\n 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：\uf07d 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。\uf07d EC50 指加入抑制剂后，细胞死亡一半所需的浓度。\uf07d 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。
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SKU:K1236	\xa0	M. Wt:431.53	\xa0
Formula:C26H29N3O3	\xa0	Solubility:DSMO 86 mg/mL Water <1 mg/ml Ethanol <1 mg/ml	\xa0
Purity:>99%	\xa0	Storage:2 years at -20 degrees centigrade	\xa0
CAS No.:897016-82-9	\xa0	\xa0	\xa0
Chemical NameN-benzyl-2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)acetamide

\t\t\t\t\t\tSKU:K1236\t\t\t\xa0\t\t\tM. Wt:431.53\t\t\t\xa0\t\t\t\t\t\t\tFormula:C26H29N3O3\t\t\t\xa0\t\t\tSolubility:DSMO 86 mg/mL Water <1 mg/ml Ethanol <1 mg/ml\t\t\t\xa0\t\t\t\t\t\t\tPurity:>99%\t\t\t\xa0\t\t\tStorage:2 years at -20 degrees centigrade\t\t\t\xa0\t\t\t\t\t\t\tCAS No.:897016-82-9\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\t\t\tChemical NameN-benzyl-2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)acetamide\t\t\t\t\t\t\t\tSKU:K1236\t\t\t\xa0\t\t\tM. Wt:431.53\t\t\t\xa0\t\t\t\t\tSKU:K1236SKU:SKU:K1236\t\t\t\xa0\xa0\t\t\tM. Wt:431.53M. Wt:M. Wt:431.53\t\t\t\xa0\xa0\t\t\t\t\t\t\tFormula:C26H29N3O3\t\t\t\xa0\t\t\tSolubility:DSMO 86 mg/mL Water <1 mg/ml Ethanol <1 mg/ml\t\t\t\xa0\t\t\t\t\tFormula:C26H29N3O3Formula:Formula:C26H29N3O3\t\t\t\xa0\xa0\t\t\tSolubility:DSMO 86 mg/mL Water <1 mg/ml Ethanol <1 mg/mlSolubility:Solubility:DSMO 86 mg/mL Water <1 mg/ml Ethanol <1 mg/ml\t\t\t\xa0\xa0\t\t\t\t\t\t\tPurity:>99%\t\t\t\xa0\t\t\tStorage:2 years at -20 degrees centigrade\t\t\t\xa0\t\t\t\t\tPurity:>99%Purity:Purity:>99%\t\t\t\xa0\xa0\t\t\tStorage:2 years at -20 degrees centigradeStorage:Storage:2 years at -20 degrees centigrade\t\t\t\xa0\xa0\t\t\t\t\t\t\tCAS No.:897016-82-9\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\tCAS No.:897016-82-9CAS No.:CAS No.:897016-82-9\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\t\t\t\tChemical NameN-benzyl-2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)acetamide\t\t\t\t\tChemical NameN-benzyl-2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)acetamideChemical NameChemical NameN-benzyl-2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)acetamide\t\t\tBiological Activity
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Description	KX2-391 can inhibit Src with IC50 of 72 nM.
Targets	Src	\xa0	\xa0	\xa0	\xa0	\xa0
\xa0	\xa0	\xa0	\xa0	\xa0	\xa0	\xa0
IC50	72 nM	\xa0	\xa0	\xa0	\xa0	\xa0
In vitro	As a small molecule and non-ATP competitive inhibitor, KX2-391 can inhibit Src tyrosine kinase signaling inhibitor with an IC50 of 72 nM by targeting the substrate binding pocket of Src.[1] KX2-391 can also inhibit tubulin polymerization.[2] \t\t\tFor cell lines \t\t\tKX2-391 can inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation.
IN vivo	In pre-clinical animal models of cancer, orally administered KX2-391 was shown to inhibit primary tumor growth and to suppress metastasis. In combination with certain chemotherapeutic agents, KX2-391 can reduce the doses of some current cytotoxic agents. [3] KX2-391 is currently in Phase-2 testing for solid tumors. [2]

\t\t\t\t\t\tDescription\t\t\tKX2-391 can inhibit Src with IC50 of 72 nM.\t\t\t\t\t\t\tTargets\t\t\tSrc\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\t\t\tIC50\t\t\t72 nM\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\t\t\tIn vitro\t\t\tAs a small molecule and non-ATP competitive inhibitor, KX2-391 can inhibit Src tyrosine kinase signaling inhibitor with an IC50 of 72 nM by targeting the substrate binding pocket of Src.[1] KX2-391 can also inhibit tubulin polymerization.[2]
\t\t\tFor cell lines
\t\t\tKX2-391 can inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation.\t\t\t\t\t\t\tIN vivo\t\t\tIn pre-clinical animal models of cancer, orally administered KX2-391 was shown to inhibit primary tumor growth and to suppress metastasis. In combination with certain chemotherapeutic agents, KX2-391 can reduce the doses of some current cytotoxic agents. [3] KX2-391 is currently in Phase-2 testing for solid tumors. [2]\t\t\t\t\t\t\t\tDescription\t\t\tKX2-391 can inhibit Src with IC50 of 72 nM.\t\t\t\t\tDescriptionDescription\t\t\tKX2-391 can inhibit Src with IC50 of 72 nM.KX2-391 can inhibit Src with IC50 of 72 nM.\t\t\t\t\t\t\tTargets\t\t\tSrc\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\tTargetsTargets\t\t\tSrcSrc\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\t\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\t\t\t\tIC50\t\t\t72 nM\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\xa0\t\t\t\t\tIC50IC50\t\t\t72 nM72 nM\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\xa0\xa0\t\t\t\t\t\t\tIn vitro\t\t\tAs a small molecule and non-ATP competitive inhibitor, KX2-391 can inhibit Src tyrosine kinase signaling inhibitor with an IC50 of 72 nM by targeting the substrate binding pocket of Src.[1] KX2-391 can also inhibit tubulin polymerization.[2]
\t\t\tFor cell lines
\t\t\tKX2-391 can inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation.\t\t\t\t\tIn vitroIn vitro\t\t\tAs a small molecule and non-ATP competitive inhibitor, KX2-391 can inhibit Src tyrosine kinase signaling inhibitor with an IC50 of 72 nM by targeting the substrate binding pocket of Src.[1] KX2-391 can also inhibit tubulin polymerization.[2]
\t\t\tFor cell lines
\t\t\tKX2-391 can inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation.As a small molecule and non-ATP competitive inhibitor, KX2-391 can inhibit Src tyrosine kinase signaling inhibitor with an IC50 of 72 nM by targeting the substrate binding pocket of Src.[1] KX2-391 can also inhibit tubulin polymerization.[2]
\t\t\tFor cell lines
\t\t\tKX2-391 can inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation.\t\t\t\t\t\t\tIN vivo\t\t\tIn pre-clinical animal models of cancer, orally administered KX2-391 was shown to inhibit primary tumor growth and to suppress metastasis. In combination with certain chemotherapeutic agents, KX2-391 can reduce the doses of some current cytotoxic agents. [3] KX2-391 is currently in Phase-2 testing for solid tumors. [2]\t\t\t\t\tIN vivoIN vivo\t\t\tIn pre-clinical animal models of cancer, orally administered KX2-391 was shown to inhibit primary tumor growth and to suppress metastasis. In combination with certain chemotherapeutic agents, KX2-391 can reduce the doses of some current cytotoxic agents. [3] KX2-391 is currently in Phase-2 testing for solid tumors. [2]In pre-clinical animal models of cancer, orally administered KX2-391 was shown to inhibit primary tumor growth and to suppress metastasis. In combination with certain chemotherapeutic agents, KX2-391 can reduce the doses of some current cytotoxic agents. [3] KX2-391 is currently in Phase-2 testing for solid tumors. [2]\t\t\t\xa0