Glutathione
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Research Use Only
These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Research Summary
20 PubMed CitationsResearch Overview Glutathione (GSH) is a ubiquitous endogenous tripeptide that serves as the principal intracellular antioxidant and redox buffer in mammalian biology. Composed of L-glutamate, L-cysteine, and glycine, it was first isolated and named by Frederick Gowland Hopkins in 1921, though its correct tripeptide structure was not established until 1935 by Harington and Mead. Present at millimolar concentrations (0.5–10 mM) in virtually every cell, GSH participates in a vast network of antioxidant defense, detoxification, signal transduction, and immune modulation processes that are essential for cellular survival.[3][12] GSH is biosynthesized in the cytosol via a tightly regulated, two-step ATP-dependent enzymatic process. First, glutamate-cysteine ligase (GCL) catalyzes the formation of γ-glutamylcysteine from glutamate and cysteine (the rate-limiting step); then glutathione synthetase (GS) adds glycine to the C-terminal to yield the final molecule. The availability of cysteine is the primary rate-limiting factor in this synthesis. The liver serves as the principal production organ...
Glutathione — Research Data at a Glance
| Property | Value |
|---|---|
| PubMed Citations Referenced | 20 |
| Contributing Researchers | 3 |
| Storage Conditions | Lyophilized: -20°C or 2–8°C (stable long-term as dry powder); Reconstituted: aliquot immediately, store at 2–8°C short-term or -20°C long-term; protect from light, air, and moisture; avoid freeze-thaw cycles. |
| Purity Standard | ≥99% (HPLC verified, 3rd-party COA) |
| Research Use Only | Not for human consumption. RUO only. |
Overview
Research Overview
Glutathione (GSH) is a ubiquitous endogenous tripeptide that serves as the principal intracellular antioxidant and redox buffer in mammalian biology. Composed of L-glutamate, L-cysteine, and glycine, it was first isolated and named by Frederick Gowland Hopkins in 1921, though its correct tripeptide structure was not established until 1935 by Harington and Mead. Present at millimolar concentrations (0.5–10 mM) in virtually every cell, GSH participates in a vast network of antioxidant defense, detoxification, signal transduction, and immune modulation processes that are essential for cellular survival.[3][12]
GSH is biosynthesized in the cytosol via a tightly regulated, two-step ATP-dependent enzymatic process. First, glutamate-cysteine ligase (GCL) catalyzes the formation of γ-glutamylcysteine from glutamate and cysteine (the rate-limiting step); then glutathione synthetase (GS) adds glycine to the C-terminal to yield the final molecule. The availability of cysteine is the primary rate-limiting factor in this synthesis. The liver serves as the principal production organ and the main source of plasma GSH for interorgan distribution.[12][20]
The therapeutic rationale for GSH research is grounded in its role as the body's "master antioxidant." GSH directly neutralizes reactive oxygen species (ROS) and reactive nitrogen species (RNS), serves as the essential cofactor for glutathione peroxidases (GPx), and conjugates with electrophilic toxins and heavy metals via glutathione S-transferases (GSTs) for excretion (Phase II detoxification). The ratio of reduced GSH to oxidized GSSG serves as a fundamental index of cellular oxidative status; a decline in this ratio is a hallmark of oxidative stress, cellular dysfunction, and aging.[3][12]
Clinical research has established that GSH depletion is implicated in the pathology of numerous conditions. In Parkinson's disease, GSH depletion in the substantia nigra precedes neurodegeneration, and intranasal GSH (600 mg/day) improved UPDRS scores in a Phase IIb trial (P = 0.0025).[11][5] In liver disease, oral GSH (300 mg/day) significantly reduced alanine transaminase (ALT) in NAFLD patients.[8] In dermatology, both oral (250–500 mg/day) and topical (2% GSSG) glutathione demonstrated significant reductions in melanin index, wrinkles, and improvements in skin elasticity in multiple randomized controlled trials.[19][18][2] In type 2 diabetes, 1000 mg/day oral GSH significantly improved whole-body insulin sensitivity in obese males.[16] As a chemotherapy adjunct, IV glutathione (1.5 g/m²) reduced cisplatin-associated neurotoxicity in gastric and ovarian cancer patients without compromising antineoplastic efficacy.[4][15]
A key challenge in GSH research is bioavailability. Standard oral GSH has limited systemic availability due to degradation by intestinal γ-glutamyl transpeptidase (GGT), and IV administration yields a plasma half-life of less than 3 minutes. Strategies to overcome this include liposomal encapsulation, sublingual delivery, intranasal administration (which increases brain GSH >200% within 45 minutes), and the use of GSH precursors such as N-acetylcysteine (NAC).[14][20][9]
Mechanism of Action
Mechanism of Action
Glutathione (GSH) does not function through a single classical receptor-ligand interaction. Instead, it acts as a pervasive biochemical modulator of cellular redox state, enzymatic cofactor, and signaling regulator via post-translational protein modification.[3]
Primary Biochemical Targets & Binding Characteristics
| Target / Mechanism | Detail | Evidence |
|---|---|---|
| S-Glutathionylation | Reversible post-translational modification; GSH forms mixed disulfide bonds with reactive cysteine residues on target proteins (protein-SSG), acting as a redox "on/off" switch for regulatory, structural, and metabolic proteins | Ballatori et al. (2009)[3] |
| Glutathione Peroxidases (GPx) | GSH serves as the essential electron donor for GPx-catalyzed reduction of H2O2 and lipid hydroperoxides to water/alcohols, oxidizing GSH to GSSG | Ballatori et al. (2009)[3] |
| Glutathione S-Transferases (GSTs) | GSH conjugates with electrophilic xenobiotics, heavy metals (Hg, Pb), and endogenous toxins (Phase II detoxification), rendering them water-soluble for excretion | Ballatori et al. (2009)[3] |
| Metal Chelation | Six coordination sites for metal ions; thiol group has high affinity for Cu, Zn, Hg, and Pb, forming stable mercaptide complexes for mobilization and transport | Ballatori et al. (2009)[3] |
| NMDA Receptor Modulation | GSH modulates the N-methyl-D-aspartate (NMDA) receptor, regulating calcium influx in cerebellar granule cells | Ballatori et al. (2009)[3] |
| Bcl-2 Binding | GSH binds the Bcl-2 BH3-domain groove at the mitochondria, contributing to anti-apoptotic antioxidant function | Ballatori et al. (2009)[3] |
| γ-Peptide Bond Stability | Unusual γ-carboxyl linkage between glutamate and cysteine protects from intracellular peptidase hydrolysis; only cleaved by ectoenzyme γ-glutamyl transpeptidase (GGT) on external cell surfaces | Ballatori et al. (2009)[3] |
Downstream Signaling Cascades
| Pathway | Mechanism | Outcome |
|---|---|---|
| Keap1-Nrf2-ARE | Oxidative stress or electrophiles modify Keap1 cysteines, preventing Nrf2 degradation; stabilized Nrf2 translocates to nucleus and binds Antioxidant Response Element (ARE); modulated by ERK and p38 MAPK kinases | Transcription of GSH synthesis genes (GCLC, GCLM) and detoxification enzymes (GSTs)[3] |
| NF-κB Signaling | S-glutathionylation of the p50 subunit of NF-κB inhibits its DNA binding; GSH depletion activates NF-κB via ROS-mediated IκB degradation | GSH suppresses pro-inflammatory gene transcription (TNF-α, IL-1β, IL-6); depletion drives inflammation[3] |
| MAPK Pathway | Severe GSH depletion oxidizes MAPK phosphatases (MKPs), causing sustained JNK and p38 MAPK activation; GST-pi monomers bind JNK (inhibition), but dimerize under oxidative stress to release JNK | Cytochrome c release and caspase activation leading to apoptosis[3] |
| Nitric Oxide (NO) Signaling | GSH buffers NO; depletion increases free NO causing protein nitration and DNA damage; activates p53, which induces PGC-1α for antioxidant response | Modulation of NO-mediated signaling and protection against nitrosative stress[3] |
Cellular & Tissue-Level Effects
| System | Effect | Detail |
|---|---|---|
| Mitochondria | Critical for neutralizing H2O2 from electron transport chain | Transported via dicarboxylate and 2-oxoglutarate carriers; prevents mPTP opening[3] |
| Skin (Antimelanogenic) | Inhibits tyrosinase by chelating copper at active site | Shifts melanogenesis from eumelanin (dark) to pheomelanin (light); reduces melanin index, wrinkles, increases elasticity[19] |
| Nervous System | Astrocytes synthesize and release GSH for neuronal uptake | Protects dopaminergic neurons from oxidative damage; preserves mitochondrial Complex I activity[5] |
| Immune System | Essential for T-cell metabolic reprogramming and clonal expansion | GSH:GSSG ratio modulates Th1/Th2 balance; depletion favors Th2 (chronic inflammation)[14] |
| Cardiovascular | Restores endothelium-dependent vasorelaxation in aging | Increases H2S levels and mtNOS activity; inhibits mPTP opening in aged heart tissue[3] |
| Hepatoprotective | Reduces ALT and oxidative damage markers in liver tissue | Significant benefit in NAFLD and NASH models[8] |
Comparison with Related Compounds
| Compound | Relationship to GSH | Key Difference |
|---|---|---|
| L-Cysteine | Rate-limiting precursor substrate for GSH synthesis | Neurotoxic at high extracellular concentrations; GSH is the non-toxic storage form[3] |
| N-Acetylcysteine (NAC) | Deacetylated precursor used to replenish intracellular GSH | Better oral bioavailability than GSH; widely used clinically as GSH booster[7] |
| GSSG (Oxidized Glutathione) | Disulfide dimer formed when GSH is oxidized | Accumulation is toxic; cells maintain GSH:GSSG ratio >100:1 via Glutathione Reductase + NADPH[3] |
| Liposomal Glutathione | GSH encapsulated in phospholipid vesicles | Enhanced oral absorption bypassing GGT degradation; elevates body stores and immune markers[14] |
| Glutathione Monoethyl Ester (GEE) | Synthetic analog designed for enhanced cell penetration | Bypasses transport limitations; crosses blood-brain barrier more effectively than native GSH[3] |
Research Applications
Research Applications
Glutathione is investigated across a broad spectrum of research domains, with evidence spanning preclinical animal models to randomized controlled clinical trials:
1. Neurodegenerative Diseases (Parkinson's, Alzheimer's)
GSH depletion in the substantia nigra is one of the earliest biochemical changes in Parkinson's disease, preceding mitochondrial Complex I dysfunction and dopaminergic neuron loss. Intranasal GSH (200–600 mg/day) demonstrated significant improvement in UPDRS Total scores (-4.6 points, P = 0.0025) in a Phase IIb RCT, and a single 200 mg intranasal dose increased brain GSH levels >200% within 45 minutes (P < 0.001) as measured by magnetic resonance spectroscopy.[11][5][13]
2. Hepatoprotection (NAFLD, NASH, Cirrhosis)
GSH is extensively studied for its hepatoprotective effects. Oral GSH (300 mg/day for 4 months) significantly reduced ALT levels (p < 0.05) in NAFLD patients. In NASH patients, 300 mg/day for 3 months decreased both ALT and 8-OHdG (DNA oxidative damage marker) significantly. However, 500 mg/day GSH for 12 weeks showed no significant effect in liver cirrhosis.[8]
3. Dermatology & Skin Research
| Study | Intervention | Key Result | Ref |
|---|---|---|---|
| Weschawalit et al. (2017) | 250 mg oral GSH or GSSG/day, 12 weeks | Significant wrinkle reduction (P = 0.006); increased skin elasticity; melanin index reduction in >40 year group | [19] |
| Arjinpathana et al. (2012) | 500 mg oral GSH/day, 4 weeks | Significant melanin index reduction in sun-exposed areas (face/wrists) vs placebo | [2] |
| Watanabe et al. (2014) | 2% GSSG lotion, twice daily, 10 weeks | Significant reduction in melanin index (p < 0.05), TEWL (p < 0.05), and wrinkles (p < 0.01) | [18] |
4. Diabetes & Metabolic Syndrome
Research highlights a correlation between GSH insufficiency and T2DM complications. Oral GSH (1000 mg/day, 3 weeks) significantly increased whole-body insulin sensitivity in obese males with and without T2DM (NCT02948673). In a larger trial (n=360), 500 mg/day for 6 months as adjunct therapy significantly decreased oxidative damage markers and improved HbA1c in patients >55 years.[16]
5. Oncology & Chemotherapy Support
IV glutathione (1.5 g/m²) administered before cisplatin chemotherapy demonstrated neuroprotective effects in randomized trials of advanced gastric cancer and ovarian cancer, reducing neurotoxicity and nephrotoxicity without compromising antineoplastic efficacy.[4][15]
6. Respiratory Conditions (Cystic Fibrosis, IPF)
Inhaled/aerosolized glutathione (600 mg BID) is investigated for replenishing GSH in the epithelial lining fluid of the lungs. Oral reduced L-glutathione improved growth in pediatric cystic fibrosis patients. Results on FEV1 improvement have been mixed across studies.[17]
7. Viral Infections & Immune Function
GSH depletion is linked to impaired host immune responses and severe outcomes in HIV and COVID-19. Liposomal glutathione supplementation elevated body stores of GSH and markers of immune function (including natural killer cell activity) in healthy adults.[14]
8. Male Infertility
Intramuscular GSH (600 mg) was studied in a placebo-controlled, double-blind crossover trial for male infertility, targeting oxidative stress in seminal plasma that damages sperm DNA and motility.[10]
9. Cardiovascular Aging
In aged Wistar rats, intraperitoneal GSH (52 mg/kg) increased total heart glutathione by 40% (p = 0.0027), reduced superoxide generation 2.5-fold, and restored endothelium-dependent vasorelaxation, demonstrating significant cardiovascular rejuvenation potential.[3]
Biochemical Characteristics
| Property | Value |
|---|---|
| Molecular Formula | C₁₀H₁₇N₃O₆S |
| Molecular Weight | 307.32 g/mol |
| CAS Number | 70-18-8 |
| PubChem CID | 124886 |
| Sequence (3-Letter) | γ-Glu-Cys-Gly |
| Sequence (1-Letter) | γ-E-C-G |
| IUPAC Name | (2S)-2-Amino-5-({(2R)-1-[(carboxymethyl)amino]-1-oxo-3-sulfanylpropan-2-yl}amino)-5-oxopentanoic acid |
| Structure | Tripeptide with gamma-peptide linkage between γ-carboxyl of glutamate and α-amino of cysteine; contains free thiol (sulfhydryl) group; forms intermolecular disulfide bond (GSSG) upon oxidation |
| Origin | Endogenous tripeptide synthesized in virtually all mammalian cells from L-glutamate, L-cysteine, and glycine via a two-step ATP-dependent enzymatic process (GCL and GS) |
| Classification | Endogenous Tripeptide Antioxidant / Redox Modulator / Research Compound |
| Half-Life | Plasma half-life < 3 minutes (IV administration); intracellular turnover regulated by γ-glutamyl cycle |
| Bioavailability | Low oral bioavailability due to intestinal hydrolysis by γ-glutamyl transpeptidase (GGT); enhanced by liposomal or sublingual delivery |
Identifiers
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|---|---|
| Synonyms | |
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| InChI |
Preclinical Research Summary
Research Summary
Key Clinical Studies
| Study | Design / Population | Key Findings | Ref |
|---|---|---|---|
| Richie et al. (2015) Eur J Nutr | RCT, n=54 healthy adults; 250 mg or 1000 mg oral GSH/day, 6 months | 1000 mg/day: significant increase in GSH in erythrocytes, plasma, lymphocytes, buccal cells (p < 0.05). 250 mg: no significant difference vs placebo | [12] |
| Mischley et al. (2017) J Parkinson's Dis | Phase IIb RCT, n=45 PD patients; 300 or 600 mg/day intranasal GSH, 12 weeks | 600 mg/day: UPDRS Total improved -4.6 points (P = 0.0025); Motor sub-score improved -2.2 points (P = 0.0485) | [11] |
| Honda et al. (2017) BMC Gastroenterol | Open-label pilot, n=34 NAFLD patients; 300 mg oral GSH/day, 4 months | Significant reduction in ALT (p < 0.05); non-significant improvements in liver stiffness | [8] |
| Søndergård et al. (2021) Appl Physiol Nutr Metab | RCT, n=20 obese males ± T2DM; 1000 mg oral GSH/day, 3 weeks | Whole-body insulin sensitivity significantly increased; skeletal muscle GSH increased ~19% | [16] |
| Weschawalit et al. (2017) Clin Cosm Invest Derm | RCT, n=57 healthy females; 250 mg oral GSH or GSSG/day, 12 weeks | Significant wrinkle reduction (P = 0.006); increased skin elasticity; melanin reduction in >40 yrs subgroup | [19] |
| Cascinu et al. (1995) J Clin Oncol | RCT, advanced gastric cancer; 1.5 g/m² IV GSH before cisplatin | Neuroprotective effect; reduced cisplatin-associated neurotoxicity without compromising chemotherapy efficacy | [4] |
| Smyth et al. (1997) Ann Oncol | RCT, ovarian cancer; IV GSH with cisplatin | Reduced toxicity; improved quality of life; no reduction in antineoplastic efficacy | [15] |
| Sinha et al. (2018) Eur J Clin Nutr | RCT; liposomal GSH supplementation | Elevated body stores of GSH; enhanced markers of immune function including natural killer cell activity | [14] |
Key Preclinical Studies
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Strutynska et al. (2023) | Aged male Wistar rats; 52 mg/kg i.p., acute | Heart GSH +40% (p=0.0027); superoxide reduced 2.5x; H2O2 reduced 2.3x; restored vasorelaxation; inhibited mPTP opening | [3] |
| Cai et al. (2003) | BALB/c mice; oral GSH; influenza A/X-31 | Decreased viral titers in both lung and trachea homogenates | [3] |
| Chinta et al. (2007) | In vivo GSH depletion in dopaminergic midbrain neurons | Inducible GSH alterations result in nigrostriatal degeneration, confirming causative role of GSH loss in PD pathology | [5] |
Dosage Summary
| Setting | Dose | Route / Duration | Notes |
|---|---|---|---|
| In Vitro | 0.5–10 mM | Cell culture | Physiological intracellular concentration range |
| Animal (Rat) | 52 mg/kg | Intraperitoneal; acute | LD50 > 5 g/kg (mice, oral) |
| Human — Oral (antioxidant) | 250–1000 mg/day | Oral capsules; 4 weeks–6 months | 1000 mg/day required for 6 months to significantly elevate body stores[12] |
| Human — Oral (skin) | 250–500 mg/day | Oral; 4–12 weeks | Significant melanin and wrinkle reduction[19][2] |
| Human — Intranasal | 200–600 mg/day | Intranasal atomization; 12 weeks | Brain GSH >200% increase within 45 min[11] |
| Human — IV | 1.5 g/m² | Intravenous; before chemotherapy | Neuroprotective adjunct to cisplatin[4] |
| Human — Topical | 2% GSSG lotion | Twice daily; 10 weeks | Significant reduction in melanin index, wrinkles, TEWL[18] |
| Human — Inhaled | 600 mg BID | Nebulized | Respiratory conditions; contraindicated in asthma[17] |
Safety Profile
| Route | Safety Assessment | Adverse Events |
|---|---|---|
| Oral | GRAS status; well-tolerated; LD50 > 5 g/kg (mice) | Mild: flatulence, loose stools, flushing, weight gain[12] |
| Topical | Generally well-tolerated | Mild erythema, pruritus; typically self-resolving[19] |
| Intranasal | Phase IIb safety established | One withdrawal (tachycardia/cardiomyopathy, resolved upon cessation)[11] |
| Intravenous | Significant safety concerns | 32% adverse event rate; hepatotoxicity, anaphylaxis, Stevens-Johnson syndrome reported |
| Inhaled | Contraindicated in asthma | Risk of bronchospasm |
&x26A0;&xFE0F; Important Disclaimer
This product is sold strictly for in-vitro research and laboratory use only. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. For Laboratory Research Only. Not for human use, medical use, diagnostic use, or veterinary use.
About This Research Profile
This research profile was compiled from peer-reviewed sources and publicly available scientific literature. All articles and product information provided on this website are for informational and educational purposes only. The information presented here does not constitute medical advice and should not be relied upon as a substitute for consultation with a qualified healthcare professional.
Authors & Attribution
✍️ Article Author
Helmut Sies, MD
Helmut Sies, MD, is a pioneering biochemist who formulated the concept of "oxidative stress" and is recognized as a "Redox Pioneer" by the journal Free Radical Biology and Medicine. He received his MD from the University of Munich (1967) and his Habilitation in Physiological Chemistry and Physical Biochemistry (1972), with training at the University of Tübingen and the University of Munich. He is affiliated with Heinrich Heine University of Düsseldorf. Dr. Sies elucidated the role of glutathione as an antioxidant and its physiology, quantified central redox systems including antioxidant GSH in subcellular compartments, and discovered that ebselen is a glutathione peroxidase mimic. His foundational work spans over four decades and has shaped the entire field of redox biology and antioxidant research. Key publications include "Hydroperoxide metabolism in mammalian organs" (1979), "Glutathione and its role in cellular functions" (1999, Free Radical Biology and Medicine), and "Oxidative stress: introductory remarks" (1985). Helmut Sies is being referenced as one of the leading scientists involved in Glutathione research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →🎓 Scientific Journal Author
Alton Meister, PhD
Alton Meister, PhD, was a distinguished biochemist and professor who was instrumental in the surge of glutathione research during the 1980s. He is credited with elucidating the γ-glutamyl cycle, the central metabolic pathway governing glutathione synthesis, transport, and degradation. Meister also developed the use of buthionine sulfoximine (BSO) as a potent and specific inhibitor of glutathione synthesis, a method that became a widely adopted tool for studying GSH deficiency in experimental systems. His work established the mechanistic foundation for understanding how cells synthesize, utilize, and recycle this critical antioxidant. His landmark publications include "Glutathione" (1983, Annual Review of Biochemistry), "On the discovery of glutathione" (1988), and "Glutathione metabolism and its selective modification" (1988, Journal of Biological Chemistry). Alton Meister is being referenced as one of the leading scientists involved in Glutathione research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Alton Meister, PhD is being referenced as one of the leading scientists involved in the research and development of Glutathione. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
🔬 Contributing Researcher
Laurie K. Mischley, ND, PhD
Laurie K. Mischley, ND, PhD, is a neuroscience researcher and clinician-scientist who has led the most advanced clinical trials investigating intranasal glutathione for Parkinson's disease. She conducted the Phase I/IIa safety and tolerability trial (2015, Movement Disorders), which established the safety of intranasal GSH and demonstrated preliminary efficacy over placebo on UPDRS scores. Her Phase IIb randomized, double-blind, placebo-controlled trial (2017, Journal of Parkinson's Disease; NCT02424708) demonstrated that 600 mg/day intranasal GSH significantly improved Total UPDRS scores (-4.6 points, P = 0.0025) and Motor sub-scores (-2.2 points, P = 0.0485) over 12 weeks. Critically, her CNS uptake study (2016, npj Parkinson's Disease) demonstrated that a single 200 mg intranasal dose increased brain GSH levels by over 200% within approximately 45 minutes (P < 0.001) as measured by magnetic resonance spectroscopy, providing target validation that intranasally administered GSH reaches the central nervous system. Laurie K. Mischley is being referenced as one of the leading scientists involved in Glutathione research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Laurie K. Mischley, ND, PhD is being referenced as one of the leading scientists involved in the research and development of Glutathione. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
Referenced Citations
Allen J, Bradley RD. Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers. Journal of Alternative and Complementary Medicine, 17(9), 827-833, 2011.
PubMedArjinpathana N, Asawanonda P. Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study. Journal of Dermatological Treatment, 23(2), 97-102, 2012.
PubMedBallatori N, Krance SM, Notenboom S, Shi S, Tieu K, Hammond CL. Glutathione dysregulation and the etiology and progression of human diseases. Biological Chemistry, 390(3), 191-214, 2009.
PubMedCascinu S, Cordella L, Del Ferro E, et al. Neuroprotective effect of reduced glutathione on cisplatin-based chemotherapy in advanced gastric cancer: a randomized, double-blind, placebo-controlled trial. Journal of Clinical Oncology, 13(1), 26-32, 1995.
PubMedChinta SJ, Kumar MJ, Hsu M, et al. Inducible alterations of glutathione levels in adult dopaminergic midbrain neurons result in nigrostriatal degeneration. Journal of Neuroscience, 27(51), 13997-14006, 2007.
PubMedHandog EB, Datuin MS, Singzon IA. 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. International Journal of Dermatology, 55(2), 153-157, 2016.
PubMedHolmay MJ, Terpstra M, Coles LD, et al. N-Acetylcysteine boosts brain and blood glutathione in Gaucher and Parkinson diseases. Clinical Neuropharmacology, 36(4), 103-106, 2013.
PubMedHonda Y, Kessoku T, Sumida Y, et al. Efficacy of glutathione for the treatment of nonalcoholic fatty liver disease: an open-label, single-arm, multicenter, pilot study. BMC Gastroenterology, 17(1), 96, 2017.
PubMedKovacs-Nolan J, Rupa P, Matsui T, et al. In vitro and ex vivo uptake of glutathione (GSH) across the intestinal epithelium and fate of oral GSH after in vivo supplementation. Journal of Agricultural and Food Chemistry, 62(39), 9499-9506, 2014.
PubMedLenzi A, Culasso F, Gandini L, Lombardo F, Dondero F. Placebo-controlled, double-blind, cross-over trial of glutathione therapy in male infertility. Human Reproduction, 8(10), 1657-62, 1993.
PubMedMischley LK, Leverenz JB, Lau RC, et al. A randomized, double-blind phase I/IIa study of intranasal glutathione in Parkinson's disease. Movement Disorders, 30(12), 1696-1701, 2015.
PubMedRichie JP, Nichenametla S, Neidig W, et al. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. European Journal of Nutrition, 54(2), 251-263, 2015.
PubMedSechi G, Deledda MG, Bua G, et al. Reduced intravenous glutathione in the treatment of early Parkinson's disease. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 20(7), 1159-1170, 1996.
PubMedSinha R, Sinha I, Calcagnotto A, et al. Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function. European Journal of Clinical Nutrition, 72(1), 105-111, 2018.
PubMedSmyth JF, Bowman A, Perren T, et al. Glutathione reduces the toxicity and improves quality of life of women diagnosed with ovarian cancer treated with cisplatin: results of a double-blind, randomised trial. Annals of Oncology, 8(6), 569-73, 1997.
PubMedSøndergård SD, Cintin I, Kuhlman AB, et al. The effects of 3 weeks of oral glutathione supplementation on whole body insulin sensitivity in obese males with and without type 2 diabetes: a randomized trial. Applied Physiology, Nutrition, and Metabolism, 46(9), 1133-1142, 2021.
PubMedVisca A, Bishop CT, Hilton S, Hudson VM. Oral reduced L-glutathione improves growth in pediatric cystic fibrosis patients. Journal of Pediatric Gastroenterology and Nutrition, 60(6), 802-810, 2015.
PubMedWatanabe 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, 7, 267-274, 2014.
PubMedWeschawalit S, Thongthip S, Phutrakool P, Asawanonda P. Glutathione and its antiaging and antimelanogenic effects. Clinical, Cosmetic and Investigational Dermatology, 10, 147-153, 2017.
PubMedWitschi A, Reddy S, Stofer B, Lauterburg BH. The systemic availability of oral glutathione. European Journal of Clinical Pharmacology, 43(6), 667-669, 1992.
PubMedRUO Disclaimer
For Research Use Only (RUO). This product is intended solely for in-vitro research and laboratory experimentation. It is not a drug, food, cosmetic, or medical device and has not been approved by the FDA for any human or veterinary use. It must not be used for therapeutic, diagnostic, or any other non-research purpose. Pure US Peptide does not condone or encourage the use of this product for anything other than strictly defined research applications. Users assume full responsibility for compliance with all applicable regulations and guidelines.
Certificate of Analysis (COA)
Every batch is strictly tested by accredited third-party laboratories (ISO 17025) to ensure 99%+ purity.
Latest Lab Report
Storage & Handling
Summary
Lyophilized: -20°C or 2–8°C (stable long-term as dry powder); Reconstituted: aliquot immediately, store at 2–8°C short-term or -20°C long-term; protect from light, air, and moisture; avoid freeze-thaw cycles.
Lyophilized Powder
Store at -20°C for optimal long-term stability, or at 2–8°C for routine storage. The dry powder form is relatively stable but must be kept in tightly sealed, opaque containers to protect from light and moisture. Glutathione is highly susceptible to oxidation in the presence of air and elevated humidity (water activity >0.3).
Reconstituted Solution
Dissolve in sterile water or PBS (Phosphate Buffered Saline). Aqueous GSH solutions oxidize rapidly to GSSG when exposed to air. Aliquot stock solutions immediately after preparation to minimize freeze-thaw cycles. Store aliquots at -20°C and use promptly after thawing. For short-term use, keep at 2–8°C and consume within 24 hours.
Quality & Handling
Supplied as a white crystalline powder. Purity: ≥98% by HPLC. Identity verified by HPLC, mass spectrometry (307.32 g/mol), and enzymatic recycling assay. Incompatible with strong oxidizing agents. In laboratory settings, prepared solutions should be temperature-controlled and protected from light until immediately before use. CAS: 70-18-8, PubChem CID: 124886.
Related Research Compounds
5-Amino 1MQ
50mg
NAD+
1000mg
MOTS-C
40mg