| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 100mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
| 2g | 电议 |
Cell lines | NIH-3T3 cells, HUVECs |
Preparation method | The solubility of this compound in DMSO is > 10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Applications | In serum-starved NIH-3T3 cells expressing VEGFR2 or PDGFRβ, Sunitinib inhibited VEGF-dependent VEGFR2 phosphorylation and PDGF-dependent PDGFRβ phosphorylation. Sunitinib inhibited VEGF-induced proliferation of serum-starved HUVECs with IC50 of 40 nM, and inhibited PDGF-induced proliferation of NIH-3T3 cells overexpressing PDGFRβ or PDGFRα with IC50 of 39 nM and 69 nM, respectively. |
Animal models | Tumor xenograft mouse models bearing HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435 cells |
Dosage form | Oral dosing, 20-80 mg/kg/day, once daily |
Application | Sunitinib (20-80 mg/kg/day) exhibited broad and potent dose-dependent anti-tumor activity against a variety of tumor xenograft models including HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435. Sunitinib (80 mg/kg/day for 21 days) led to complete tumor regression in six of eight mice, without tumor re-growing during a 110-day observation period after the end of treatment. Sunitinib treatment significantly decreased tumor MVD, with ~40% reduction in SF763T glioma tumors. SU11248 completely inhibited additional tumor growth of luciferase-expressing PC-3M xenografts, despite no reduction in tumor size. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | Sunitinib malate, also called sunitinib, is a novel, oral, multi-targeted , small molecule oxindole tyrosine kinase inhibitor which inhibits multiple receptor tyrosine kinases including platelet-derived growth factor receptor ( and (, vascular endothelial growth factor receptor 1, 2 and 3, c-KIT, FLT3 kinase, colony-stimulating factor 1 receptor and RET kinase [2][3] [4]. The IC50 of sunitinib is approximately 10-20 ng/ml to NB cell lines, which is within the clinically relevant human trough serum concentration (50-100 ng/ml) [1]. Receptor tyrosine kinases activated a number of different intracellular signaling pathways [5]. In neuroblastoma (NB) cell lines, SKN-BE (2), NUB-7, SH-SY5Y and LAN-5, sunitinib significantly inhibited cell proliferation after a treatment for 48 hours, in a concentration-dependent manner [1]. Treatment with 20, 30 or 40 mg/kg of sunitinib made NOD/SCID mice inoculated with xenograft tumor cells show significant reduction (P<0.05) in primary tumor growth (%T/C: 49% for SK-N-BE (2) and 55% for NB12 tumor, T/C: average treated tumor mass/average control tumor mass). Treatment with different doses of sunitinib (20, 30 or 40 mg/kg) for 14 days resulted in a dramatic decrease in the numbers and size of metastatic sites and a significant difference in liver weight in mice injected intravaneously with 106 SK-N-BE(2) cells for 7 days compared with the control group [1]. References: |
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