Methyl pyruvate
Based on 1 Customer Validation
Methyl pyruvate is a p53/p21 axis inhibitor, intrinsic apoptosis inhibitor, cytotoxic agent, ATP production enhancer, proteasome function restorer, TDP-43 localization normalizer, ATP-sensitive potassium (K+ATP) channel inhibitor, depolarizer, and insulin secretagogue.Methyl pyruvate turns off apoptotic pathways, induces cancer cell death, acts as a substrate for dimeric dihydrodiol dehydrogenase, enhances TCA cycle activity, rescues proteasome impairment and TDP-43 mislocalization, inhibits K+ATP channels independent of ATP, depolarizes pancreatic β-cell membranes, modulates insulin secretion, and enters pancreatic β-cell mitochondria via a specific transporter.Methyl pyruvate can be used for the research of lung adenocarcinoma, ovarian clear cell adenocarcinoma, breast adenocarcinoma, amyotrophic lateral sclerosis, and type II diabetes.
For research use only. We do not sell to patients.
- Purity: 99.81%
- CAS No.: 600-22-6
- Formula: C4H6O3
- Molecular Weight:102.09
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Storage:
Store at room temperature 3 years.
In solvent -80°C, 2 years , -20°C, 1 year
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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
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Apoptosis Compound Library
HY-L003
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Membrane Transporter/Ion Channel Compound Library
HY-L011
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Anti-Cancer Compound Library
HY-L025
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Mitochondria-Targeted Compound Library
HY-L089
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Glucose Metabolism Compound Library
HY-L092
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Human Metabolite Library
HY-L123
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Highly Selective Activators Library
HY-L159
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Cell Death Library
HY-L162
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Bioactive Compound Library Max
HY-L181
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MCE Bioactive Compound Library
HY-L001V
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Bioactive Compound Library
HY-L001
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Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library
HY-L199
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High-Throughput Bioactive Compound Library
HY-L205
Biological Activity
Methyl pyruvate (1-2 mM; 4-48 h) inhibits the proliferation of RMG-1, A549 and MDA-MB 231 cancer cell lines, enhances the proliferation-inhibiting effect of irinotecan on these cancer cells, and protects MRC-5 normal lung fibroblasts from irinotecan-induced cell death[1].
Methyl pyruvate (2 mM; 4-48 h) induces apoptosis in p53 wild-type RMG-1 and A549 cancer cells, triggers only limited necrosis in p53-mutant MDA-MB 231 cancer cells, and protects MRC-5 normal lung fibroblasts from irinotecan-induced cell death by regulating cell cycle progression and inhibiting apoptosis[1].
Methyl pyruvate (2 mM; 4-48 h) attenuates the p53/p21-mediated pathway and mitochondrial apoptotic pathway in normal MRC-5 lung fibroblasts by downregulating the transcription of pro-apoptotic genes, while upregulating the expression of pro-apoptotic genes in RMG-1, A549 and MDA-MB 231 cancer cell lines[1].
Methyl pyruvate (2 mM; 4-48 h) regulates the expression of p53, cytochrome c and RBBP6 proteins, thereby inhibiting the apoptotic pathway in MRC-5 normal lung fibroblasts, while upregulating the expression of pro-apoptotic proteins in RMG-1, A549 and MDA-MB 231 cancer cell lines[1].
Methyl pyruvate (2 mM; 48 h) combined with irinotecan upregulates pro-apoptotic and stress response pathways in A549 cancer cells, while upregulating pro-survival, pro-angiogenic and metabolic pathways in MRC-5 normal lung fibroblasts[1].
Methyl pyruvate (5 μM; 48 h) rescues ATP depletion in Neuro2A cells overexpressing σ1RE102Q, both under basal conditions and tunicamycin (HY-A0098)-induced endoplasmic reticulum stress[3].
Methyl pyruvate (5 μM; 48 h) rescues proteasome dysfunction in Neuro2A cells overexpressing σ1RE102Q, and this effect is valid under both basal conditions and tunicamycin-induced endoplasmic reticulum stress[3].
Methyl pyruvate (5 μM; 48 h) inhibits the induction of autophagy in Neuro2A cells overexpressing σ1RE102Q under basal conditions, and reduces the enhanced level of autophagy during tunicamycin-induced endoplasmic reticulum stress[3].
Methyl pyruvate (5 μM; 48 h) reduces the apoptosis level of Neuro2A cells overexpressing σ1RE102Q under basal conditions[3].
Methyl pyruvate (5 μM; 48 h) rescues σ1RE102Q-induced cytoplasmic mislocalization of TDP-43 in Neuro2A cells, and this effect is observed under both basal conditions and tunicamycin-induced endoplasmic reticulum stress[3].
Methyl pyruvate (5-20 mM; 1 h) stimulates insulin release from isolated mouse islets in the absence of glucose, with the maximal effect observed at a concentration of 5 mM; at 5 mM, it enhances glucose-induced insulin secretion, while at 20 mM, it inhibits glucose-induced insulin secretion; in addition, its insulinotropic effect is inhibited by diazoxide but not potentiated by high K+ [4].
Methyl pyruvate (5-20 mM) depolarizes the membrane potential of mouse pancreatic β cells in a concentration-dependent manner, and maintains the depolarized state at concentrations of 10 mM and 20 mM[4].
Methyl pyruvate (1 mM; 10 min) stimulates ATP production in isolated pancreatic β-cell mitochondria, and its mitochondrial uptake is mediated by pyruvate transporters combined with malic acid (HY-Y1311) or glutamic acid[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human lung embryonic fibroblast (MRC-5), human ovarian clear cell adenocarcinoma (RMG-1), human lung adenocarcinoma (A549), human breast adenocarcinoma (MDA-MB 231)
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Concentration:1 mM, 2 mM
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Incubation Time:4 h, 24 h, 48 h; 20 h followed by 24-hour recovery (MRC-5)
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Result:Inhibited proliferation of RMG-1, A549, and MDA-MB 231 cancer cell lines at 2 mM alone.
Enhanced proliferation inhibition in cancer cells when combined with irinotecan, including reversing irinotecan resistance in RMG-1 cells.
Protected MRC-5 normal lung fibroblasts against irinotecan-induced cell death at 2 mM; cells treated with the combination survived in drug-free medium without exponential growth during the observation window, whereas cells treated with irinotecan alone did not recover.
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Cell Line:human lung embryonic fibroblast (MRC-5), human ovarian clear cell adenocarcinoma (RMG-1), human lung adenocarcinoma (A549), human breast adenocarcinoma (MDA-MB 231)
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Concentration:2 mM
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Incubation Time:4 h, 24 h, 48 h; 24-hour recovery (MRC-5)
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Result:Induced apoptotic cell death in p53 wild-type RMG-1 and A549 cancer cells after 48 h.
Induced necrotic cell death in ~25% of p53 mutant MDA-MB 231 cancer cells after 48 h.
Transiently unlocked irinotecan-induced G0/G1 cell cycle arrest in RMG-1 cells before inducing apoptosis.
Prevented irinotecan-induced cell death in MRC-5 fibroblasts, with most cells arrested at G0/G1 during treatment and progressing to S-phase and G2/M during recovery; minimal cell death was observed.
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Cell Line:human lung embryonic fibroblast (MRC-5), human ovarian clear cell adenocarcinoma (RMG-1), human lung adenocarcinoma (A549), human breast adenocarcinoma (MDA-MB 231)
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Concentration:2 mM
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Incubation Time:4 h, 24 h, 48 h; 24-hour recovery (MRC-5)
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Result:Abrogated transcription of p21, Bax, caspase 9, and caspase 3, and reduced cytochrome c expression in MRC-5 fibroblasts alone or combined with irinotecan.
Enhanced p53 transcription after 48 h (except RMG-1 and MRC-5) and upregulated pro-apoptotic gene expression in cancer cell lines with combination treatment.
Caused transient depletion of p21 and caspase 3 transcripts between 4-24 h, followed by reappearance at 48 h alongside p53 depletion and MDM2 mRNA increase in RMG-1 cells with combination treatment.
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Cell Line:human lung embryonic fibroblast (MRC-5), human ovarian clear cell adenocarcinoma (RMG-1), human lung adenocarcinoma (A549), human breast adenocarcinoma (MDA-MB 231)
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Concentration:2 mM
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Incubation Time:4 h, 24 h, 48 h; 24-hour recovery (MRC-5)
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Result:Reduced p53 protein levels, depleted cytochrome c, and caused differential expression of RBBP6 isoforms (isoform 1 expressed in first 24 h of treatment and depleted during recovery, isoform 3 upregulated during recovery) in MRC-5 fibroblasts with combination treatment.
Increased p53 and cytochrome c protein levels (except MDA-MB 231) and altered RBBP6 expression (reduced in RMG-1 cells, increased in other cancer cells) in cancer cell lines with combination treatment.
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Cell Line:mouse neuroblastoma Neuro2A cells overexpressing σ1Rᴱ102Q (with or without tunicamycin-induced ER stress)
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Concentration:5 μM
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Incubation Time:48 h
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Result:Significantly inhibited the increase in the LC3-II/total LC3 ratio induced by σ1Rᴱ102Q overexpression under basal conditions.
Tended to suppress the further increase in the LC3-II/total LC3 ratio seen in σ1Rᴱ102Q-overexpressing cells treated with tunicamycin.
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Cell Line:mouse neuroblastoma Neuro2A cells overexpressing σ1Rᴱ102Q (with or without tunicamycin-induced ER stress)
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Concentration:5 μM
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Incubation Time:48 h
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Result:Significantly inhibited apoptosis induced by σ1Rᴱ102Q overexpression under basal conditions.
Reduced the percentage of TUNEL-positive cells from ~28% to ~15%.
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Cell Line:mouse neuroblastoma Neuro2A cells overexpressing σ1Rᴱ102Q (with or without tunicamycin-induced ER stress)
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Concentration:5 μM
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Incubation Time:48 h
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Result:Inhibited the extra-nuclear localization of TDP-43 seen in σ1Rᴱ102Q-overexpressing cells under basal conditions, reducing the percentage of affected cells from ~72% to ~35%.
Reduced the extra-nuclear TDP-43 localization in σ1Rᴱ102Q-overexpressing cells treated with tunicamycin, decreasing the percentage of affected cells from ~90% to ~45%.
Chemical Information
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CAS No. 600-22-6
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Appearance Liquid (Density: 1.073±0.06 g/cm3)
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Molecular Weight 102.09
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Formula C4H6O3
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Color Colorless to light yellow
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SMILES
O=C(OC)C(=O)C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Store at room temperature 3 years
In solvent -80°C 2 years -20°C 1 year
Solvent & Solubility
DMSO : 200 mg/mL (1959.06 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Purity & Documentation
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Data Sheet (290 KB)
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SDS (466 KB)
- English - EN (466 KB)
- Français - FR (466 KB)
- Deutsch - DE (466 KB)
- Norwegian - NO (466 KB)
- Español - ES (466 KB)
- Swedish - SV (466 KB)
- Italian - IT (466 KB)
- Korean - KR (466 KB)
- Portuguese - PT (466 KB)
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Handling Instructions (2659 KB)
References
[1]. Monchusi B, et al. Methyl pyruvate protects a normal lung fibroblast cell line from irinotecan-induced cell death: Potential use as adjunctive to chemotherapy. PloS one. 2017;12(8):e0182789. [Content Brief]
[2]. Sato K, et al. Purification and characterization of dimeric dihydrodiol dehydrogenase from dog liver. Journal of biochemistry. 1994 Sep;116(3):711-7. [Content Brief]
[3]. Tagashira H, et al. Methyl pyruvate rescues mitochondrial damage caused by SIGMAR1 mutation related to amyotrophic lateral sclerosis. Biochimica et biophysica acta. 2014 Dec;1840(12):3320-34. [Content Brief]
[4]. Lembert N, et al. Methyl pyruvate initiates membrane depolarization and insulin release by metabolic factors other than ATP. The Biochemical journal. 2001 Mar 01;354(Pt 2):345-50. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 9.7953 mL | 48.9764 mL | 97.9528 mL | 244.8820 mL |
| 5 mM | 1.9591 mL | 9.7953 mL | 19.5906 mL | 48.9764 mL | |
| 10 mM | 0.9795 mL | 4.8976 mL | 9.7953 mL | 24.4882 mL | |
| 15 mM | 0.6530 mL | 3.2651 mL | 6.5302 mL | 16.3255 mL | |
| 20 mM | 0.4898 mL | 2.4488 mL | 4.8976 mL | 12.2441 mL | |
| 25 mM | 0.3918 mL | 1.9591 mL | 3.9181 mL | 9.7953 mL | |
| 30 mM | 0.3265 mL | 1.6325 mL | 3.2651 mL | 8.1627 mL | |
| 40 mM | 0.2449 mL | 1.2244 mL | 2.4488 mL | 6.1220 mL | |
| 50 mM | 0.1959 mL | 0.9795 mL | 1.9591 mL | 4.8976 mL | |
| 60 mM | 0.1633 mL | 0.8163 mL | 1.6325 mL | 4.0814 mL | |
| 80 mM | 0.1224 mL | 0.6122 mL | 1.2244 mL | 3.0610 mL | |
| 100 mM | 0.0980 mL | 0.4898 mL | 0.9795 mL | 2.4488 mL |
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