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首页-小分子抑制剂&激动剂-Tyrosine Kinase-c-Fms (CSF1R)-Vimseltinib
Vimseltinib

Chemical Structure : Vimseltinib

CAS No.: 1628606-05-2

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Vimseltinib (DCC-3014, DCC3014)

货号: PC-38376Not For Human Use, Lab Use Only.

Vimseltinib (DCC-3014) is a potent, selective, orally active inhibitor of colony-stimulating factor 1 receptor (CSF1R/c-Fms), inhibits CSF1R phosphorylated juxtamembrane domain (JMD) with IC50 of 2.8 nM, 100-fold less potency against fully phosphorylated CSF1R (IC50=290 nM).

规格 价格 库存 数量
5 mg ￥1880 In stock
10 mg ￥2780 In stock
25 mg ￥4580 In stock
50 mg ￥7280 In stock
100 mg Get quote
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纯度 & COA & 质检文件 纯度: >98% (HPLC) Select Batch:

生物&药学活性

Vimseltinib (DCC-3014) is a potent, selective, orally active inhibitor of colony-stimulating factor 1 receptor (CSF1R/c-Fms), inhibits CSF1R phosphorylated juxtamembrane domain (JMD) with IC50 of 2.8 nM, 100-fold less potency against fully phosphorylated CSF1R (IC50=290 nM).
Vimseltinib (DCC-3014) exhibits approximately 20-fold weaker affinity for unphosphorylated CSF1R (Kd=79 nM) versus the JMD phosphorylated form (Kd=3.6 nM).
Vimseltinib (DCC-3014) displays high selectivity (>100-fold) for CSF1R kinase against a panel of approximately 300 human kinases.
Vimseltinib (DCC-3014) potently inhibited CSF1-stimulated phosphorylation of CSF1R in the human THP1 mononuclear cell line with IC50 of 19 nM, inhibited proliferation of M-NFS-60 cells with IC50 of 10.1 nM.
Vimseltinib (DCC-3014) inhibited CSF1R signaling in monocytes in human whole blood with an average IC50 of 403 nM, as measured the levels of phosphorylated ERK (downstream of CSF1R activation).
Vimseltinib (DCC-3014) inhibited tumor growth and bone degradation in mouse cancer models.

物理化学性质&存储条件

分子量 431.500
分子式 C23H25N7O2
外观性状 Solid
CAS No.
储存条件
固体粉末
-20°C 12 个月; 4°C 6 个月
配置液
-80°C 6 个月; -20°C 6 个月
Shipping
Solubility

10 mM in DMSO
Chemical Name/SMILES

2-(isopropylamino)-3-methyl-5-(6-methyl-5-((2-(1-methyl-1H-pyrazol-4-yl)pyridin-4-yl)oxy)pyridin-2-yl)pyrimidin-4(3H)-one

参考文献

1. Smith BD, et al. Mol Cancer Ther. 2021 Nov;20(11):2098-2109.

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