Glutathione trisulfide TFA
Based on 1 Customer Validation
Glutathione trisulfide TFA (GSSSG TFA) is an orally active, blood-brain barrier permeable neuroprotective agent. Glutathione trisulfide TFA inactivates intracellular tyrosinase, regulates the expression of Cars2, Cbs, MITF and TYR, inhibits α-MSH (HY-P0252)-induced melanogenesis, and restores intracellular persulfide levels reduced by α-MSH. Glutathione trisulfide TFA scavenges free radicals, quenches ROS, reduces Paclitaxel (HY-B0015)-induced superoxide production, upregulates the expression of antioxidant protein genes, and inhibits oxidative stress-induced cell death. Glutathione trisulfide TFA promotes ERK1/2 activation, prevents NF-κB p65 activation, inhibits TAK1 phosphorylation, reduces pro-inflammatory cytokine expression, and blocks microglial activation. Glutathione trisulfide TFA can be used in research related to dry age-related macular degeneration, inflammation-associated eye diseases, Alzheimer's disease, Parkinson's disease, etc.
For research use only. We do not sell to patients.
- Purity: 99.08%
- Formula: C20H32N6O12S3·xC2HF3O2
- Molecular Weight:644.70 (free base)
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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IL-6 |
IL-1β |
Cars2 |
Cbs |
MITF |
TYR |
ERK1 |
ERK2 |
NF-κB |
p65 |
TAK1 |
Glutathione trisulfide (25-100 μM; 30 min pretreatment, 24 h α-MSH (HY-P0252) incubation) TFA (GSSSG TFA) is non-cytotoxic to B16-F0 cells at 25 μM and 50 μM following 30 min pretreatment and 24 h α-MSH incubation, while 100 μM causes a modest non-significant viability reduction[1].
Glutathione trisulfide (25-50 μM; 30 min pretreatment, 24 h α-MSH incubation) TFA potently suppresses α-MSH-induced melanin production in B16-F0 cells[1].
Glutathione trisulfide (25-50 μM; 30 min pretreatment, 24 h α-MSH incubation) TFA dose-dependently downregulates Mitf and TYR gene expression in α-MSH-induced B16-F0 cells[1].
Glutathione trisulfide (25-50 μM; 30 min pretreatment, 24 h α-MSH incubation) TFA significantly upregulates Cars2 and Cbs gene expression in α-MSH-induced B16-F0 cells[1].
Glutathione trisulfide (25-50 μM; 30 min pretreatment, 24 h α-MSH incubation) TFA significantly restores α-MSH-reduced intracellular persulphide levels in B16-F0 cells[1].
Glutathione trisulfide (50 μM; 30 min pretreatment, 24 h α-MSH incubation) TFA significantly inactivates intracellular tyrosinase activity in α-MSH-induced B16-F0 cells[1].
Glutathione trisulfide (0.1-100 μM; 24 h) TFA protects SH-SY5Y cells from MPP+-induced cell death[3].
Glutathione trisulfide (0.1-2 mM; 30 min) TFA exhibits dose-dependent antioxidant radical-scavenging activity in a cell-free DPPH assay, with up to 65% scavenging activity at 2 mM[1].
Glutathione trisulfide (10-30 μM; 30 minutes) TFA attenuates Paclitaxel-induced superoxide production in cultured murine primary cortical neurons[5].
Glutathione trisulfide (25-200 µM; 6 h) TFA is non-toxic to mouse primary Müller cells and BV-2 microglial cells at concentrations up to 100 µM, while 200 µM reduces Müller cell viability[2].
Glutathione trisulfide (25-200 µM; 1 h pre-incubation, 6 h or 24 h LPS stimulation) TFA dose-dependently inhibits LPS-induced upregulation of IL-6 and Ccl2 mRNA expression and protein secretion in mouse primary Müller cells, with significant effects at concentrations of 100 and 200 µM[2].
Glutathione trisulfide (200 µM; 1 h pre-incubation, 30 or 60 min LPS stimulation) TFA inhibits LPS-induced phosphorylation of TAK1 (Ser412) in mouse BV-2 microglial cells at 30 and 60 minutes post-LPS stimulation[2].
Glutathione trisulfide (25-200 µM; 1 h pre-incubation, 6 h or 24 h LPS stimulation) TFA dose-dependently inhibits LPS-induced upregulation of TNF-α, Ccl2, IL-6, and IL-1β mRNA expression, as well as TNF-α, Ccl2, and IL-6 protein secretion in mouse BV-2 microglial cells, with significant effects starting at 25 µM for some targets[2].
Glutathione trisulfide (500 nM; 1 hour) TFA prevents Paclitaxel (HY-B0015)-induced axonal degeneration and mitochondrial fragmentation in cultured murine primary DRG neurons by restoring axonal elongation and preserving axonal mitochondrial integrity[5].
Glutathione trisulfide (10 μM; 24 hours) TFA does not alter the anti-tumor cytotoxic effect of 2 μM Paclitaxel on human breast cancer MDA-MB-231 cells[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:B16-F0 murine melanoma cells
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Concentration:25 μM; 50 μM; 100 μM
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Incubation Time:30 min (pretreatment); 24 h (α-MSH incubation)
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Result:Caused no reduction in B16-F0 cell viability at 25 μM and 50 μM.
Caused a modest, non-statistically significant reduction in cell viability at 100 μM.
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Cell Line:α-MSH-induced B16-F0 murine melanoma cells
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Concentration:25 μM; 50 μM
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Incubation Time:30 min (pretreatment); 24 h (α-MSH incubation)
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Result:Downregulated the expression of melanogenesis-related genes Mitf and TYR in a dose-dependent manner.
Induced statistically significant reductions in Mitf and TYR expression at 25 μM and 50 μM relative to α-MSH-only treated cells.\nSignificantly upregulated the expression of persulphide synthesis-related genes Cars2 and Cbs in α-MSH-treated cells.
Induced statistically significant increases in Cars2 and Cbs expression at both 25 μM and 50 μM concentrations.
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Cell Line:mouse BV-2 microglial cells
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Concentration:25-200 µM
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Incubation Time:1 h pre-incubation; 6 h LPS stimulation (mRNA); 1 h pre-incubation; 6 h or 24 h LPS stimulation (protein)
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Result:Significantly inhibited LPS-induced TNF-α mRNA expression at 50, 100, and 200 µM.
Significantly inhibited LPS-induced Ccl2 mRNA expression at 200 µM.
Significantly inhibited LPS-induced IL-6 mRNA expression at 50, 100, and 200 µM.
Significantly inhibited LPS-induced IL-1β mRNA expression at 25, 50, 100, and 200 µM.
Significantly inhibited LPS-induced TNF-α secretion at 200 µM.
Significantly inhibited LPS-induced Ccl2 secretion at 200 µM.
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Cell Line:mouse BV-2 microglial cells
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Concentration:200 µM
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Incubation Time:1 h pre-incubation; 30 or 60 min LPS stimulation
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Result:Significantly inhibited LPS-induced TAK1 phosphorylation (Ser412) at 30 minutes post-stimulation.
Significantly inhibited LPS-induced TAK1 phosphorylation (Ser412) at 60 minutes post-stimulation.
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Cell Line:human neuroblastoma SH-SY5Y cells
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Concentration:0.1-100 μM
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Incubation Time:24 h
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Result:Significantly increased cell viability relative to MPP+-treated cells at all tested concentrations.
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Cell Line:human breast cancer MDA-MB-231 cells
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Concentration:10 μM
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Incubation Time:24 hours
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Result:Resulted in 48.3% viable cells, compared to 44.9% viable cells with Paclitaxel alone.
Showed no significant difference from Paclitaxel-only group via statistical equivalence testing (10% margin), with a mean difference of 0.034 and 90% confidence interval of -0.280 to 0.357.
Glutathione trisulfide (200 mg/kg; i.p.; daily; 4 days) TFA prevents post-ischemic spinal cord injury-induced paraplegia in mice, while maintaining a 100% survival rate[3].
Glutathione trisulfide (50 mg/kg/day; oral gavage; daily; 28 days) TFA ameliorates Paclitaxel-induced mechanical allodynia in male C57BL/6J mice by preserving unmyelinated axon integrity, reducing mitochondrial swelling, and upregulating antioxidant signaling in peripheral sensory neurons[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar rats (8-10 weeks old)[2]
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Dosage:15 nmol/eye; 60 nmol/eye
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Administration:intravitreal; single co-administration with LPS
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Result:Significantly decreased LPS-induced upregulation of IL-6 mRNA in rat retinas at 15 nmol/eye dose, but did not significantly affect IL-1β or Ccl2 mRNA upregulation.
Significantly attenuated LPS-induced upregulation of IL-6, IL-1β, and Ccl2 mRNA in rat retinas at 60 nmol/eye dose.
Significantly reduced LPS-induced accumulation of Iba1-immunopositive microglia in rat retinas at 60 nmol/eye dose, lowering density from ~900 cells/mm2 (LPS alone) to ~700 cells/mm2.
Did not affect baseline microglial density when administered alone.
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Animal Model:unspecified strain[3]
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Dosage:200 mg/kg
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Administration:i.p.; daily; 4 days
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Result:Maintained BMS scores >6 in all 4 treated mice at 24, 48, and 72 hours post-SCI, with 0/4 developing paraplegia.
Achieved a 100% survival rate (4/4 mice) at 72 hours post-SCI.
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Animal Model:C57BL/6J (male, 6-7 weeks old, Paclitaxel-induced peripheral neuropathy)[5]
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Dosage:50 mg/kg/day (behavioral/histological studies); 50 mg/kg (tissue distribution studies); 50 mg/kg (gene expression studies)
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Administration:oral gavage; daily; 28 days (behavioral/histological studies); oral gavage; single dose (tissue distribution studies); oral gavage; single dose (gene expression studies)
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Result:Ameliorated Paclitaxel-induced mechanical allodynia over 28 days, but did not alter thermal hyperalgesia.
Prevented Paclitaxel-induced loss of intraepidermal nerve fibers at 4 weeks.
Increased the ratio of unmyelinated axons in sciatic nerves compared to Paclitaxel-only mice; did not affect myelinated axon count or myelin thickness (G-ratio).
Reduced Paclitaxel-induced mitochondrial swelling in unmyelinated sciatic nerve axons, with a median mitochondrial cross-sectional area of 0.041 μm2.
Detected 34S-labeled form 2 hours after oral administration at concentrations of 415 pmol/mg protein in lumbar DRG, 518 pmol/mg protein in lumbar spinal cord, 142 pmol/mg protein in brain, 158 pmol/mg protein in liver, and 58 pmol/mL in plasma; 34S-labeled reactive sulfur species (GSSH, CysSSH, CysSSSCys) were >10-fold higher than endogenous 32S-containing counterparts in all tissues.
Upregulated mRNA expression of Nrf2-dependent antioxidant genes in lumbar DRG 2 hours after co-administration with Paclitaxel.
Chemical Information
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Appearance Solid
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Molecular Weight 644.70 (free base)
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Formula C20H32N6O12S3·xC2HF3O2
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Color White to off-white
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SMILES
OC([C@@H](N)CCC(N[C@@H](CSSSC[C@@H](C(NCC(O)=O)=O)NC(CC[C@H](N)C(O)=O)=O)C(NCC(O)=O)=O)=O)=O.O=C(O)C(F)(F)F.[x]
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Synonyms
GSSSG TFA
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
DMSO : 100 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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Data Sheet (291 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Glutathione trisulfide TFA Related Classifications
HY-160906A Related Classifications
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- Glutathione trisulfide
- GSSSG
- Interleukin Related
- Tyrosinase
- ERK
- Microphthalmia Associated Transcription Factor (MITF)
- Reactive Oxygen Species (ROS)
- NF-κB
- ARPE-19 cells
- MDA-MB-231 cells
- BV-2 microglial cells
- murine primary cortical neurons
- primary mouse RPE cells
- murine primary DRG neurons
- B16-F0 cells
- SH-SY5Y cells
- primary human RPE cells
- mouse primary Müller cells
- Inhibitor
- inhibitor
- inhibit