Kinasechem是来自英国的专业的抑制剂供应商，提供覆盖几百个激酶靶点的抑制剂。 Kinasechem的产品涉及绝大多数的信号通路研究以及癌症研究，包括： PI3K-Akt signaling pathway； MAPK signaling pathway; apoptosis(凋亡)； DNA damage( DNA 损伤) RTK(受体酪氨酸激酶） 等抑制剂在生命科学研究领域的应用非常广泛。在信号通路以及癌症研究方面，很多地方需要用到抑制剂来阻抑信号通路。目前，在HIV的研究，抗感染，心血管疾病，老年痴呆症（阿兹海默症），甚至糖尿病的研究中，都会使用到抑制剂。 1、 抑制剂的一般使用方法：（1）细胞实验将抑制剂溶解于DMSO, 乙醇或者水中，稀释到需要的浓度。一般孵育48小时，也有孵育2周的实验。（2）动物实验小鼠模型：以注射为主。大鼠模型：以口服为主。（3）抗药性筛选实验长期孵育，递增性增加浓度。 2、抑制剂的几个重要参数： IC50(半抑制浓度) 指抑制剂降低对应激酶的活性到原来活性的一半的浓度。 IC50是抑制剂一个重要的指标，一般而言，IC50越小，抑制能力越强。 EC50 指加入抑制剂后，细胞死亡一半所需的浓度。 抑制剂选择性抑制剂有多重抑制剂，指同时抑制多个靶点的抑制剂。有高选择性抑制剂，仅仅抑制某些激酶的某个亚型或者结构域。比如，有的抑制剂仅仅抑制PI3K这个激酶的gamma亚型。
Information

SKU:K1174		M. Wt:509.67
Formula:C26H35N7O2S		Solubility:DSMO 102 mg/mL Water <1 mg/ml Ethanol <1 mg/ml
Purity:>99%		Storage:2 years at -20 degrees centigrade
CAS No.:936091-14-4
Chemical NameN-tert-butyl-3-(5-methyl-2-(4-(4-methylpiperazin-1-yl)phenylamino)pyrimidin-4-ylamino)benzenesulfonamide

Biological Activity

Description	As a JAK2 selective inhibitor, TG101209 can inhibit JAK2 (IC50=6 nM), FLT3 (IC50=25 nM) and RET (IC50=17 nM) kinases and JAK3 (IC50=169 nM).
Targets	JAK2	FLT3	RET	JAK3
IC50	6 nM	25 nM	17 nM	169 nM
In vitro	As a JAK2 selective inhibitor, TG101209 can inhibit JAK2 (IC50=6 nM), FLT3 (IC50=25 nM) and RET (IC50=17 nM) kinases and JAK3 (IC50=169 nM). [1] By inducing cell cycle arrest and apoptosis, and inhibiting phosphorylation of JAK2V617F, STAT5 and STAT3, TG101209 inhibit the cell proliferation of human JAK2V617F-expressing acute myeloid leukemia cell line.[1] TG101209 inhibited growth of Ba/F3 cells expressing JAK2V617F or MPLW515L mutations with an IC50 of 200 nM.TG101209 can induce cytotoxicity in a variety of multiple myeloma (MM) cell lines in dose- and time-dependent manners. TG101209 can induce apoptosis and inhibit cell cycle progression in myeloma cell lines and patient-derived plasma cells. [2] Co-treatment with BEZ235 and JAK2-TKI (TG101209 and SAR302503) synergistically induced lethal activity against the cultured and primary CD34+ MPN cells while relatively sparing the normal CD34+ HPCs.
IN vivo	Treatment with TG101209 not only prevented bleomycin-induced fibrosis but also effectively reduced skin fibrosis in TSK-1 mice. addition of TG101209 to radiation in lung xenografts produced a significant tumor growth delay (>10 days) compared with radiation alone and was well tolerated. TG101209 increased apoptosis and decreased cell proliferation and vascular density.