| 货号 (SKU) | 包装规格 | 是否现货 | 价格 | 数量 |
|---|---|---|---|---|
| P408101-1ml |
1ml |
现货  |
|
| 英文别名 | PF4691502 | 2-amino-8-((1r,4r)-4-(2-hydroxyethoxy)cyclohexyl)-6-(6-methoxypyridin-3-yl)-4-methylpyrido[2,3-d]pyrimidin-7(8H)-one |
|---|---|
| 规格或纯度 | Moligand™, 10mM in DMSO |
| 英文名称 | PF-04691502 |
| 生化机理 | PF-04691502（PF4691502）是一种 ATP 竞争性 PI3K(α/β/δ/γ)/mTOR 双抑制剂，其Ki值为 1.8 nM/2.1 nM/1.6 nM/1.9 nM，在无细胞实验中为 16 nM，对 Vps34、AKT、PDK1、p70S6K、MEK、ERK、p38 或 JNK 几乎没有活性。PF-04691502 可诱导细胞凋亡。第 2 阶段 |
| 储存温度 | -80℃储存 |
| 运输条件 | 超低温冰袋运输 |
| 作用类型 | 抑制剂 |
| 作用机制 | PI3 激酶 I 类抑制剂 |
| 产品介绍 |
PF-04691502是高效选择性PI3K/mTOR (FRAP)双重抑制剂，抑制Akt T308 (IC50 = 7.5 nM)和Akt S473 (IC50 = 3.8 nM)的磷酸化。 PI3Ks是参与细胞功能的酶家族，如细胞生长、增殖、分化、运动、存活和胞内运输，从而也参与癌症。PI3Ks的功能大多与1类PI3K 在PI3K/AKT/mTOR通路中激活蛋白激酶B (PKB，亦称Akt)相关，此信号通路与细胞静止、增殖、癌症和永生直接相关。此通路中有诸多有价值的抗癌药物治疗靶点。p110δ和p110γ亚型调节免疫应答的不同方面。 PF-04691502是一种有潜能的药物，由荧光偏振激酶试验、细胞、小鼠和其他动物试验得出PF-04691502的功能为抑制PI3K/AKT/mTOR通路中的1类PI3K和mTOR，此外，由此抑制作用，PF-04691502能抑制肿瘤。PF-04691502短时间处理能显著抑制PI3K，而对mTOR的抑制作用需要持续24-48小时。PF-04691502诱导细胞周期G1期停滞，伴随p27 Kip1的上调和Rb的下调。PF-04691502的抗肿瘤活性已在U87 (PTEN null)、SKOV3 (PIK3CA 突变)、耐gefitinib和erlotinib的非小细胞肺癌异种移植物中观察到。PF-04691502在第七天抑制肿瘤生长达到72%。FDG-PET成像表明PF-04691502显著降低葡萄糖代谢。PF-04691502处理也能显著抑制PI3K/mTOR通路活性的组织标志物p-AKT (S473)和p-RPS6 (S240/244)。 Information PF-04691502 (PF4691502) is an ATP-competitivePI3K(α/β/δ/γ)/mTORdual inhibitor withKiof 1.8 nM/2.1 nM/1.6 nM/1.9 nM and 16 nM in cell-free assays, little activity against either Vps34, AKT, PDK1, p70S6K, MEK, ERK, p38, or JNK. PF-04691502 inducesapoptosis. PF-04691502 potently inhibits recombinant class I PI3K and mTOR in biochemical assays and suppresses transformation of avian fibroblasts mediated by wild-type PI3K γ, δ, or mutant PI3Kα. In PIK3CA-mutant and PTEN-deleted cancer cell lines, PF-04691502 reduces phosphorylation of AKT T308 and AKT S473 (IC(50) of 7.5-47 nM and 3.8-20 nM, respectively) and inhibits cell proliferation (IC(50) of 179-313 nM). PF-04691502 inhibits mTORC1 activity in cells as measured by PI3K-independent nutrient stimulated assay, with an IC(50) of 32 nM and inhibits the activation of PI3K and mTOR downstream effectors including AKT, FKHRL1, PRAS40, p70S6K, 4EBP1, and S6RP. Short-term exposure to PF-04691502 predominantly inhibits PI3K, whereas mTOR inhibition persists for 24 to 48 hours. PF-04691502 induces cell cycle G(1) arrest, concomitant with upregulation of p27 Kip1 and reduction of Rb. In vivo Antitumor activity of PF-04691502 is observed in U87 (PTEN ), SKOV3 (PIK3CA mutation), and gefitinib- and erlotinib-resistant non-small cell lung carcinoma xenografts. PF-04691502 inhibits tumor growth at 7 days by 72%. FDG-PET imaging revealed that PF-04691502 reduces glucose metabolism dramatically. Tissue biomarkers of PI3K/mTOR pathway activity, p-AKT (S473), and p-RPS6 (S240/244), are also dramatically inhibited following PF-04691502 treatment. cell lines： Concentrations：0-3 mM Incubation Time：3 days Powder Purity:≥98% |
| Ki Data | PI3Kβ, Ki: 2.1 nM |
|---|
| 分子类型 | 小分子 |
|---|---|
| Canonical SMILES | COC1=CC=C(C=N1)C2=CC3=C(C)N=C(N)N=C3N(C4CCC(CC4)OCCO)C2=O |
| 分子量 | 425.48 |
| 溶解性 | Solubility (25°C) In vitro DMSO: 91 mg/mL (198.01 mM); Water: Insoluble; Ethanol: Insoluble; |
|---|
| Concentration(Compounding value) | 9.0-11.0(mmol/L) |
|---|---|
| Appearance(Colorless to light yellow liquid) | Pass |
| Record the entire process by video | Conform |
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