PF-573228产品规格:1mL(10mM)|10mg|50mg|100mg发货周期:1～3天产品价格:询价本产品仅可用于科研实验,严禁用于其他非科研用途!PF-573228是有效的和选择性的FAK抑制剂,对FAK纯化重组催化片段的IC50值为4nM。注:本品仅可用于科研实验,严禁用于临床医疗及其他用途!CAS号:869288-64-2纯度:98.72%分子式:C22H20F3N5...
PF-573228 is an ATP-competitive FAK inhibitor. In a cell-free assay, the IC50 of FAK is 4 nM. 靶点活性 FAK:4 nM 体内活性 在REF52细胞, PC3细胞, SKOV-3细胞, 及L3.6p1和F-G, MDCK细胞中,PF 573228(IC50=30-500 nM)抑制FAK Tyr397磷酸化。PF 573228(1 μM )抑制FAK磷酸化,但不抑制细胞...
PF 573228CAS 869288-64-2 C22H20F3N5O3S MW 491.49 Purity: 99%Soluble in DMSO (>100 mM) Biological Activity: Potent and selective inhibitor of focal adhesion kinase (FAK) with IC50 of 4 nM; Displays 50-250-fold selectivity over other protein kinases; a useful tool in functional study of...
PF573228是FAK 的抑制剂，IC50值为4 nM[1]。粘着斑激酶（FAK ）是一种非受体蛋白酪氨酸激酶，驻留在粘着斑部位。FAK 蛋白是由位于人染色体8q24上的FAK 基因编码，分子量为125 kDa 。FAK 是细胞活性的重要介体，如细胞粘附、生长、增殖、存活、血管生成和迁移。据报道，正常组织的FAK 要显著低于原发性和转移性...
PF-573228是粘着斑激酶FAK抑制剂,IC50为4 nM,是抗血管生成剂。 产品信息 英文别名(English Synonym) PF-573228, PF573228 靶点(Target) FAK 通路(Pathway) Protein Tyrosine Kinase--FAK CAS号(CAS NO.) 869288-64-2 分子式(Formula) C22H20F3N5O3S ...
PF-573228 is an ATP-competitive inhibitor of FAK with IC50 of 4 nM in a cell-free assay, ~50- to 250-fold selective for FAK than Pyk2, CDK1/7 and GSK-3β. PF-573228 induces apoptosis.
PF-562271 FAK inhibitor PF-562271 is an orally bioavailable small molecule and ATP-competitive focal adhesion kinase (FAK) inhibitor with potential antineoplastic and antiangiogenic activities. Quick View A11235 PF 573228 FAK Inhibitor PF 573228 is a potent and selective inhibitor of focal adhesion ki...
7f). In addition, treatment of mature 3T3-L1 adipocytes with FAK inhibitor PF573228 also increased cleaved caspase 3, further supporting a direct pro-survival signalling of FAK in mature adipocytes (Supplementary Fig. 7g). Moreover, treatment of primary isolated adipocytes with PF573228 also ...
By contrast, the FAK inhibitor PF573228 abrogated these effects induced by the increased [Cl-]i. FAK also activated the PI3K/AKT signaling pathway. In conclusion, increased [Cl-]i promotes the proliferation and wound healing ability of BEAS-2B cells by activating FAK to activate the PI3K/AKT...
Our data indicate that this indeed may be the case as low doses of FAK inhibitor PF573228 enhanced microvessel sprouting ex vivo, although 0.01 mM PF573228 does not appear to affect autopho- sphorylation of FAK at Y397 in vitro (J.P., unpublished data). Furthermore, low doses of PF...