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:K1227		M. Wt:243.69
Formula:C11H14ClNO3		Solubility:DSMO 49 mg/mL Water <1 mg/ml Ethanol 49 mg/mL
Purity:>99%		Storage:2 years at -20 degrees centigrade
CAS No.:99873-43-5
Chemical Name4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide

Biological Activity

Description	As a selective inhibitor, Droxinostat (CMH, 5809354) shows inhibition to HDAC3, HDAC6 and HDAC8 with IC50 of 16.9 uM, 2.47uM and 1.46 uM, respectively.
Targets	HDAC3	HDAC6	HDAC8
IC50	16.9 uM	2.47uM	1.46 uM
In vitro	As a selective inhibitor, Droxinostat (CMH, 5809354) shows inhibition to HDAC3, HDAC6 and HDAC8 with IC50 of 16.9 uM, 2.47uM and 1.46 uM, respectively.Droxinostat,4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide, can inhibit and reduce c-FLIP expression without inhibiting caspases-8 and caspases-10. Droxinostat can downregulate c-FLIP(L) and c-FLIP(S) mRNA and protein levels. As cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (c-FLIP) plays a major resistance factor role in the tumor necrosis factor-related apoptosis-inducing ligand TRAIL and in drug resistance. Droxinostat inhibit c-FLIP, the caspase-8 inhibitor, and cause poly(ADP-ribose) polymerase (PARP) degradation. Droxinostat reduces cell survival and induce apoptosis in MCF-7 breast cancer cells.[1] Droxinostat selectively inhibited HDAC3, HDAC6, and HDAC8 and that inhibition of these HDACs was functionally important for its ability to sensitize cells to death ligands. [2] Droxinostat can downregulate c-FLIP expression, induced caspase-8- and caspase-3/7-mediated apoptosis, and increased apoptosis in bicalutamide-treated cells. [3]
IN vivo	In SCID mice models, Droxinostat shows inhibition to PPC-1 cells.