| 包装 | 价格(元) |
| 2mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | Hep3B, JHH7, and HUH7 cells |
Preparation Method | Roblitinib was dissolved at 10 mmol/L in 100% DMSO to use |
Reaction Conditions | Roblitinib 5nM,500nM for 1h-72h |
Applications | Roblitinib inhibited FGFR4 tyrosine phosphorylation at compound concentrations needed to inhibit cell proliferation. |
Animal models | Four-week-old female BALB/c nude mice |
Preparation Method | Cells mixed with 1:1 Matrigel were subcutaneously injected into the fat pads of mice. The mice were randomized into four groups, and they were treated with vehicle, trastuzumab, Roblitinib (30 mg/kg, oral administration). The tumor volume was measured every 3 days. |
Dosage form | Roblitinib (30 mg/kg, oral administration) |
Applications | Compared with the other treatment group, the roblitinib treatment group showed decreased tumor volume. The combination of roblitinib and other drugs revealed a synergistic antitumor effect in trastuzumab-resistant breast cancer. |
| 产品描述 | Roblitinib (FGF-401) is a 1,8-naphthyridine pyridine derivative[5].Roblitinib binds to an inactive (autoinhibited brake, closed activation segment) DFG-Din enzyme form; the ligand binds covalently to FGFR4 and is classified as a Type VI inhibitor[7]. Roblitinib as an orally active and highly selective FGFR4 inhibitor with an IC50 of 1.9 nM without off-target effects[3]. Roblitinib has antitumor activity[4] 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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