1094048-77-7
中文名稱
I-OME-AG 538
英文名稱
I-OME-AG 538
CAS
1094048-77-7
分子式
C17H12INO5
分子量
437.19
MOL 文件
1094048-77-7.mol
1094048-77-7 結(jié)構(gòu)式
基本信息
中文別名
化合物 T11593 英文別名
I-OME-AG 538TYRPHOSTIN I-OME-AG 538
I-OME-TYRPHOSTIN AG 538
α-Cyano-(3-methoxy-4-hydroxy-5-iodocinnamoyl)-(3′,4′-dihydroxyphenyl)ketone
ALPHA-CYANO-(3-METHOXY-4-HYDROXY-5-IODOCINNAMOYL)-(3',4'-DIHYDROXYPHENYL)KETONE
I-OMe-AG 538, α-Cyano-(3-methoxy-4-hydroxy-5-iodocinnamoyl)-(3μ,4μ-dihydroxyphenyl)ketone
物理化學(xué)性質(zhì)
儲(chǔ)存條件-20°C
溶解度DMSO : 50 mg/mL (114.37 mM; Need ultrasonic)
形態(tài)solid
顏色Yellow to orange
InChI1S/C17H12INO5/c1-24-15-6-9(5-12(18)17(15)23)4-11(8-19)16(22)10-2-3-13(20)14(21)7-10/h2-7,20-21,23H,1H3/b11-4+
InChIKeyHSRMHXWCTRFVHK-NYYWCZLTSA-N
SMILESCOc1cc(cc(I)c1O)\C=C(/C#N)C(=O)c2ccc(O)c(O)c2
I-OME-AG 538價(jià)格(試劑級(jí))
| 報(bào)價(jià)日期 | 產(chǎn)品編號(hào) | 產(chǎn)品名稱 | CAS號(hào) | 包裝 | 價(jià)格 |
| 2026/06/05 | HY-135680 | I-OMe-Tyrphostin AG 538 | 1094048-77-7 | 1 mg | 540元 |
| 2026/06/05 | HY-135680 | I-OME-AG 538 I-OMe-Tyrphostin AG 538 | 1094048-77-7 | 5mg | 1500元 |
| 2026/06/05 | HY-135680 | I-OMe-Tyrphostin AG 538 | 1094048-77-7 | 10 mM * 1 mLin DMSO | 1650元 |
常見問題列表
生物活性
I-OMe-Tyrphostin AG 538 (I-OMe-AG 538) 是 IGF-1R 激酶的特異性抑制劑。I-OMe-Tyrphostin AG 538 抑制 IGF-1R 介導(dǎo)的信號(hào)傳導(dǎo)，并優(yōu)先對(duì)營養(yǎng)缺乏的 PANC1 細(xì)胞產(chǎn)生細(xì)胞毒性。I-OMe-Tyrphostin AG 538 是具有 ATP 競(jìng)爭(zhēng)性的 PI5P4Kα抑制劑，IC50 為 1 μM。靶點(diǎn)
IC50: 1 μM (PI5P4Kα)
體外研究
I-OMe-Tyrphostin AG 538 (I-OMe-AG 538) (0.1-1000 μM; 24 hours) is cytotoxic to PANC-1 cells in nutrient-deprived medium.
I-OMe-Tyrphostin AG 538 (0-3 μM; 1 hour) blocks phosphorylation of IGF-1R, Akt and Erk.
Cell Viability Assay
| Cell Line: | PANC-1 cells |
| Concentration: | 0.1, 1, 10, 1000 μM |
| Incubation Time: | 24 hours |
| Result: | Cytotoxic to PANC-1 cells in nutrient-deprived medium. |
Western Blot Analysis
| Cell Line: | PANC-1 cells (stimulation with 50 ng/ml IGF-1 for 10 min) |
| Concentration: | 0.03, 0.3, 3 μM |
| Incubation Time: | 1 hour |
| Result: | Blocked phosphorylation of IGF-1R, Akt and Erk. |