中文同义词:
(5E)-5-[[5-(4-氟苯基)-2-呋喃基]亚甲基]-2,4-噻唑烷二酮;PI3KΓ抑制剂(CAY10505)
英文同义词:
CAY10505;(5E)-5-[[5-(4-Fluorophenyl)-2-furanyl]methylene]-2,4-thiazolidinedione;(E)-5-((5-(4-fluorophenyl)furan-2-yl)methylene)thiazolidine-2,4-dione;CAY10505 ( 5E)-5-[[5-(4-Fluorophenyl)-2-furanyl]methylene]-2,4-thiazolidinedione;CAY10505, >=98%;2,4-Thiazolidinedione, 5-[[5-(4-fluorophenyl)-2-furanyl]methylene]-, (5E)-;CAY10505 USP/EP/BP
相关类别:
细胞生物学试剂;小分子抑制剂，天然产物;Akt;mTOR;PI3K;PI3K/Akt/mTOR;Inhibitors
酸度系数(pKa)
7.21±0.20(Predicted)
生物活性
CAY10505 是一种有效的选择性 PI3Kγ 抑制剂，作用于神经元细胞，IC50 为 30 nM。
靶点
PI3Kγ
30 nM (IC 50 , Neurons)
PI3Kγ
30 nM (IC 50 , Neurons)
体外研究
A class IB PI3Kγ isoform inhibitor CAY10505 at 200 nM (IC 50 =30 nM) partially reduces the baicalein-induced Akt phosphorylation in neurons. The pharmacological PI3K inhibitor CAY10505 (PIK3CG) is tested on an extended panel of multiple myeloma (MM) cell lines and freshly isolated primary MM samples. MM cells are CAY10505-treated for 3 d (MM cell lines) or 5 d (primary MM cells) respectively, and survival is analysed by flow cytometry (annexin V-FITC/PI staining). Treatment of bone marrow stromal cells (BMSCs)-co-cultured primary MM samples with the PIK3CA inhibitor CAY10505 results in anti-survival effects (mean survival relative to DMSO-treated controls: CAY10505: 84±14%, tested at 10 μM).
体内研究
Administration of CAY10505 (0.6 mg/kg, p.o.), Losartan (25 mg/kg, p.o.), or Atorvastatin (30 mg/kg, p.o.) significantly increases serum nitrite and (or) nitrate concentrations in hypertensive rats. Acetylcholine (ACh) and Sodium nitroprusside (SNP) produce endothelium-dependent and-independent relaxation in isolated rat aortic ring precontracted with Phenylephrine (3 μM), in a dose dependent manner. Administration of CAY10505 (0.6 mg/kg,p.o.), Losartan (25 mg/kg, p.o.), or Atorvastatin (30 mg/kg, p.o.) significantly prevents hypertension-induced attenuation of ACh-induced endothelium-dependent relaxation. Deoxycorticosterone acetate salt (DOCA, 40 mg/kg, s.c.) induced hypertension markedly attenuates acetylcholine-induced endothelium-dependent relaxation, but does not affect SNP-induced endotheliumindependent relaxation.
