| CAS NO: | 915769-50-5 |
| 包装 | 价格(元) |
| 5mg | 电议 |
| 25mg | 电议 |
| 100mg | 电议 |
| Cas No. | 915769-50-5 |
| 别名 | 多韦替尼,TKI258 lactate hydrate; CHIR-258 lactate hydrate |
| 化学名 | 4-amino-5-fluoro-3-(6-(4-methylpiperazin-1-yl)-1H-benzo[d]imidazol-2-yl)quinolin-2(1H)-one 2-hydroxypropanoate hydra |
| Canonical SMILES | FC1=C(C(N)=C(C2=O)C3=NC4=C(N3)C=C(N5CCN(C)CC5)C=C4)C(N2)=CC=C1.CC(O)C(O)=O.O |
| 分子式 | C24H29FN6O5 |
| 分子量 | 500.52 |
| 溶解度 | ≥ 168.2mg/mL in Water |
| 储存条件 | Store at -20℃ |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
| 产品描述 | Description: IC50: ~10 nmol/L for FGFR1–3 Fibroblast growth factor receptor 1 (FGFR1) and FGFR2 amplifications are observed in approximately 10% of breast cancers and are related to poor outcomes. Dovitinib (TKI258) is an oral tyrosine kinase inhibitor (TKI) against FGFR1–3, VEGFR1–3, and platelet-derived growth factor receptor (PDGFR). In vitro: Dovitinib decreased the concentrations of pFRS2 and pERK/MAPK in a dose-dependent manner in FGFR1 amplified and FGFR2 amplified cell lines. The IC50 for cell growth inhibition was 190 and 180 nmol/L in MDA-MB-134 and SUM52, respectively. Conversely, IC50 values were more than 2,000 nmol/L in the 11 breast cancer cell lines that had neither FGFR1 nor FGFR2 amplification [1]. In vivo: In vivo model (HBCx-2 breast cancer primary xenograft, with 8 FGFR1 gene copies), dovitinib prevented tumor growth at the 30 mg/kg dose and caused tumor regression at the 50 mg/kg dose. Similarly, dovitinib caused tumor regression in HBCx-3 xenografts when administered at a dose of 40 mg/kg daily until day 35 [1]. Clinical trial: Eighty-one patients were enrolled in the trial. Unconfirmed response or stable disease for over 6 months was observed in 5 and 1 patient(s) with FGFR1-amplified/HR-positive and FGFR1-nonamplified/HR-positive breast cancer. When qPCR-identified amplifications in FGFR1, FGFR2, or FGF3 were grouped to define an FGF pathway–amplified breast cancer in HR-positive patients, the mean reduction in target lesions was 21.1% compared with a 12.0% increase in patients that did not present with FGF pathway–amplified breast cancer [1]. Reference: |
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