Peptigrade

Endogenous antioxidant / detoxification

Glutathione

L-Glutathione (reduced) — γ-L-glutamyl-L-cysteinyl-glycine·Also known as: GSH, Reduced glutathione, γ-Glu-Cys-Gly, Glutathiol

FDARegulatory status

Glutathione is an endogenous tripeptide, not a drug. No FDA-approved glutathione product exists for IV detoxification, skin whitening, or general antioxidant indications. FDA issued an alert (2019, reaffirmed in subsequent compounding guidance) warning consumers against IV injectable glutathione marketed for skin lightening, citing unapproved new-drug status and sterility/contamination risk from compounders. Oral and sublingual glutathione are sold as dietary supplements under DSHEA — legal to sell, not evaluated for efficacy. Acetaminophen overdose hepatotoxicity is treated with N-acetylcysteine (Acetadote, FDA-approved 2004), a GSH precursor — not with GSH itself.

WADARegulatory status

Not prohibited. Glutathione is not listed on the 2026 WADA Prohibited List (in force January 1, 2026) in any section. It is an endogenous metabolite and is not distinguishable from physiological baseline.

Regulatory note ·Legal status is split by route. Oral capsules, liposomal tinctures, and sublingual sprays are sold as dietary supplements. Injectable (IV/IM) glutathione is only legal in the U.S. when dispensed by a licensed compounding pharmacy under a valid patient-specific prescription; FDA has repeatedly flagged non-compliant online marketing of IV glutathione for cosmetic skin whitening as an unapproved new drug claim. The Philippines FDA issued a 2011 public warning against IV glutathione skin-whitening after reports of Stevens-Johnson syndrome, toxic epidermal necrolysis, thyroid dysfunction, and renal failure — the most commonly cited safety evidence against the cosmetic IV indication.

§ The quick take

TL;DR · Editor’s summary

Glutathione is not a drug candidate in the usual sense — it is the body's most abundant intracellular thiol, produced de novo by every mammalian cell at 0.5–10 mM, and the rate-limiting substrate for Phase II detoxification (GST conjugation), glutathione peroxidase, and protein S-glutathionylation. The honest grading question is not 'does GSH do anything' — it does — but 'does supplementing exogenous GSH by any route produce a clinical benefit beyond supplying the same cysteine + glycine precursors more cheaply.' For the best-studied endpoint — restoration of erythrocyte GSH and oxidative-stress biomarkers (F2-isoprostanes, oxidized LDL, 8-OHdG) in deficient older adults — Sekhar (2011, Am J Clin Nutr) is a replicated B-grade RCT, but the precursors used were cysteine and glycine, not GSH. Oral GSH has ~1% bioavailability due to intestinal γ-glutamyltransferase hydrolysis (Witschi 1992); plasma GSH rises modestly after oral dosing in rats but the mechanism is debated between intact absorption vs precursor resynthesis.

For cosmetic skin whitening — the dominant commercial indication — the evidence is poor-quality and the FDA issued a 2019 alert against IV marketing; the Philippines FDA flagged Stevens-Johnson syndrome, TEN, thyroid dysfunction, and renal failure from compounded cosmetic infusions. For acetaminophen-overdose hepatoprotection the effective drug is NAC (FDA-approved 2004), not GSH. The IV 'detox' drip sold in wellness clinics has no controlled-trial evidence and is mechanistically implausible given a ~10-minute plasma half-life (Aebi 1991).

The Parkinson's IV trial (Hauser 2009) was negative. The case for oral GSH or GlyNAC in deficient populations is real but narrow; every other marketed claim is substantially weaker than the marketing suggests.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for Glutathione, sorted by strength of evidence.

B

Restoration of GSH and oxidative-stress biomarkers in deficient populations

Promising

Sekhar (2011, Am J Clin Nutr) randomized cysteine + glycine supplementation in GSH-deficient elderly adults restored erythrocyte GSH synthesis rate, GSH concentration, and reduced F2-isoprostane and oxidized-LDL biomarkers to young-adult levels within 14 days. Replicated in HIV (Nguyen 2014) and type-2 diabetes (Sekhar 2011 companion) cohorts. Biomarker endpoint, not a clinical outcome.

9 studiesUpdated 2026-04-20
A

Acetaminophen-overdose hepatoprotection (as NAC, not GSH)

Strong

N-acetylcysteine — the cysteine precursor that drives hepatic GSH resynthesis — is FDA-approved (Acetadote, 2004) for prevention of hepatotoxicity after acetaminophen overdose based on Prescott 1979 and Smilkstein 1988 cohorts. IV glutathione itself has not been shown to substitute for NAC in this indication; the grade attaches to NAC, not exogenous GSH.

12 studiesUpdated 2026-04-20
D

Skin whitening / lightening (IV or oral)

Weak

Weschawalit (2017, Clin Cosmet Investig Dermatol) oral GSH 250 mg BID × 12 weeks in 60 women showed small melanin-index reduction on some sites but not others; Arjinpathana (2012) oral 500 mg/d × 4 weeks in 60 subjects showed borderline melanin-index change. Handog (2016) buccal GSH pilot in 30 women showed modest change. No IV trial meets FDA's standard for efficacy; mechanism (tyrosinase eumelanin-to-pheomelanin shunting) is in-vitro only. FDA (2019) and Philippines FDA (2011) have actively warned against the IV cosmetic use.

8 studiesUpdated 2026-04-20
D

Parkinson's disease motor symptoms

Weak

Hauser (2009, Mov Disord) double-blind RCT of IV GSH 1400 mg 3×/week × 4 weeks in 21 PD patients showed no difference from placebo on UPDRS. Mischley (2015) intranasal GSH 600 mg/d × 3 months in 45 patients showed UPDRS improvement vs placebo but the effect did not persist off-treatment. Earlier open-label Sechi (1996) suggested benefit but lacked a control arm. Evidence is inconsistent and under-powered.

6 studiesUpdated 2026-04-20
C

Non-alcoholic fatty liver disease (NAFLD)

Mixed

Honda (2017, BMC Gastroenterol) open-label oral GSH 300 mg/d × 4 months in 34 NAFLD patients reduced ALT (median 52 → 44 U/L) with inconsistent imaging response; no placebo arm. Small pilot-level signal only; no Phase 2 RCT.

3 studiesUpdated 2026-04-20
D

Autism spectrum disorder behavioral symptoms

Weak

Kern (2011) open-label transdermal and oral GSH in 26 autistic children showed increases in plasma cysteine and sulfate but no validated behavioral endpoint improvement. No placebo-controlled trial. Mechanistic plausibility tied to reported GSH depletion in ASD cohorts (James 2004) does not establish efficacy.

4 studiesUpdated 2026-04-20
Pend.

General 'detoxification' (IV glutathione push)

Pending · Below evidence threshold

No peer-reviewed controlled trial supports IV glutathione 'detox' drips as marketed by concierge wellness clinics. The claim conflates the biochemist's meaning of glutathione conjugation (endogenous Phase II metabolism in hepatocytes) with the lay-marketing meaning of 'removing toxins from the body.' IV glutathione plasma half-life is ~10 minutes (Aebi 1991); systemic bolus does not meaningfully raise intracellular GSH in the tissues that actually perform xenobiotic conjugation.

1 studiesUpdated 2026-04-20
Ins.

Longevity / anti-aging (as stand-alone GSH)

Insufficient

Age-related decline in erythrocyte GSH is well-documented (Sekhar 2011). Whether raising GSH with exogenous supplementation extends healthspan in humans has not been tested. GlyNAC combination trials (Kumar 2023, Sekhar 2023) are ongoing — but those test cysteine + glycine precursors, not GSH itself.

2 studiesUpdated 2026-04-20

§ Why this grade

Sub-scores for this outcome.

Restoration of GSH and oxidative-stress biomarkers in deficient populations

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

5 / 5

GSH biosynthesis (Lu 2013), GPx/GR redox cycle (Marí 2020), GST conjugation (Hayes 2005), and S-glutathionylation signaling (Mailloux 2024) are well-characterized at the enzymatic, structural, and cellular level. This is one of the best-understood metabolic systems in biology. The gap is not mechanism — it is whether exogenous supplementation productively intersects it.

Human studies (count + quality)

4 / 5

Sekhar 2011 (Am J Clin Nutr) is a well-designed RCT showing cysteine + glycine supplementation restores erythrocyte GSH synthesis rate, GSH concentration, F2-isoprostanes, and oxidized-LDL to young-adult levels in deficient elderly. Replicated in HIV (Nguyen 2014) and diabetes cohorts. Caveat: the supplement was precursors, not GSH itself — making this less a test of oral GSH than of cysteine + glycine sufficiency.

Effect vs placebo

4 / 5

Biomarker effect sizes vs placebo are large and consistent — erythrocyte GSH roughly doubled and F2-isoprostane fell ~30% within 14 days in Sekhar 2011. The biomarker-to-clinical-outcome linkage is not established — no downstream mortality, cognition, or frailty outcome has been powered.

Long-term safety data

3 / 5

Oral cysteine + glycine at the doses used in Sekhar's work is well-tolerated over months. NAC has decades of human safety data across acetaminophen, pulmonary, and psychiatric use. Long-term (multi-year) exogenous oral GSH safety is less characterized; no repeat-dose IV glutathione safety cohort exists in healthy adults.

Side effect profile

4 / 5

Oral GSH and oral NAC/GlyNAC are generally well-tolerated (GI upset, sulfurous taste). IV glutathione carries a distinct profile — anaphylaxis, Stevens-Johnson syndrome, TEN, thyroid dysfunction, renal failure (Philippines FDA 2011; FDA 2019 alert) — largely from compounded cosmetic product rather than pharmaceutical-grade use. The route-specificity of the safety profile is a meaningful rubric input.

Regulatory status

3 / 5

Endogenous metabolite; not a scheduled drug. Oral GSH sold as dietary supplement under DSHEA. NAC is FDA-approved as Acetadote for acetaminophen overdose. IV glutathione for cosmetic use is an unapproved new drug per FDA's 2019 alert. WADA does not prohibit it. The 3 reflects the split — partial regulatory acceptance (NAC) for a neighboring indication, not full acceptance of exogenous GSH.

§ What the science says

How Glutathione
works.

Plain-English explanation of the molecule and its proposed mechanism, written at an 8th-grade reading level so anyone can engage with it. Every claim is linked to a primary source below.

What it is

Glutathione is the endogenous tripeptide γ-L-glutamyl-L-cysteinyl-glycine (C₁₀H₁₇N₃O₆S, 307.32 Da, CAS 70-18-8, PubChem CID 124886). It is synthesized in the cytoplasm of nearly every mammalian cell in two ATP-dependent steps: γ-glutamylcysteine ligase (GCL, formerly γ-GCS) condenses glutamate and cysteine (the rate-limiting step, feedback-inhibited by GSH), and glutathione synthetase adds glycine. The unusual γ-peptide bond between glutamate's side-chain γ-carboxyl and cysteine's α-amino group resists most peptidases — only γ-glutamyltransferase (GGT) can cleave it — which is why exogenous GSH is efficiently hydrolyzed on the gut brush border and on the vascular endothelium. Intracellular concentrations reach 0.5–10 mM (>90% reduced form in healthy tissue), establishing GSH as the single largest non-protein thiol pool in the body. It is not a 'peptide therapeutic' — it is a ubiquitous metabolite, which makes the evidence framing fundamentally different from exogenous peptides like BPC-157 or semaglutide.

How it works

  1. 01

    Glutathione peroxidase (GPx) — primary peroxide defense

    Glutathione peroxidases are selenoprotein enzymes that reduce hydrogen peroxide and lipid hydroperoxides using GSH as the two-electron donor: 2 GSH + H₂O₂ → GSSG + 2 H₂O. GPx1 (cytosolic) and GPx4 (membrane-associated, lipid-peroxide-specific) are the dominant forms; GPx4 knockout is embryonic lethal and its activity is the gatekeeper of ferroptosis. Mitochondria lack catalase, so mitochondrial GSH + GPx is the sole enzymatic defense against matrix-generated H₂O₂ (Marí 2020, Antioxidants; Lu 2013, Mol Aspects Med). Resulting GSSG is reduced back to GSH by glutathione reductase using NADPH — the redox cycle that couples GSH metabolism to the pentose phosphate pathway.

  2. 02

    Glutathione S-transferase (GST) — Phase II detoxification

    The cytosolic GST superfamily (α, μ, π, θ, ζ classes in humans) catalyzes nucleophilic attack of the GSH thiolate on electrophilic xenobiotics and reactive endogenous metabolites (α,β-unsaturated aldehydes, quinones, epoxides), forming GSH conjugates that are exported via MRP1/MRP2 transporters and processed through the mercapturic-acid pathway (GGT → dipeptidase → N-acetyltransferase) for renal elimination (Hayes 2005, Annu Rev Pharmacol Toxicol). This is the biochemist's 'detoxification' — hepatocyte-localized conjugation, not the infusion-clinic marketing term.

  3. 03

    Cysteine reservoir and the rate-limiting role of cysteine

    De novo GSH synthesis is rate-limited by intracellular cysteine, not glycine or glutamate. Cysteine is the scarce, autoxidation-prone input; this is why NAC (N-acetylcysteine) rescues hepatic GSH in acetaminophen overdose and why GlyNAC (glycine + NAC) supplementation (Sekhar 2023, Nutrients; Kumar 2023, J Gerontol) reliably raises erythrocyte GSH in deficient elderly adults. Oral GSH is less efficient than oral cysteine precursors because most ingested GSH is hydrolyzed at the brush border before reaching the portal circulation (Witschi 1992, Eur J Clin Pharmacol).

  4. 04

    Protein S-glutathionylation — redox signaling

    Reversible formation of mixed disulfides between GSH and protein cysteine residues (Protein-SSG) is now recognized as a major redox post-translational modification, regulating metabolic enzymes (GAPDH, pyruvate kinase), signaling proteins (PTP1B, NF-κB), and apoptotic caspases (Mailloux 2024, Redox Biol). Glutaredoxins (Grx1/Grx2) and sulfiredoxin catalyze deglutathionylation. This positions GSH not just as an antioxidant buffer but as a signaling cofactor — and complicates the 'more GSH is better' intuition that drives consumer marketing.

  5. 05

    Pharmacokinetics of exogenous GSH — why route matters

    Oral GSH: Witschi (1992) administered 3 g oral GSH to 7 healthy volunteers and observed no significant rise in plasma GSH, concluding oral bioavailability is effectively zero; more recent analogue and liposomal work (Richie 2015; the 2025 N-methylated analogue work in MDPI Pharmaceutics) has tried to circumvent brush-border GGT hydrolysis with mixed results. IV GSH: Aebi (1991, Eur J Clin Pharmacol) administered 2 g IV to 5 volunteers and showed plasma GSH cleared with a half-life of ~10 minutes; total GSH disappears from the circulation within ~90 minutes. Intranasal: Mischley (2013) showed modest brain GSH increase on MRS, the basis of the Mischley 2015 PD trial. The short plasma half-life is the mechanistic argument against IV 'detox drips': a bolus that clears in 10 minutes does not meaningfully raise hepatocyte intracellular GSH.

  6. 06

    Proposed skin-whitening mechanism (and why it does not justify IV use)

    In-vitro work (Villarama 2005; del Rosario-Blasco 2008) shows that GSH at millimolar concentrations in melanocyte culture shifts tyrosinase product distribution away from eumelanin toward lighter pheomelanin, and that GSH inhibits tyrosinase activity. Translating this to systemic IV dosing requires that a plasma GSH spike reaches melanocyte intracellular pools at the required concentration for long enough to matter — a chain of assumptions not supported by the pharmacokinetic data above. The controlled oral trials (Arjinpathana 2012; Weschawalit 2017; Handog 2016) show small and inconsistent melanin-index changes that do not translate reliably to patient-reported outcomes.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Restoration of GSH and oxidative-stress biomarkers in elderly/deficient adults

    Sekhar 2011 (Am J Clin Nutr) RCT, replicated in HIV (Nguyen 2014) and T2D cohorts — endpoint is biomarker, not clinical

  • Acetaminophen overdose (via NAC precursor, not GSH itself)

    FDA-approved (Acetadote 2004) on strength of Prescott 1979 and Smilkstein 1988 — GSH per se is not the approved drug

  • Cosmetic skin whitening (oral, IV, sublingual)

    Small RCTs (Arjinpathana 2012; Weschawalit 2017; Handog 2016) with modest melanin-index changes; FDA 2019 alert against IV marketing; Philippines FDA 2011 adverse-event warnings

  • Parkinson's disease

    Hauser 2009 IV RCT negative; Mischley 2015 intranasal small RCT positive but non-durable

  • Non-alcoholic fatty liver disease

    Honda 2017 open-label oral GSH — ALT decline without placebo control

  • Autism spectrum disorder

    Kern 2011 open-label transdermal/oral — biomarker changes only, no validated behavioral endpoint

  • Cystic fibrosis lung inflammation

    Bishop 2005 inhaled GSH pilot — no subsequent Phase 3

  • Chemotherapy-induced peripheral neuropathy (cisplatin, oxaliplatin)

    Cascinu 2002 IV GSH Phase 3 showed reduced neuropathy incidence with cisplatin; conflicting results in subsequent trials and in oxaliplatin indication

  • 'IV detox' / wellness drip

    No controlled trial; mechanistically implausible at observed PK; unapproved-new-drug claim per FDA

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    Whether any oral or sublingual GSH formulation raises intracellular GSH in the tissues that matter (hepatocytes, neurons, melanocytes) better than giving the same cost in NAC + glycine. Head-to-head trials of oral GSH vs GlyNAC are not published.

  • !

    Whether long-term exogenous GSH supplementation affects de novo GSH synthesis via feedback inhibition of γ-glutamylcysteine ligase. No human study has characterized this loop across months of dosing.

  • !

    Human pharmacokinetics of liposomal, N-methylated, and proliposome analogues beyond manufacturer-funded pilot studies. The Park 2025 N-methylated GSH 16× bioavailability claim is rat-only.

  • !

    Safety of repeated IV glutathione in healthy adults for cosmetic use. The Philippines FDA 2011 alert cited Stevens-Johnson syndrome, TEN, thyroid dysfunction, renal failure, and sepsis from contaminated compounded product — but no controlled safety cohort exists.

  • !

    Whether GSH supplementation in cancer patients is net beneficial or net harmful. GSH protects normal tissue from chemotherapy oxidative damage (Cascinu 2002) but also protects tumor cells from the same mechanism (Traverso 2013); GST-π overexpression is a resistance marker in cisplatin-treated tumors.

  • !

    Whether the modest Parkinson's intranasal signal (Mischley 2015) survives replication in a larger sample with a longer open-label extension. The 2026-planned multi-site trial has not reported.

  • !

    The clinical relevance of 'oxidative stress biomarker improvement' as a surrogate endpoint. F2-isoprostane and oxidized-LDL reductions in Sekhar 2011 were real — but no study has linked those reductions to downstream mortality, disability, or disease-incidence outcomes.

  • !

    Drug–drug interactions — particularly with chemotherapeutics cleared via GSH-conjugation (cisplatin, chlorambucil, cyclophosphamide metabolites), acetaminophen, and nitrates — are poorly characterized for exogenous GSH dosing.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing Glutathioneand tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • Glutathione IV Drips — What the Evidence Actually Says

    Medlife Crisis·MD, Cardiology

    Walks through the pharmacokinetic argument (Aebi 1991 ~10-minute plasma half-life) and the FDA 2019 alert. Explicit that IV 'detox' marketing is not supported by the controlled literature.

    Verified credentials

  • GlyNAC and the Science of Restoring Glutathione in Aging

    Peter Attia MD·MD, Internal Medicine / Longevity

    Covers Sekhar 2011 and the Kumar 2023 GlyNAC trial. Makes the explicit case that precursor supplementation (glycine + NAC) is a better-evidenced intervention than oral GSH itself for older adults.

    Verified credentials

  • I Tried IV Glutathione for 30 Days — My Skin Transformation

    Anonymous beauty influencer·Unverified

    Testimonial format with no objective measurement, no control, undisclosed product sourcing. Representative of the cosmetic-IV marketing FDA flagged in 2019. Do not weight against published evidence.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 21 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation

    Sekhar RV, Patel SG, Guthikonda AP, et al. · Am J Clin Nutr · 2011

    RCTPMID 21289193
  2. [02]

    Deficient cysteine and glutathione synthesis in HIV infection: dietary glutathione supplementation corrects deficiency

    Nguyen D, Hsu JW, Jahoor F, Sekhar RV · J Clin Endocrinol Metab · 2014

    RCTPMID 24500941
  3. [03]

    GlyNAC supplementation improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, and multiple aging hallmarks in older adults: a randomized clinical trial

    Kumar P, Osahon OW, Sekhar RV · J Gerontol A Biol Sci Med Sci · 2023

    RCTPMID 36415974
  4. [04]

    The systemic availability of oral glutathione

    Witschi A, Reddy S, Stofer B, Lauterburg BH · Eur J Clin Pharmacol · 1992

    PilotPMID 1362956
  5. [05]

    High-dose intravenous glutathione in man. Pharmacokinetics and effects on cyst(e)ine in plasma and urine

    Aebi S, Assereto R, Lauterburg BH · Eur J Clin Pharmacol · 1991

    PilotPMID 2060532
  6. [06]

    Glutathione and its antiaging and antimelanogenic effects

    Weschawalit S, Thongthip S, Phutrakool P, Asawanonda P · Clin Cosmet Investig Dermatol · 2017

    RCTPMID 28761342
  7. [07]

    Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study

    Arjinpathana N, Asawanonda P · J Dermatolog Treat · 2012

    RCTPMID 22475713
  8. [08]

    An open-label, single-arm trial of the safety and efficacy of a novel preparation of glutathione as a skin-lightening agent in Filipino women

    Handog EB, Datuin MS, Singzon IA · Int J Dermatol · 2016

    Open-labelPMID 26904424
  9. [09]

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

    Hauser RA, Lyons KE, McClain T, Carter S, Perlmutter D · Mov Disord · 2009

    RCTPMID 19230029
  10. [10]

    Central nervous system uptake of intranasal glutathione in Parkinson's disease

    Mischley LK, Leverenz JB, Lau RC, et al. · NPJ Parkinson's Disease · 2015

    RCTPMID 25758290
  11. [11]

    Efficacy of glutathione for the treatment of nonalcoholic fatty liver disease: an open-label, single-arm, multicenter, pilot study

    Honda Y, Kessoku T, Sumida Y, et al. · BMC Gastroenterol · 2017

    Open-labelPMID 28789631
  12. [12]

    Neuroprotective effect of reduced glutathione on oxaliplatin-based chemotherapy in advanced colorectal cancer: a randomized, double-blind, placebo-controlled trial

    Cascinu S, Catalano V, Cordella L, et al. · J Clin Oncol · 2002

    RCTPMID 11896090
  13. [13]

    Glutathione transferases

    Hayes JD, Flanagan JU, Jowsey IR · Annu Rev Pharmacol Toxicol · 2005

    Systematic reviewPMID 15987822
  14. [14]

    Glutathione synthesis

    Lu SC · Mol Aspects Med · 2013

    Systematic reviewPMID 23089296
  15. [15]

    Mitochondrial glutathione: recent insights and role in disease

    Marí M, de Gregorio E, de Dios C, et al. · Antioxidants (MDPI) · 2020

    Systematic reviewPMID 33023001
  16. [16]

    Role of glutathione in cancer progression and chemoresistance

    Traverso N, Ricciarelli R, Nitti M, et al. · Oxid Med Cell Longev · 2013

    Systematic reviewPMID 22080474
  17. [17]

    Dysregulation of glutathione homeostasis in neurodegenerative diseases

    Johnson WM, Wilson-Delfosse AL, Mieyal JJ · Nutrients · 2012

    Systematic reviewDOI
  18. [18]

    FDA alert: injectable glutathione marketed for skin lightening is an unapproved new drug; compounding risk

    U.S. Food and Drug Administration, Office of Compounding Quality and Compliance · FDA · 2019

    RegulatoryLink
  19. [19]

    Philippines FDA advisory on unregistered intravenous glutathione for skin whitening — adverse events including Stevens-Johnson syndrome, TEN, thyroid dysfunction, renal failure

    Philippine Food and Drug Administration · FDA Philippines · 2011

    RegulatoryLink
  20. [20]

    FDA approval of Acetadote (IV N-acetylcysteine) for prevention of hepatotoxicity from acetaminophen overdose

    U.S. Food and Drug Administration · FDA Orange Book (NDA 021539) · 2004

    RegistrationLink
  21. [21]

    WADA 2026 Prohibited List (in force January 1, 2026) — glutathione not listed

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink

§ Adjacent peptides

Worth reading
alongside this.

Compare

BPC-157

Adjacent injectable-peptide category with a similar 'strong mechanism, thin human evidence' profile. Different mechanism entirely (tissue repair, not antioxidant defense) but similar evidence-discipline exercise.

Read its grades

Compare

GHK-Cu

Cosmetic-adjacent peptide with modest controlled topical evidence and a large gap between marketing claims and clinical data — closest neighbor on the skin-claim axis.

Read its grades

Compare

Melanotan II

The opposite side of the pigmentation marketing axis — tanning rather than whitening — and the better-characterized cautionary tale on unregulated injectable cosmetics.

Read its grades

Where to research further

Looking for Glutathione
for laboratory research?

Peptigrade does not sell peptides. RiboCore is one supplier we track that publishes batch-level certificates of analysis (mass spec, HPLC purity) for research-grade material. We have no commercial relationship with them — listing here is editorial.

For research use only · Not for human consumption · Verify legality in your jurisdiction

View at RiboCoreHow we evaluate suppliers →