| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
Cell lines | Mesencgymal stem cells(MSCs) |
Preparation Method | PKM2-IN-1 (10 mM) was dissolved in dimethyl sulfoxide (DMSO) and stored at -80℃ for subsequent experiments. MSCs were seeded into a 12-well plate and induced in adipogenic medium containing PKM2-IN-1 (10 μM). |
Reaction Conditions | PKM2-IN-1 10 μM |
Applications | Increasing the concentration of PKM2-IN-1 gradually promoted adipogenesis confirming the role of PKM2 activity in the TRAF4-mediated inhibition of adipogenic differentiation, 10 μM PKM2-IN-1 increased adipogenesis in the TRAF4-overexpressing group |
Animal models | BALB/c nude mice subcutaneously injected with SK-OV-3 cells |
Preparation Method | Once the tumor reached 200 cm3, the mice were randomly divided into two groups (n = 5 per group). PKM2-IN-1 (5 mg/kg body weight) dissolved in 1 ml of solvent was administered orally every 2 days for 31 days. |
Dosage form | 5 mg/kg PKM2-IN-1 orally every 2 days for 31 days |
Applications | PKM2-IN-1 treatment markedly decreased the tumor volume and tumor weight, compared with the control group. Meanwhile, no significant weight reduction was detected in the mouse treated with PKM2-IN-1, suggesting that PKM2-IN-1 did not cause any major organ toxicity. Thus, use of specific PKM2 inhibitors to block the glycolytic pathway and target cancer cell metabolism represents a promising therapeutic approach for treating PKM2-overexpressing ovarian cancer. |
| 产品描述 | PKM2-IN-1 is a pyruvate kinase M2 (PKM2) inhibitor with an IC50of 2.95μM[5]. In MSCs, Increasing the concentration of PKM2-IN gradually promoted adipogenesis confirming the role of PKM2 activity in the TRAF4-mediated inhibition of adipogenic differentiation, 10 μM PKM2-IN increased adipogenesis in the TRAF4-overexpressing group[1]. In the Huh7 cell line, PKM2-IN-1 inhibited CCL20-mediated PKM2 expression and nuclear localization without affecting the phosphorylation of ERK1/2. Furthermore, PKM2-IN-1 inhibited CCL20-mediated aerobic glycolysis and reduced the ability of Huh7 cells to consume glucose and produce lactate and ATP[3].PKM2-IN-1 decreased lactate product and glucose uptake in Eca109 and Ec9706 cells[4].PKM2-IN-1 can induce cytotoxicity in HNSCC cells without affecting their glycolysis rate or oxygen consumption[7].PKM2-IN-1 highly increased late apoptosis in U87MG glioma cells without G2-phase arrest[8] In mice, PKM2-IN-1 treatment markedly decreased the tumor volume and tumor weight, compared with the control group. Meanwhile, no significant weight reduction was detected in the mouse treated with PKM2-IN-1, suggesting that PKM2-IN-1 did not cause any major organ toxicity. Thus, use of specific PKM2 inhibitors to block the glycolytic pathway and target cancer cell metabolism represents a promising therapeutic approach for treating PKM2-overexpressing ovarian cancer[6].In hearts of 7-day-old mice, PKM2-specific inhibitor PKM2-IN-1 significantly blocked the proliferation of cardiomyocytes in HRR groups, indicating HRR-induced proliferation of cardiomyocytes was fully abolished by PKM2-IN-1[2] References: |
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