产品说明书

	同义名 :	-
	CAS号 :	1458630-17-5
	货号 :	A1328181
	分子式 :	C18H17F3N6O2
	纯度 :	97%
	分子量 :	406.362
	MDL号 :	MFCD24849399
	存储条件：	粉末 Inert atmosphere,Room Temperature 液体 -20°C:3-6个月-80°C:12个月
	溶解度 :	-
	动物实验配方：

生物活性

描述

CHR-6494 TFA is a potent haspin inhibitor with an IC50 value of 2 nM. CHR-6494 TFA inhibits the phosphorylation of histone H3 threonine 3. CHR-6494 TFA induces apoptosis in cancer cells, such as melanoma and breast cancer. CHR-6494 TFA can be used in cancer research[1][2][3 ].CHR-6494 TFA dose-dependently inhibited the growth of HCT-116, HeLa, MDA-MB-231, and Wi-38 cancer cells with IC50 values of 500 nM, 473 nM, 752 nM, and 1059 nM, respectively, at a concentration range of <105 nM for 72 h. At a concentration of 500 nM, CHR-6494 TFA inhibited the growth of cancer cells with IC50 values of 500 nM, 473 nM, 752 nM, and 1059 nM, respectively. At a concentration of 500 nM, CHR-6494 TFA causes a mitotic catastrophe with abnormal morphology of the mitotic spindle and centrosome amplification, and up-regulates the spindle assembly checkpoint protein BUB1 and the mitotic arrest marker cytosolic protein B1[1].CHR-6494 TFA has inhibitory activity against melanoma cell lines, including BRAFV600E mutant, NRAS mutant and wild-type cells, with IC50 values ranging from 396 nM to 1229 nM. At 300 nM and 600 nM concentrations for 72 hours, CHR-6494 TFA induced apoptosis and increased caspase 3/7 activity to 3-fold and 6-fold, respectively, in COLO-792 cells, and to 8.5-fold and 16-fold, respectively, in RPMI-7951 melanoma cells[2].At the concentration of 50 and 200 nM for 1 week, CHR-6494 TFA enhanced the antiproliferative effect of MLN8237 in MDA-MB-231 and SKBR3 breast cancer cells, and increased apoptosis[3].

实验方案
	1mg	5mg	10mg
1 mM 5 mM 10 mM	2.46mL 0.49mL 0.25mL	12.30mL 2.46mL 1.23mL	24.61mL 4.92mL 2.46mL

参考文献

[1]Huertas D, et al. Antitumor activity of a small-molecule inhibitor of the histone kinase Haspin. Oncogene. 2012 Mar 15;31(11):1408-18. [2]Han L, et al. Anti-Melanoma Activities of Haspin Inhibitor CHR-6494 Deployed as a Single Agent or in a Synergistic Combination with MEK Inhibitor. J Cancer. 2017 Aug 25;8(15):2933-2943. [3]Chen A, et al. CRISPR/Cas9 screening identifies a kinetochore-microtubule dependent mechanism for Aurora-A inhibitor resistance in breast cancer. Cancer Commun (Lond). 2021 Feb;41(2):121-139.