SU 6656 is a selective inhibitor of Src family kinases, with IC50 of 280 nM, 20 nM, 130 nM, and 170 nM for Src, Yes, Lyn, and Fyn, respectively.

Src:280 nM, Lyn:130 nM, Fyn:170 nM, YES:20 nM

在NIH 3T3细胞中，SU 6656以0.3-0.4 μM的IC50抑制了PDGF激活的S期启动。SU 6656还能抑制PDGF和血清介导的NIH 3T3细胞增殖，以及表皮生长因子和集落刺激因子1（colony-stimulating factor 1）激活的正常及集落刺激因子1受体转染NIH 3T3细胞的DNA合成。SU6656阻断了PDGF激活的c-Myc诱导和ERK2激活。[1] 在Jurkat T细胞中预处理SU 6656能够增加VSV-G荧光素酶活性。[2] SU 6656抑制TGF-β促进的近端上皮HKC-8细胞内CTGF mRNA和蛋白的上调，也减少了自分泌生长因子暴露细胞中的CTGF表达。SU 6656干扰Aurora激酶活性，导致细胞分裂受阻和多叶核的形成。[3]

SU 6656 显著且剂量依赖性地减轻了小鼠中由美卡明引起的实验性尼古丁撤断综合征。[4] 每日一次给药（1.5、3、6 mg/kg, i.p.）显著且剂量依赖性地减轻了纳洛酮引起的吗啡撤断综合征。[5]

Biochemical kinase assays for IC50 determination and kinetic studies: IC50 measurements are made using poly-Glu–Tyr (4:1), or, in the case of Lck, poly-Lys–Tyr (4:1) as a peptide substrate. The divalent cation is 20 mM MgCl2 (in the case of Src, Fyn, Yes, Lyn, Csk, Frk, or Abl) or 10 mM MnCl2 (in the case of FGFR1, IGF1R, Lck, or Met). The ?nal ATP concentrations are as follows: Src, 10 μM; Fyn, 6 μM; Yes, 100 μM; Lyn, 2 μM; Csk, 10 μM; Frk, 10 μM; Abl, 4 μM; FGFR1, 10 μM; IGF1R, 2 μM; Lck, 2 μM; Met, 5 μM; PDGFR, 6 μM. IC50 measurements of PDGFRb autophosphorylation are determined on immunoprecipitated PDGFRb. Km values are calculated using the Eadie-Hofstee method.

HKC-8 cells are seeded at different cells densities (10,000 cells/cm2 and 50,000 cells/cm2) and cultured in the presence or absence of SU 6656 for 24 and 48 h. Bright ?eld pictures of cells are recorded by Olympus CK40 microscope using Leica DC Viewer software.(Only for Reference)