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ACTB-1003
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
ACTB-1003图片
CAS NO:939805-30-8
包装与价格:
包装价格(元)
5mg电议
10mg电议
50mg电议
100mg电议

产品介绍
ACTB-1003 (ACTB-1003) 是一种口服激酶抑制剂,对 FGFR1、VEGFR2 和 Tie-2 的 IC50 分别为 6、2 和 4 nM。
Cas No.939805-30-8
别名ACTB-1003
化学名1-(4-(4-amino-6-(methoxymethyl)-7-(morpholinomethyl)pyrrolo[2,1-f][1,2,4]triazin-5-yl)-2-fluorophenyl)-3-(2-fluoro-5-(trifluoromethyl)phenyl)urea
Canonical SMILESCOCC1=C(CN2CCOCC2)N3N=CN=C(N)C3=C1C4=CC=C(NC(NC5=CC(C(F)(F)F)=CC=C5F)=O)C(F)=C4
分子式C27H26F5N7O3
分子量591.53
溶解度≥ 18.15mg/mL in DMSO
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

EOC317 (ACTB-1003) is an oral kinase inhibitor with IC50s of 6, 2 and 4 nM for FGFR1, VEGFR2 and Tie-2.

EOC317 (ACTB-1003) is an oral kinase inhibitor with multiple modes of action, targeting cancer mutations via FGFR inhibition FGFR1 (IC50=6 nM), angiogenesis through inhibition of VEGFR2 (2 nM), Tie-2 (4 nM), and induces apoptosis likely by targeting RSK (5 nM) and p70S6K (32 nM). EOC317 is highly active with dose-dependent tumor growth inhibition in cell lines with FGFR genetic alterations-OPM2 human multiple myeloma and the murine leukemia Ba/F3-TEL-FGFR1. OPM2 cells harbor the FGFR3 t(4:14) translocation, FGFR3 K650E mutation and PTEN deletion while the Ba/F3-TEL-FGFR1 cells are driven by FGFR1 over-expression[1].

EOC317 (ACTB-1003) is shown to inhibit tumor angiogenesis evident by the inhibition of CD31 staining in tumor sections. EOC317 is combinable with 5-FU or paclitaxel without diminishing the activity or increasing the toxicity of these chemotherapy agents in the HCT-116 colon tumor xenograft model[1].

References:
[1]. Patel K, et al. ACTB-1003: An oral kinase inhibitor targeting cancer mutations (FGFR), angiogenesis (VEGFR2, TEK), and induction of apoptosis (RSK and p70S6K). Journal of Clinical Oncology 28, no. 15 DOI: 10.1200/jco.2010.28.15_suppl.e13665