| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Preparation Method | Biochemical selectivity of GSK2636771 was tested using the PI3-Kinase HTRF Assay, as well as the entire panel of GSK in-house kinase selectivity assays. Affinity-enrichment-based chemoproteomics using kinobeads was performed. Briefly, 14 lipid and atypical kinases were enriched from a standard mixture of extracts derived from HeLa, K562, and Jurkat cells using a compound-derivatized bead matrix. The enriched proteins were identified by quantitative mass spectrometry analysis, enabling the simultaneous assessment of binding specificity, and potency for all detected affinity-captured proteins. |
Applications | GSK2636771 is a potent, orally bioavailable, adenosine triphosphate-competitive, selective inhibitor of PI3Kβ with an apparent Ki value of 0.89 nmol/L (IC50 = 5.2 nmol/L), >900-fold selectivity over p110α and p110γ, and >10-fold selectivity over p110δ isoforms, while sparing other PI3K superfamily kinases. |
Cell lines | PTEN-deficient PC3 prostate and BT549 and HCC70 breast cancer cell lines |
Preparation Method | Cell viability was determined after 72 hours of treatment with indicated concentrations of the p110β selective inhibitors GSK2636771 and AZD6482 in 3 p110β-reliant breast and prostate cancer cell lines, 7 PTEN wild-type EEC cells, and 17 PTEN-mutant EEC cells. |
Reaction Conditions | 1-10uM GSK2636771 for 72 hours |
Applications | Upon 72 hours treatment with the p110β inhibitors GSK2636771 and AZD6482, cell viability was significantly more decreased in the control cells [ p110β-reliant PTEN-deficient PC3 prostate and BT549 and HCC70 breast cancer cell lines] than in PTEN-mutant and PTEN wild-type EEC cells. |
Animal models | Female athymic nude mice (4-5-week-old) |
Preparation Method | Female athymic nude mice were injected subcutaneously with ZR75-1/FR cells resuspended in matrigel. On the same date, mice were implanted subcutaneously with a 17β-estradiol pellet, and fulvestrant treatment was initiated. Four weeks after implantation, tumor-bearing mice were randomized to treatment with vehicle, GSK2636771 (30 mg/kg/d, orally), BYL719, or the combination, all with a fulvestrant treatment backbone. |
Dosage form | GSK2636771 (30 mg/kg/d, orally) |
Applications | Inhibition of ER/p110β or ER/p110α/βby GSK2636771 induced rapid tumor regression, whereas ER/p110α inhibition had no significant early effect on growth compared to continued ER inhibition alone. |
| 产品描述 | GSK2636771 is a potent adenosine triphosphate competitive oral inhibitor of PI3Kβ, with an IC50 of 5.2 nmol/L against the catalytic subunit, p110β, whilst showing >900-fold selectivity over p110α and p110γ, and >10-fold selectivity over p110δ[3,4]. Upon 72 hours treatment with the p110β inhibitors GSK2636771 and AZD6482, cell viability was significantly more decreased in the control cells [ p110β-reliant PTEN-deficient PC3 prostate and BT549 and HCC70 breast cancer cell lines] than in PTEN-mutant and PTEN wild-type EEC cells[1]. GSK2636771 showed a certain inhibitory effect on several CRPC cell lines including C4-2B cell sublines, and BL140 showed a stronger inhibitory effect than GSK2636771[6]. Inhibition of ER/p110β or ER/p110α/βby GSK2636771 induced rapid tumor regression, whereas ER/p110α inhibition had no significant early effect on growth compared to continued ER inhibition alone[2]. To explore the therapeutic potential of simultaneously targeting Cx43 and PIK3CB/p110β, αCT1 is combined with TGX-221 or GSK2636771, two PIK3CB/p110β-selective inhibitors. These two different treatments synergistically inactivate PI3K and sensitize glioblastoma cells to temozolomide in vitro and in vivo[5]. Combining anti-OX40 with GSK2636771, a PI3Kβ-selective inhibitor, delayed tumor growth and extended the survival of mice with PTEN-null melanomas[7]. References: |
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