AG-1478 NEW
| Price | $45 | $61 | $114 |
| Package | 5mg | 10mg | 25mg |
| Min. Order: | |
| Supply Ability: | 10g |
| Update Time: | 2024-11-01 |
Product Details
| Product Name: AG-1478 | CAS No.: 153436-53-4 |
| Purity: 99.71% | Supply Ability: 10g |
| Release date: 2024/11/01 |
Product Introduction
Bioactivity
| 名稱 | AG-1478 |
| 描述 | AG-1478 (NSC-693255) (Tyrphostin AG-1478) is a selective EGFR inhibitor. |
| 細胞實驗 | Cells are exposed to different concentrations of AG-1478 for 72 hours in 96-well plates. The effects of AG-1478 on cell growth are examined using an Alamar Blue assay. A 20-μL aliquot of Alamar Blue is added to each well, and its absorbance is determined using a Spectromax Scanning Micro plate Reader. The effects of AG-1478 are expressed as percentage of growth inhibition using untreated cells as the control (0% inhibition). Cellular DNA synthesis is determined using a [3H]thymidine incorporation assay. (Only for Reference) |
| 體外活性 | Co-administration of 0.4 mg AG-1478 with a single dose of 25 μCi 90Y-CHX-A''-DTPA-hu3S193 results in significantly enhanced potency compared to the drugs administered separately. AG-1478 blocks phosphorylation of EGFR at tumor sites and inhibits growth in xenograft models of A431 cells overexpressing wt EGFR and glioma expressing de2-7 EGFR. Even subtherapeutic doses of AG-1478 significantly increase the potency of cytotoxic drugs. The combination of AG-1478 and temozolomide shows synergistic antitumor activity against human glioma xenografts. |
| 體內(nèi)活性 | At a concentration of 0.25 μM, AG-1478 effectively inhibits Ang II, Ca2+ ionophore, and EGF-induced MAPK activation in VSMCs, without affecting fosinopril or platelet-derived growth factor-BB (PDGF-BB)-induced MAPK activation. AG-1478 also suppresses EGF-induced mitosis in BaF/ERX and LIM1215 cells, with IC50 values of 0.07 μM and 0.2 μM, respectively. Furthermore, AG-1478 inhibits the function of ABC (ATP-binding cassette) transport proteins, such as ABCB1 and ABCG2, showing a more significant effect on ABCG2. In comparison to cells expressing endogenous wild-type EGFR or overexpressing exogenous wild-type EGFR (with IC50 values of 34.6 μM and 48.4 μM respectively), AG-1478 preferentially inhibits U87 mg cells expressing ΔEGFR, with an IC50 of 8.7 μM. It also preferentially inhibits tyrosine kinase activity and autophosphorylation of ΔEGFR over endogenous or overexpressed exogenous wild-type EGFR. |
| 存儲條件 | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| 溶解度 | Ethanol : < 1 mg/mL H2O : < 1 mg/mL (insoluble or slightly soluble) DMSO : 4.23 mg/mL (13.4 mM), Sonication is recommended. |
| 關鍵字 | diseases | encephalomyocarditis | HCV | virus | HER1 | obesity | EGFR | cardiovascular | Influenza Virus | myocardial | injury | ErbB-1 | EMCV | Hepatitis C virus | antiviral | AG 1478 | NSC693255 | Tyrphostin AG 1478 | Epidermal growth factor receptor | inhibit | Inhibitor | cancer | NSC-693255 | chemotherapy | AG-1478 | Tyrphostin AG1478 |
| 相關產(chǎn)品 | Rifampicin | Acetylcysteine | α-Vitamin E | Sorafenib | Nitazoxanide | Curcumin | Artemisinin | Naringenin | Gefitinib | Salcomine | Crystal Violet | Pazopanib |
| 相關庫 | 細胞凋亡化合物庫 | 經(jīng)典已知活性庫 | 膜蛋白靶向化合物庫 | 酪氨酸激酶分子庫 | 激酶抑制劑庫 | 抗乳腺癌化合物庫 | 抗病毒庫 | 抑制劑庫 | 已知活性化合物庫 | 抗癌活性化合物庫 |
Company Profile Introduction
Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers.
TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.
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United States- Since: 2011-01-07
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