EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73442_C
酪氨酸激酶抑制剂；抑制KDR、PDGFR、KIT、RET、FLT-3、ABL、ALK
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总览
SU5416是一种酪氨酸激酶抑制剂，其最广为人知的特性是作为激酶插入域（KDR/VEGFR2/FLK1）的ATP竞争性抑制剂。除了抑制KDR（IC₅₀=1 μM）外，SU5416还抑制PDGFR（IC₅₀=20 μM）、KIT（IC₅₀=30 nM）、RET（IC₅₀=170 nM）、FLT-3（IC₅₀=160 nM）、ABL（IC₅₀=11 μM）和ALK（IC₅₀=1.2 μM）。 SU5416不抑制EGFR或FGFR酪氨酸激酶（IC₅₀> 100 μM；Fong et al.; Litz; Mologni et al.）。
癌症研究
·阻止血管生成，从而抑制多种癌症的肿瘤生长、催化和血管化（Litz; Fong et al.）。
·抑制RET介导的NIH-3T3小鼠成纤维细胞和Ba/F3小鼠前B细胞转化（Mologni et al.）。
疾病建模
·在缺氧条件下，可引起SuHx大鼠模型中的肺动脉高压（de Raaf et al.; Mizuno et al.）。
免疫学
·抑制TGFβ1活化并延缓大鼠伤口愈合（Haroon et al.）。
细胞类型
癌细胞及细胞系
种属
人，小鼠，非人灵长类，其他物种，大鼠
研究领域
血管生成细胞研究，癌症，疾病建模，免疫
CAS 编号
204005-46-9
化学式
C₁₅H₁₄N₂O
纯度
≥98%
通路
酪氨酸激酶
靶点
ABL，ALK，FLT-3，KDR，KIT，PDGFR，RET
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
相关材料与文献
技术资料 (3)
文献 (5)
The multi-targeted kinase inhibitor SU5416 inhibits small cell lung cancer growth and angiogenesis, in part by blocking Kit-mediated VEGF expression
Lung Cancer 2004
Abstract
SU5416 is a multi-targeted kinase inhibitor that potentially has the ability to directly block tumor growth by inhibiting Kit signaling,as well as blocking angiogenesis by inhibiting vascular endothelial growth factor receptor (VEGFR) signaling. Previous work has demonstrated that SU5416 efficiently blocks Kit-mediated growth of small cell lung cancer (SCLC) in vitro. To determine the drug's effect on in vivo growth of SCLC,we studied its activity,alone and in combination with carboplatin,in chemotherapy-resistant H526,and chemotherapy-sensitive H209 murine xenograft models. SU5416 efficiently inhibited Kit activity in vivo when administered on a twice-weekly schedule. When administered over a 3-week period to animals bearing established tumors,it inhibited growth by at least 70%. It was at least as effective as carboplatin in suppressing growth of H526 xenografts. However,the combination with carboplatin was not superior to the most active single agent in either xenograft model at the doses and schedule utilized. SU5416 clearly inhibited growth in part by inhibiting angiogenesis,with microvessel density dropping by approximately 50% in treated xenografts. In addition to the recognized mechanism of inhibition of VEGFR,we uncovered a novel mechanism of angiogenesis suppression by demonstrating reduced VEGF expression in SU5416-treated xenografts. In vitro,stem cell factor treatment of the H526 cell line enhanced expression of VEGF,which was efficiently blocked with SU5416. Thus,we have demonstrated that SU5416 can inhibit SCLC growth by directly inhibiting tumor cell proliferation and by inhibiting angiogenesis,in part by inhibiting Kit-mediated VEGF expression. These data suggest that kinase inhibitors that target both Kit and VEGFR could play an important role in the treatment of SCLC,as well as other malignancies that express Kit.
Inhibition of RET tyrosine kinase by SU5416.
Journal of molecular endocrinology 2006
Abstract
Thyroid neoplasia is frequently associated with rearranged during transfection (RET) proto-oncogene mutations that cause hyperactivation of RET kinase activity. Selective inhibition of RET-mediated signaling should lead to an efficacious therapy. SU5416 is a potent inhibitor of vascular endothelial cell growth factor receptor,c-Kit,and FLT-3 receptor tyrosine kinases presently used in clinical trials. We found that SU5416 inhibits RET with similar potency,both in cell-free assays and in cells,thus causing proliferation arrest in oncogenic RET-transfected cells and in papillary thyroid carcinoma (PTC) cells expressing the RET/PTC1 oncogene,but not in RET-negative control cells. SU5416 inhibited RET-mediated signaling through the extracellular signal regulated kinase (ERK) and JNK pathways. In addition,we show that a naturally occurring MEN2 mutation at codon 804 confers resistance to SU5416,but not to the related compound SU4984. We provide a possible explanation to these results by using molecular docking. Finally,SU5416 was also assessed against an array of 52 tyrosine and serine/threonine kinases.
Severe pulmonary arterial hypertension induced by SU5416 and ovalbumin immunization.
American journal of respiratory cell and molecular biology 2012
Abstract
The combination of chronic hypoxia and treatment of rats with the vascular endothelial growth factor (VEGF) receptor blocker,SU5416,induces pulmonary angio-obliteration,resulting in severe pulmonary arterial hypertension (PAH). Inflammation is thought to contribute to the pathology of PAH. Allergic inflammation caused by ovalbumin (OVA) immunization causes muscularization of pulmonary arteries,but not severe PAH. Whether disturbance of the immune system and allergic inflammation in the setting of lung endothelial cell apoptosis causes PAH is unknown. We investigated the effects of OVA-allergic inflammation on the development of PAH initiated by VEGF blockade-induced lung endothelial cell apoptosis. OVA-immunized rats were treated with SU5416 to induce pulmonary vascular endothelial cell apoptosis. The combination of OVA and SU5416 treatment resulted in severe angio-obilterative PAH,accompanied by increased IL-6 expression in the lungs. c-Kit(+) and Sca-1(+) cells were found in and around the lung vascular lesions. Pan-caspase inhibiton,dexamethasone treatment,and depletion of B-lymphocytes using an anti-CD20 antibody suppressed this remodeling. OVA immunization also increased lung tissue hypoxia-induced factor-1α and VEGF expression. Our results also suggest that the increased expression of hypoxia-induced factor-1α and IL-6 induced by the allergic lung inflammation may be a component of the pathogenesis of PAH.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 204005-46-9 |
| Chemical Formula | C₁₅H₁₄N₂O |
| 纯度 | ≥ 98% |
| Target | ABL, ALK, FLT-3, KDR, KIT, PDGFR, RET |
| Pathway | Tyrosine Kinase |
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