GSK2636771 - PI3K 抑制剂 - 生命科学试剂 - MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEGSK2636771Cat. No.: HY-15245CAS No.: 1372540-25-4分式: CHFNO分量: 433.42作靶点: PI3K作通路: PI3K/Akt/mTOR储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性数据体外实验 DMSO : 10.6 mg/mL (24.46 mM; Need ultrasonic and warm

2、ing)Mass Solvent1 mg 5 mg 10 mg Concentration制备储备液1 mM 2.3072 mL 11.5362 mL 23.0723 mL5 mM 0.4614 mL 2.3072 mL 4.6145 mL10 mM 0.2307 mL 1.1536 mL 2.3072 mL请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液，并请注意储备液的保存式和期限。BIOLOGICAL ACTIVITY物活性 GSK2636771有效，选择性和可服的 PI3K 抑制剂，Ki和IC50分别为0.89，5.2 nM，p110和p110的选择性900倍，p110同种型的

3、选择性10倍。IC50 & Target p110体外研究GSK2636771 treatment causes cell viability significantly more decreased in the control cells (p110-reliantPTEN-deficient PC3 prostate and BT549 and HCC70 breast cancer cell lines) than in PTEN-mutant and1/2 Master of Small Molecules 您边的抑制剂师www.MedChemEPTEN wild-type EEC

4、cells. Inhibition of p110 by GSK2636771 or AZD6482 leads to a marked decrease ofAKT phosphorylation only in the control prostate and breast cancer cell lines, whereas only marginal effectson AKT activation are observed in EEC cells 1.体内研究 GSK2636771 is a p110 inhibitor, and the p110 primes cells for

5、 response to growth factor stimulation. Whilep110 inhibition suppresses cell and tumor growth, dual targeting of p110/ enhances apoptosis andprovides sustained tumor response in mice model 2.PROTOCOLCell Assay 1 Cells are plated in 96-well microtiter plates at densities ranging from 1,500 to 15,000

6、cells/well, optimized foruntreated control cells to be 80-90% confluent at the endpoint of the experiment. After 24 h, cells are treatedwith serial dilutions (100 pM to 10 M) of the PI3K pathway inhibitors GDC-0941, A66, TGX-221,GSK2636771, AZD6482, Temsirolimus, AZD8055, PF-04691502, and of the MAP

7、K pathway inhibitorsAZD6244, PD0325901, AZD628, and PLX4032. Cell viability is assessed after 72 h of treatment byincubation with CellTiter Blue for 1.5 h. The drug concentration required for survival of 50% of cells relative tountreated cells is determined using GraphPad Prism version 5.0 d. Cell l

8、ines that fail to achieve the SF50 toa given drug are nominally assigned as the highest concentration screened (10 M). At least threeindependent experiments in triplicate per cell line/targeted drug are performed. Association between amutation and response to a targeted agent is determined using a F

9、ishers exact test, and a two-tailed Pvalue.MCE has not independently confirmed the accuracy of these methods. They are for reference only.户使本产品发表的科研献 Sci Transl Med. 2018 Jul 18;10(450). pii: eaaq1093. Mol Pharmacol. 2016 Dec;90(6):726-737. Harvard Medical School LINCS LIBRARYSee more customer valid

10、ations on HYPERLINK / www.MedChemEREFERENCES1. Weigelt B, et al. PI3K pathway dependencies in endometrioid endometrial cancer cell lines. Clin Cancer Res. 2013, 19(13), 3533-3544.2. Hosford SR, et al. Combined inhibition of both p110 and p110 isoforms of phosphatidylinositol 3-kinase is required for sustainedtherapeutic effect in PTEN-deficient, ER+ breast cancer. Clin Cancer Res. 2016 Nov 30McePdfHeightCaution: Product has not been fully