Evidence Grade E — Very limited evidence. 0 published studies. 261 registered clinical trials.
Medically reviewed by a licensed medical professional
Glutathione is the body's primary built-in antioxidant — a tripeptide found in virtually every human cell. While technically a peptide, it functions as a metabolic workhorse rather than a signalling molecule. Oral supplements, liposomal formulations, and intravenous infusions are widely marketed in wellness and skin-lightening contexts. It has no pharmaceutical approval for any therapeutic use.
Glutathione (Peptide-Adjacent) is also known by these brand and alternate names:
No published studies found on PubMed.
Glutathione has no pharmaceutical marketing authorisation for any therapeutic indication. A 6-month randomised controlled trial of oral glutathione showed increased blood levels and immune cell function. Smaller studies have investigated skin-lightening effects.
The evidence base for supplemental glutathione is mixed. Oral bioavailability has historically been questioned, though liposomal formulations may improve absorption. Intravenous glutathione is marketed through wellness clinics but has not been evaluated in rigorous clinical trials for any specific indication. Glutathione is a naturally occurring molecule with well-characterised biochemistry — the question is whether supplementation provides clinically meaningful benefit.
Glutathione's biochemistry is well established: it neutralises reactive oxygen species, participates in detoxification reactions, and maintains other antioxidants in their active forms. These are normal cellular functions. The therapeutic question is whether exogenous supplementation meaningfully augments these processes beyond what the body already produces — and whether this translates to clinical benefit.
Research suggests a 6-month randomised trial established that oral glutathione supplements do raise blood levels, resolving an earlier debate about bioavailability. Small trials have shown skin-lightening effects. Safety for oral supplementation appears excellent. However, no large-scale placebo-controlled trials (over 500 participants) exist for any clinical outcome, no data extend beyond 6 months, and most trials are small (20-80 participants) with high individual variability. Intravenous glutathione infusions marketed through wellness clinics have not been evaluated in rigorous trials. Some regulatory agencies have issued advisories against IV glutathione for skin whitening.
PeptideTrace tracks 261 registered clinical trials for Glutathione (Peptide-Adjacent) sourced from ClinicalTrials.gov.
Expanded Access Treatment Protocol With DCA for Patients With PDCD
SPI-1005 in Adults Receiving Cochlear Implant
Tolerability of Enteral NAC in Infants
Therapeutics for Moderate and Severe Dengue
Adia Med of Winter Park LLC Chronic Kidney Disease Research Study
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Glutathione (GSH) is a tripeptide (gamma-L-glutamyl-L-cysteinyl-glycine) with an unusual gamma-peptide bond. Its molecular weight is 307.32 Da with molecular formula C10H17N3O6S (CAS 70-18-8). It exists predominantly in reduced form (GSH, >98%) with an oxidized disulfide form (GSSG). IV glutathione has a plasma half-life of approximately 1.6 minutes. Standard oral bioavailability is estimated at 3-5% versus IV. Intracellular GSH concentration is 1-10 mM (80-85% cytosolic, 10-15% mitochondrial). Delivery routes include IV, oral, liposomal, sublingual, and nebulized. N-acetylcysteine (NAC) serves as a key precursor.
GSH is the primary endogenous antioxidant, serving as electron donor for glutathione peroxidase (GPx) enzymes reducing hydrogen peroxide and lipid hydroperoxides. It is the conjugation substrate for glutathione S-transferases (GSTs) in Phase II detoxification. The glutaredoxin system uses GSH-dependent thiol-disulfide oxidoreductases to regulate protein thiol redox state, modulating NF-kB, AP-1, and Nrf2 signaling. Anti-melanogenic mechanism involves tyrosinase inhibition and shifting melanogenesis from eumelanin (dark) to pheomelanin (light). GSH levels regulate T-cell proliferation, NK cell cytotoxicity, and cytokine balance.
Richie et al. (2015, Eur J Nutr, N=54, 6-month RCT) showed oral GSH 1000 mg/day increased erythrocyte GSH by 30-35% (p<0.05) with 260% increase in buccal cells and more than 2-fold increase in NK cell cytotoxicity. A liposomal GSH pilot (Sinha et al. 2018, N=12) showed 40% whole blood GSH increase within 2 weeks. For skin lightening, Arjinpathana & Asawanonda (2012, N=60, double-blind RCT) showed melanin index reduction with 500 mg/day. A larger trial (Duperray et al. 2022, N=124, 12-week RCT) showed skin lightening with L-Cystine plus GSH combination. For Parkinson's, the only proper RCT (Hauser et al. 2009, N=21) of IV GSH showed no significant improvement over placebo.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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Vancomycin is marketed as Vancocin and Firvanq (approved 1958, with oral solution Firvanq approved 2018). It is the standard treatment for serious MRSA infections (bloodstream infections, endocarditis, pneumonia, bone infections) and is first-line for severe C. difficile colitis. Vancomycin requires therapeutic drug monitoring — blood levels must be checked regularly to ensure the dose is effective without causing kidney damage or hearing loss. The rise of vancomycin-resistant enterococci (VRE) and occasional vancomycin-intermediate S. aureus (VISA) strains represent ongoing challenges. Despite being nearly 70 years old, vancomycin remains irreplaceable for many serious infections, though newer alternatives like daptomycin and the lipoglycopeptides offer advantages in specific settings.
Zilucoplan is marketed as Zilbrysq (approved October 2023) for anti-acetylcholine receptor antibody-positive generalised myasthenia gravis in adults. Administered as a daily subcutaneous self-injection. In the RAISE trial, zilucoplan showed statistically significant improvements in both activities of daily living and quantitative muscle strength scores compared to placebo, with improvements evident from week one. Its key differentiator from existing complement inhibitors (eculizumab, ravulizumab) is the self-injectable format — those alternatives require hospital-based intravenous infusions. As with all complement inhibitors, patients require meningococcal vaccination before starting treatment due to increased susceptibility to meningococcal infection.
Daptomycin is marketed as Cubicin (approved September 2003). It is indicated for complicated skin and soft tissue infections and S. aureus bloodstream infections including right-sided endocarditis. Administered as a once-daily intravenous infusion. A key limitation is that daptomycin cannot be used for pneumonia — lung surfactant inactivates the drug. In the bacteraemia trial, daptomycin was non-inferior to vancomycin with significantly lower rates of kidney problems (11% versus 26%). Creatine kinase (CK) levels must be monitored during treatment, as daptomycin can cause muscle toxicity. Generics became available after patent expiry, significantly reducing cost.
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
