeks.7 Split-face design makes each woman her own control. That removes most of the variation that sinks small skin studies. Neither the women nor the investigators knew which side had which.7

Melanin index on the treated side fell from 272.8 to 243.5 while the placebo side went from 274.1 to 265.5, a separation that held from week one onward and reached P < 0.001 by week ten.7 Wrinkle and keratin measures also favored the treated side at several timepoints; elasticity did not differ.7 One woman had mild facial redness on days two and three that cleared by day four, and every participant finished.7

Two cautions belong with that result. The compound is oxidized glutathione, GSSG, not the reduced form sold in vials, and the paper does not claim the two behave alike.7 The authors also work for the company that supplied the GSSG. That is the same company that supplied the capsules in the six-month oral trial and funds its lead author.17 A single manufacturer sits behind the two most favorable results on this page. That does not make either wrong. It means neither has been independently reproduced.

Is injectable glutathione approved anywhere?

One narrow medical purpose in one country carries an approval. Cosmetic use carries none anywhere this page checked.

The Philippine FDA advisory on this is unusually specific. It states that "injectable glutathione is approved by FDA Philippines as an adjunct treatment in cisplatin chemotherapy," and separately that "the FDA has not approved any injectable products for skin lightening."8 Those two sentences sit in the same document, and people quoting either one tend to drop the other.

The advisory also records that "there are also no published guidelines for appropriate dosing regimens and duration of treatment" for the cosmetic use.8 A regulator saying no dosing guidance exists is a stronger statement than a website saying the evidence is thin.

In the United States no injectable glutathione product is FDA approved for any purpose.

What human evidence exists for intramuscular or subcutaneous (SubQ) glutathione?

This page could find none. The search itself is the finding.

Searching for controlled human studies of intramuscular or subcutaneous glutathione returns no journal articles. Every result on the first page of those searches was a seller's blog, a supplement marketer or a clinic page. Several carry titles promising exactly what a reader wants: route comparisons, bioavailability figures, peak-level data. None of them cites a trial, because there does not appear to be one to cite.

That absence needs stating precisely. It does not mean injected glutathione does nothing. A substance can work without a published trial behind it, and glutathione given intravenously plainly reaches the bloodstream. What it means is that any number you read comparing subcutaneous to intramuscular absorption, or stating how long a shot lasts, was not measured in a person and published. It was asserted by someone selling the vial.

Our guide on why so many peptides have no human evidence covers how this pattern arises across the category.

Does the route change the glutathione dosage?

The route changes the dose completely. The figures in circulation mix all of them together.

The published figures sit in different units of magnitude and in different contexts. Richie used 250 and 1,000 mg a day by mouth over six months.1 Griese used 646 mg nebulized every 12 hours.3 Mischley used 300 and 600 mg a day intranasally.4 Hauser used 1,400 mg intravenously three times a week.5

Those are four different routes, four different schedules and four different diseases or populations. That is four reasons the figures do not transfer, and not one of the four studies was designed to let them. Lining those numbers up next to each other produces a ratio that means nothing.

A single "250 to 1,000 mg" range quoted without a route attached is therefore an oral figure doing duty for everything. Our own compound page carried exactly that problem and flagged it for correction. If you see that range on a vial listing, it came from a swallowing study.

No published study has given the same people glutathione by two different routes and compared what happened. Without that, there is no conversion factor between routes, and anyone offering one has made it up.

Does timing around exercise change what glutathione does?

Nobody has tested timing as a variable.

A 2019 review of glutathione and its precursors in athletes collects what exists.4 Individual studies dose before exercise, and the review quotes several: 6 mmol/kg given to mice an hour before exercise, 1,800 mg of N-acetylcysteine 45 minutes before a test in humans, an infusion running before and through exercise, six grams daily for three days before a rowing test.9 Those are all pre-exercise by design.

Not one of them compares pre-exercise dosing against post-exercise, or morning against evening. The review never raises the question, because no study in it was built to answer it.9

A fair word for the other side: there is a plausible mechanistic reason to think timing could matter, since exercise itself depletes glutathione and generates the reactive molecules it clears. Plausible is where that argument stops, because a mechanism that would predict an effect is not a measurement of one. Advice to take glutathione at a particular point around training extrapolates from the fact that some studies happened to dose before exercise. Those studies were not testing when to dose.

What are the side effects of glutathione injections?

A regulator has named specific harms. No systematic adverse event record exists for the homemade version.

The Philippine FDA advisory names toxic effects on the liver, kidneys and nervous system, raises Stevens-Johnson syndrome as a possibility, notes theoretical long-term skin cancer concerns, and warns about transmission of infectious agents including HIV and hepatitis B and C from injection practice.8 Where vitamin C is given alongside it, the advisory adds kidney stone risk in acidic urine and reports hemodialysis following large vitamin C doses in people with G6PD deficiency.8

Our existing compound record also lists asthma as a contraindication, because inhaled forms have triggered attacks.

The one controlled trial of cosmetic IV use puts numbers on some of that. Every one of the 25 treated women reported at least one adverse effect and none of the 25 controls did, with deranged liver function in 32% and anaphylactic shock in one person.6 That happened in a hospital with clinicians present, and the 32% figure is hard to wave off on those terms.

Trials in the medical indications read differently. Hauser reported adverse events similar between groups with no withdrawals for them.5 Griese reported similar incidence between groups.3 Both used pharmaceutical-grade product under supervision, and neither was giving 1,200 mg with vitamin C twice weekly.

The gap between a supervised infusion and a bathroom is real on top of all of that. Infection risk and product sterility do not come from the molecule. Our guide on when an injection site reaction means stop and get seen covers which reactions need attention, and it applies here whatever the compound.

How many sellers list a route nobody has studied?

Almost all of them: 127 of the 130 sellers with a glutathione listing also sell a vial. What matters is how those listings split by form.

In our October 21, 2026 vendor capture, glutathione appeared in 191 single-compound listings across 130 sellers. A hundred and seventy-eight of those 191 are vials. Seven are liquids, four are sprays and two are dissolving strips. Not one is a capsule or a tablet.10

Vials are sold to be injected. The injected routes are the two with no published human trial, and the one intravenous study in the record ran four weeks in 21 people.5 Meanwhile the route with the six-month trial behind it, the one that actually raised glutathione in blood, red cells and lymphocytes, is a capsule, and the capsule is sold by none of these 130 sellers.110

So the market and the evidence point in opposite directions, almost perfectly. The gap this whole page describes, stated in listings.

What would settle the route question?

One study design would answer most of this. Nobody has run it.

It would need:

  • the same participants given glutathione by two or more routes, in a crossover, so the comparison is within-person
  • blood and tissue glutathione measured on each route, not just blood
  • an outcome someone would notice, since the nebulized trial showed delivery and effect are separable3
  • long enough to matter, meaning months and not weeks on the oral trial's evidence1
  • enough participants that a null result means something, since 21 does not5

An experiment of that shape does not exist. Until it does, what the evidence supports is narrow.

Oral dosing demonstrably raises a blood marker. Nebulized and intranasal delivery both reached the target tissue and both failed against placebo. Intravenous use has one small null pilot and one narrow approved medical indication abroad. The liposomal form has a 12-person study with no control group. The two injected routes people actually buy have never been studied in a person at all.

Common questions

Is injected glutathione better than oral?

Nobody has compared them in the same people. Oral has a six-month randomized trial in 54 adults showing a 30 to 35% rise in blood glutathione. Intramuscular and subcutaneous have no published human trial of any size.

Does oral glutathione get absorbed?

Yes. A six-month blinded trial against placebo, in 54 adults, found glutathione up 30 to 35% in red cells, plasma and lymphocytes at 1,000 mg a day, and up 260% in cheek cells. The supplement was supplied by a manufacturer, so independent replication would help.

How much glutathione should I take by injection?

No published study supports a number. The dose figures in circulation come from oral studies at 250 to 1,000 mg a day, a nebulized trial at 646 mg twice daily, and an intravenous Parkinson's pilot at 1,400 mg three times a week. None of those was chosen to transfer to another route.

Is there a conversion between oral and injected glutathione doses?

No. No study has given the same people glutathione by two routes and compared the result, so there is no measured ratio between them. Any conversion factor you are shown was not derived from data.

What is the strongest glutathione trial?

The nebulized cystic fibrosis trial, with 153 participants over six months, blinded and placebo-controlled. It is also negative: lung function did not differ from placebo at p = 0.180, and no reduction in oxidative damage markers was seen even though the drug reached the airway.

Does IV glutathione work for Parkinson's?

The one randomized trial, in 21 people over four weeks, found no significant difference. Scores improved 2.8 units more on glutathione during treatment at p = 0.32, then worsened 3.5 units more afterward at p = 0.54. The authors call it a possible mild effect needing a larger study.

Is glutathione injection approved by the FDA?

Not in the United States, for any purpose. In the Philippines, injectable glutathione is approved as an adjunct in cisplatin chemotherapy, and the Philippine FDA states separately that no injectable product is approved there for skin lightening.

Is IV glutathione safe for skin whitening?

In the one trial with a saline control, every treated subject had at least one adverse effect and no control did. Deranged liver function affected 32% and one person had anaphylactic shock. The Philippine FDA separately names toxic effects on the liver, kidneys and nervous system and raises Stevens-Johnson syndrome as a possibility.

Does IV glutathione actually lighten skin?

Not significantly. A trial of twelve injections over six weeks found 37.5% improved against 18.7% on saline, at p = 0.054. At six months it was one woman in sixteen against none. The authors state that their study does not recommend glutathione for skin lightening.

Is an IV glutathione drip worth it?

The only controlled test of the cosmetic drip found no significant benefit at p = 0.054, and every treated subject had an adverse effect. For Parkinson's, the one randomized trial in 21 people also found no difference. No trial has tested a drip for general wellness.

Does topical glutathione work?

On pigment, in one trial, yes. A split-face trial in 30 women using a 2% oxidized glutathione lotion twice daily for ten weeks saw melanin index drop to 243.5 on the treated side against 265.5 on the placebo side, at P < 0.001. The form tested was oxidized glutathione, not the reduced form sold in vials.

Does subcutaneous glutathione work?

No published human study has tested it. Pages offering subcutaneous absorption figures or peak-level data are not citing trials, because none were found.

Glutathione IM vs IV: is there a difference?

Not one that has been measured. Intravenous has two published trials, a Parkinson's pilot and a skin-lightening trial, both null. Intramuscular has none. No study has given the same people both routes, so a claim that one absorbs better is not coming from data.

Should I take glutathione before or after a workout?

No study has tested timing as a variable. Some studies happened to dose before exercise, and dosing before exercise is not the same as comparing before against after. No review found a study that made the comparison.

Does glutathione help athletic performance?

A 2019 review collects small studies on glutathione and its precursors reporting less fatigue and longer endurance, much of it in animals or in small human groups. The review draws no firm conclusion about performance and spends its conclusion on doping risk instead.

Is liposomal glutathione better than regular oral glutathione?

No study has compared them in the same people. The liposomal evidence is a 12-person uncontrolled pilot over one month. The plain oral evidence is a 54-person blinded trial against placebo, run over six months. The weaker design produced the bigger percentages.

Does intranasal glutathione work?

Not against placebo. A 45-person blinded trial in Parkinson's found every arm improved, including saline, and neither glutathione dose beat placebo at week 12, at p = 0.5581 and p = 0.3817.

Should I take NAC instead?

N-acetylcysteine is a glutathione precursor and it has more human exercise and Parkinson's literature behind it than glutathione itself does. This page did not assess whether it works, and a precursor having more studies is not the same as it having better results.

Can nebulized glutathione trigger asthma?

Asthma is listed as a contraindication for inhaled forms because they have triggered attacks. In the 153-person cystic fibrosis trial, overall adverse event rates were similar between the glutathione and placebo groups.

Why do injection reactions get reported if there are no trials?

Reports come from clinical case literature and regulator advisories, not from trials, since no trial of intramuscular or subcutaneous glutathione exists. Infection and sterility risk come from injection practice and product quality, not from the molecule.

How long does glutathione last in the body?

Its measured half-life is in minutes, and that figure describes the intravenous route. Oral glutathione behaves differently, and the six-month oral trial measured stored levels in tissue compartments rather than circulating half-life.

Sources

Sources

  1. Richie JP Jr, Nichenametla S, Neidig W, Calcagnotto A, Haley JS, Schell TD, Muscat JE. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. European Journal of Nutrition. 2014. DOI 10.1007/s00394-014-0706-z. Tier: full text read via an open copy of the published PDF at national-toxic-encephalopathy-foundation.org; the publisher page was not opened and the volume and page numbers are not in the copy read. Six-month randomized, double-blind, placebo-controlled trial, 54 non-smoking adults, 250 or 1,000 mg/day oral. At six months on the high dose, mean glutathione up 30 to 35% in erythrocytes, plasma and lymphocytes and 260% in buccal cells; low dose up 17% in whole blood and 29% in erythrocytes; reported as P<0.05 without exact values. Oxidized to reduced ratio fell in both dose groups at six months. Natural killer cytotoxicity more than twofold higher than placebo at three months in the high-dose group (P<0.05). Levels returned to baseline after a one-month washout in most cases. Discussion notes 76% of subjects were female, that findings should not be generalized to men without caution, and that the supplement was provided by Kyowa Hakko Bio Co., Ltd., from which the lead author reports research support. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10
  2. Sinha R, Sinha I, Calcagnotto A, Trushin N, Haley JS, Schell TD, Richie JP. Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function. European Journal of Clinical Nutrition. 2018;72(1):105-111. DOI 10.1038/ejcn.2017.132. PMID 28853742. Registered NCT02278822. Tier: abstract read via an institutional repository record at pure.psu.edu; the publisher page was not opened and PubMed returned a browser verification page. A one-month pilot in 12 healthy adults at 500 or 1,000 mg/day of oral liposomal glutathione, assessed at baseline and at 1, 2 and 4 weeks. The abstract does not state that the study was randomized or placebo-controlled, and no control arm is described, so this page treats it as uncontrolled. Rises appeared by week 1 and peaked at week 2, all P<0.05: whole blood up to 40%, erythrocytes 25%, plasma 28%, peripheral blood mononuclear cells 100%. Plasma 8-isoprostane fell 35% and the oxidized to reduced ratio fell 20%, both P<0.05. Natural killer cytotoxicity up to 400% higher by week 2 and lymphocyte proliferation up to 60% higher after 2 weeks, both P<0.05. No differences between the two dose groups. The abstract states that "statistical power was limited due to the small sample size in this study" and the authors describe the findings as preliminary. James P. Richie is an author here and the lead author of the oral trial at note 1, so the two results come from the same group. ↩1 ↩2 ↩3 ↩4 ↩5
  3. Griese M, Kappler M, Eismann C, et al., and the Glutathione Study Group. Inhalation treatment with glutathione in patients with cystic fibrosis. A randomized clinical trial. American Journal of Respiratory and Critical Care Medicine. 2013 Jul 1;188(1):83-89. DOI 10.1164/rccm.201303-0427OC. PMID 23631796. Registered NCT00506688 and EudraCT 2005-003870-88. Tier: abstract read at source via the PubMed listing; the full text behind the publisher link was not retrieved, so no adverse event breakdown or confidence intervals are quoted. Randomized, double-blind, placebo-controlled. People with cystic fibrosis aged 8 or older with FEV1 40 to 90% predicted. 646 mg glutathione in 4 mL (n = 73) or placebo (n = 80) nebulized every 12 hours via an investigational eFlow nebulizer for six months. Primary endpoint absolute FEV1, pre-post difference P = 0.180 and area under the curve P = 0.205, neither differing between groups. An exploratory analysis found a 100 mL or 2.2% predicted advantage, significant at three months and not later. No reduction in pulmonary exacerbations and no quality-of-life improvement. Sputum glutathione and metabolites rose, demonstrating delivery, with no sign of reduced oxidative stress to proteins or lipids and no anti-inflammatory or antiproteolytic effect. Adverse event incidence similar between groups. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7
  4. Mischley LK, Lau RC, Shankland EG, Wilbur TK, Padowski JM. Phase IIb study of intranasal glutathione in Parkinson's disease. Journal of Parkinson's Disease. 2017;7(2):289-299. DOI 10.3233/JPD-161040. Published online April 20, 2017. PMID 28436395. Registered NCT02424708. Tier: abstract and record page read at source via the publisher at journals.sagepub.com; the full text was not retrieved and the page truncates the author list, so additional authors may be omitted above. Double-blind, placebo-controlled, 45 people with Hoehn and Yahr stage 1 to 3 Parkinson's, randomized to intranasal saline, 100 mg glutathione or 200 mg glutathione three times daily for three months with a one-month washout, corresponding to 300 and 600 mg per day. Primary outcome was change in total and motor UPDRS, testing whether phase I/IIa improvements reproduced. All cohorts improved including placebo. High-dose group improved on total UPDRS by 4.6 points (SD 4.7, P = 0.0025) and motor UPDRS by 2.2 points (SD 3.8, P = 0.0485) from baseline. Neither glutathione group was superior to placebo; between-group P values at week 12 against placebo were 0.5581 for 300 mg/day and 0.3817 for 600 mg/day on total UPDRS. Placebo total UPDRS fell 3.4 points (SD 6.2), P = 0.0590, which the authors describe as a more robust placebo response than prior Parkinson's studies; placebo motor scores did not improve. No standardized effect sizes are reported. One high-dose participant developed cardiomyopathy and withdrew; other withdrawals included sinus irritation and headaches in the placebo arm and under-eye puffiness in the 300 mg/day arm. Authors conclude the data do not suggest intranasal glutathione is superior to placebo after three months. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7
  5. Hauser RA, et al. Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson's disease. Movement Disorders. 2009. DOI 10.1002/mds.22401. PMID 19230029. Tier: abstract read via a reproduction at researchgate.net; the publisher page refused retrieval and PubMed returned a browser verification page, so the full author list, volume and pages are not confirmed here and the attribution to Hauser 2009 is taken from how other pages in that record cite it. Randomized, placebo-controlled, double-blind pilot in people with Parkinson's whose motor symptoms were not adequately controlled. 21 randomized, 11 to glutathione and 10 to placebo, with one glutathione participant withdrawing before any post-randomization assessment. 1,400 mg intravenously three times a week for four weeks, then eight weeks of observation. No named primary outcome; objective was safety, tolerability and preliminary efficacy, with UPDRS used for efficacy. ADL plus motor scores improved 2.8 units more on glutathione during treatment (P = 0.32) and worsened 3.5 units more over the following eight weeks (P = 0.54). Adverse events similar in both groups with no withdrawals for them. Authors state glutathione was well tolerated with no safety concerns identified, and describe a possible mild symptomatic effect needing confirmation. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7
  6. Zubair S, Hafeez S, Mujtaba G. Efficacy of intravenous glutathione vs. placebo for skin tone lightening. Journal of Pakistan Association of Dermatologists. 2016;26(3):177-181. jpad.com.pk. Tier: full text read at source as the publisher PDF. Placebo-controlled trial at a dermatology department in Multan, Pakistan, January 2014 to August 2015. 50 female participants aged 25 to 47 randomized to two groups of 25. Group A received GSH Detox forte 1,200 mg with ascorbic acid, 5 mL diluted in 10 mL distilled water, intravenously over 30 minutes twice weekly for six weeks, 12 injections total; group B received intravenous normal saline. Skin tone graded on Taylor hyperpigmentation scale cards at two sun-protected sites by two independent observers at baseline, after 12 injections, and at 2, 4 and 6 months. Nine group A participants were excluded from analysis, eight for deranged liver function tests and one for anaphylactic shock, with matched controls excluded, leaving 16 per group. Efficacy at end of treatment 6 of 16 (37.5%) against 3 of 16 (18.7%), P = 0.054, not significant. At 2 months 18.7% against 12.5%; at 4 months 18.7% against 0; at 6 months 1 of 16 (6.2%) against 0. Adverse effects in group A as originally enrolled (n = 25): warmth during injection 11 (44%), abdominal cramps 10 (40%), deranged liver functions 8 (32%), feeling of heart sinking 7 (28%), diarrhea 4 (16%), paresthesia 4 (16%), dizziness 3 (12%), anaphylactic shock 1 (4%), vomiting 1 (4%). All group A subjects reported at least one adverse effect and no group B subject reported any. The paper does not describe the randomization method or blinding of participants, and the two groups were drawn at a single center. Authors conclude that glutathione "is not very effective for skin tone lightening," that it "loses its efficacy with time," and that "our study does not recommend glutathione for skin lightening." ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9
  7. Watanabe F, Hashizume E, Chan GP, Kamimura A. Skin-whitening and skin-condition-improving effects of topical oxidized glutathione: a double-blind and placebo-controlled clinical trial in healthy women. Clinical, Cosmetic and Investigational Dermatology. 2014;7:267-274. DOI 10.2147/CCID.S68424. dovepress.com. Tier: full text read at source via the publisher. No PMID is displayed on the publisher page and none is asserted here. Randomized, double-blind, matched-pair, placebo-controlled split-face trial. 80 Filipino women screened, 30 enrolled, aged 30 to 50, mean 36.1 (SD 5.3), Fitzpatrick phototype III or IV, selected for a small left-right melanin difference and a face melanin index of 200 to 350. About 0.5 g of a 2% w/w oxidized glutathione (GSSG) lotion applied to one side of the face twice daily for 10 weeks, with an identical GSSG-free lotion on the other side, both at pH 6.46. Participants avoided other whiteners, moisturizers, makeup and oral vitamin C, E and A on the test sites. Primary outcome melanin index by Mexameter MX18 at the cheekbone. Melanin index mean (SD): placebo side 274.13 (25.82) at week 0 and 265.50 (25.81) at week 10; GSSG side 272.77 (26.17) at week 0 and 243.47 (26.31) at week 10, lower than placebo from week 1 through week 10 and P < 0.001 at week 10. Moisture higher on the GSSG side at weeks 8 and 9; curvature index for wrinkles lower at weeks 6 and 10; keratin index lower from weeks 6 to 10; elasticity no difference. Investigator-rated whitening score of 2 or more at week 10 in 66.7% against 3.3%, subject-rated 76.7% against 23.3%. One subject had mild whole-face erythema on days 2 to 3, resolved by day 4 without stopping either lotion; no adverse reactions attributed to GSSG; all subjects completed. The paper states the study received no specific outside grant and the authors declare no conflicts, while the authors are affiliated with Kyowa Hakko Bio Co., Ltd., which supplied the GSSG; lotions were made by Cathy Chemical Industry Co., Ltd. Methods name the Wilcoxon signed-rank test while the abstract names analysis of variance, which the paper does not reconcile. Authors describe the mechanism as speculative and note the absence of long-term safety data. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
  8. Philippine Food and Drug Administration. FDA Advisory No. 2019-182, unsafe use of glutathione as a skin lightening agent. fda.gov.ph. Tier: read at source; the page does not display a date beyond the advisory number. Quoted lines: "toxic effects on the liver, kidneys, and nervous system"; Stevens Johnson Syndrome named as "a possibility"; "theoretical concerns about the long term skin cancer risk"; "transmission of infectious agents, such as HIV, hepatitis C and B"; "There are also no published guidelines for appropriate dosing regimens and duration of treatment"; "The FDA has not approved any injectable products for skin lightening"; "Injectable glutathione is approved by FDA Philippines as an adjunct treatment in cisplatin chemotherapy". On co-administered vitamin C it states that "Vitamin C injection may form kidney stones if the urine is acidic" and that "Large doses of Vitamin C have resulted in hemodialysis" in people with G6PD deficiency. ↩1 ↩2 ↩3 ↩4
  9. Grucza K, Chołbiński P, Kwiatkowska D, Szutowski M. Effects of supplementation with glutathione and its precursors on athlete performance. Biomedical Journal of Scientific and Technical Research. 2019;12(4):001-008. DOI 10.26717/BJSTR.2019.12.002293. biomedres.us. Tier: read at source. A narrative review covering glutathione and precursors including N-acetylcysteine, cysteine-rich whey, L-glutamine and alpha-lipoic acid, much of it animal work or small human studies. Oral glutathione entries include 1 g/day for two weeks in men and mouse studies at 6 mmol/kg intraperitoneally and 500 to 1,000 mg/kg. Dosing timings quoted in individual studies: mice given 6 mmol/kg one hour before exercise; 1,800 mg N-acetylcysteine 45 minutes before an exercise test; an N-acetylcysteine infusion before and throughout exercise; 6 g for three days before a six-minute maximal rowing test. The review does not test or compare timing as a variable and does not discuss morning against evening dosing. Its conclusion focuses on the link between supplement use and doping risk rather than on performance benefit. ↩1 ↩2
  10. Peptide Decoding vendor pricing master, generated October 21, 2026. peptidedecoding.com/prices. Our own data, computed for this page from the pricing master in the project, counting one priced product at one seller as a listing. The master holds 14,492 listings across 206 sellers. Filtering every row whose compound field or listed product name contains "glutathione" returns 194 rows. Three are excluded as multi-compound items, one glutathione, thymosin alpha-1 and vilon aerosol spray, one NAD+ and glutathione pack and one TUDCA and S-acetyl glutathione pair, leaving 191 single-compound listings across 130 distinct sellers. By form: 178 vials, 7 solutions, 4 sprays and 2 dissolving strips, with no capsule or tablet anywhere in the set. 165 of the 191 were in stock at capture. Most common sizes were 1500 mg (90 listings) and 600 mg (44). ↩1 ↩2

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