| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 25mg | 电议 |
| 100mg | 电议 |
Preparation Method | 4μL of serial dilutions of Lenvatinib (E7080) were mixed in a 96-well round plate with 10μL of enzyme (KDR), 16μL of poly (GT) solution (250 ng) and 10μL of ATP solution (1μmol/L ATP) (final concentration of DMSO was 0.1%).The kinase reaction was initiated by adding ATP solution to each well. After 30-min incubation at 30℃, the reaction was stopped by adding 0.5 mol/L EDTA (10μL/well) to the reaction mixture in each well. HTRF solution (50μL/well) was added to the reaction mixture, and then kinase activity was determined by measurement of fluorescence with a time-resolved fluorescence detector at an excitation wavelength of 337 nm and an emission wave-lengths of 620 and 665 nm. |
Reaction Conditions | 4μL,30 min |
Applications | Lenvatinib (E7080) inhibited KDR with IC50values of 4.0 nM. |
Cell lines | 8505C and TCO1 cell |
Preparation Method | The cells were grown in 96-well microplates in a final volume of 100 μL culture medium per well. The cells were incubated with 0.1 to 50 μM Lenvatinib (E7080) for 48 h. Then, 50 μL of the XTT labeling mixture was added to each well to a final XTT concentration of 0.3 mg/mL. After incubation of the microplate for 4 h in 5% CO2 at 37 ℃ in a humidified incubator, the formazan dye formed was quantified using a scanning multiwell spectrophotometer. |
Reaction Conditions | 0.1 to 50 μM Lenvatinib (E7080) for 48 h |
Applications | The half-maximal inhibitory concentrations (IC50) for Lenvatinib (E7080) treatment of 8505C and TCO1 cells were 24.26 and 26.32 μM, respectively. |
Animal models | Female BALB/c nude mice (8–12 weeks old, 20–25 g) |
Preparation Method | H146 tumor cells (6.5×106) were implanted subcutaneously into the flank region of mice. Twelve days after inoculation, mice were randomized into control (n=12) and treatment groups (n=6) and this point in time was identified as day 1. Lenvatinib (E7080) were suspended in 0.5% methylcellulose and saline, and administered orally twice a day for Lenvatinib (E7080) from day 1 to day 21. Tumor volume was measured on the indicated days and calculated. |
Dosage form | Administer orally twice a day for Lenvatinib (E7080) |
Applications | Oral administration of Lenvatinib (E7080) inhibited the growth of H146 tumor at 30 and 100 mg/kg in a dose-dependent manner and caused tumor regression at 100 mg/kg. |
| 文献引用 | |
| 产品描述 | E7080, known as lenvatinib, is an oral multitargeted tyrosine kinase inhibitor including VEGF, FGF and SCF receptors that has been shown to improve the survival rate of patients with radioiodine-refractory thyroid cancer. Lenvatinib (E7080) had antitumor activity against HCC PDX models, likely through its potent anti-angiogenic activity[1]. Lenvatinib (E7080) inhibited Flt-1, KDR, Flt-4 with IC50values of 22, 4.0 and 5.2 nM, respectively. Lenvatinib (E7080) inhibited FGFR1 and FDGFR tyrosine kinases. In addition to these kinases, Lenvatinib (E7080) also inhibited KIT kinase with an IC50value of 100 nM[2]. The half-maximal inhibitory concentrations (IC50) for Lenvatinib (E7080) treatment of 8505C and TCO1 cells were 24.26 and 26.32 μM, respectively[3]. The novel multi-targeted kinase inhibitor Lenvatinib (E7080), which inhibited both KDR and KIT kinases, showed a more potent antitumor efficacy against H146 tumor than imatinib. Oral administration of Lenvatinib (E7080) inhibited the growth of H146 tumor at 30 and 100 mg/kg in a dose-dependent manner and caused tumor regression at 100 mg/kg[2]. Lenvatinib (E7080) at 10 and 30 mg/kg inhibited the tumor growth of both PDXs, LI0050 and LI0334[1]. Lenvatinib (E7080), as compared with placebo, was associated with significant prolongation of progression-free survival and an improved response rate (64.8% vs. 1.5%) among patients with iodine-131–refractory differentiated thyroid cancer[4]. References: |
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