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TAM Receptor

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TAM Receptor

结构式 货号 产品名称 CAS号
Batiraxcept 结构式
 BCP49357 Batiraxcept 2268717-61-7
Batiraxcept is an ultra-high affinity decoy protein that captures GAS6, preventing it from activating AXL signaling.
Ningetinib 结构式
 BCP46143 宁格替尼 1394820-69-9
Ningetinib is a novel tyrosine kinase inhibitor, targeted at c-Met, Axl, VEGFR-2, Mer and Flt3.
Gilteritinib hemifumarate 结构式
 BCP40569 富马酸吉瑞替尼 1254053-84-3
Gilteritinib, also known as ASP2215, is a potent FLT3/AXL inhibitor, which showed potent antileukemic activity against AML with either or both FLT3-ITD and FLT3-D835 mutations.
DS-1206b 结构式
 BCP40272 DS-1206b 1855860-24-0
DS-1206b is a selective and potent AXL kinase inhibitor with IC50 of 1.3 nM.
RU-301 结构式
 BCP35046 RU-301 1110873-99-8
RU-301 is a novel pan-tam inhibitor, blocking the interface between tam ig1 ectodomain and gas6 lg domain, potently inhibiting axl reporter cell lines and native tam receptors cancer cell lines.
TAM-IN-2 结构式
 BCP34892 TAM-IN-2 2135642-56-5
TAM-IN-2 is a TAM inhibitor extracted from patent US 20170275290 A1, pyrrolotriazine compound 0904.
UNC2541 结构式
 BCP33929 UNC2541 1612782-86-1
UNC2541 is a potent and Mer tyrosine kinase (MerTK)-specific inhibitor, binds in the MerTK ATP pocket, with an IC50 of 4.4 nM, more selective over Axl, Tyro3 and Flt3. UNC2541 inhibits phosphorylated MerTK (pMerTK; EC50, 510 nM).
ONO7475 结构式
 BCP33232 ONO7475 1646839-59-9
ONO-7475 is a potent and orally active Axl/Mer inhibitor. ONO-7475 targets and binds to both Axl and Mer, and prevents their activity.
BMS 777607 结构式
 BCP13190 BMS 777607 1196681-44-3
BMS 777607 is a novel, selective and orally available ATP-competitive MET kinase inhibitor that primarily targets several MET family members, including RON, MET, Tyro-3 and AxI, with half maximal inhibitory concentration IC50 of 1.8 nmol/L, 3.9 nmol/L, 4.3 nmol/L and 1.1 nmol/L respectively.
S49076 HCl 结构式
 BCP29576 S49076 HCl 1265966-31-1
S49076 is an effective inhibitor of MET, AXL/MER, and FGFR1/2/3. S49076 potently blocked cellular phosphorylation of MET, AXL, and FGFRs and inhibited downstream signaling in vitro and in vivo.
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