Methyl pyruvate

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 σ₁R^E102Q, 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 σ₁R^E102Q, 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 σ₁R^E102Q 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 σ₁R^E102Q under basal conditions^[3].
Methyl pyruvate (5 μM; 48 h) rescues σ₁R^E102Q-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.