SU 6668

Discontinued Product

3335 has been discontinued.

View all PDGFR products.
说明: PDGFR, VEGFR and FGFR inhibitor
别名: TSU68,Orantinib
化学名: 5-[1,2-Dihydro-2-oxo-3H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-propanoic acid
纯度: ≥99% (HPLC)
说明书
引用文献 (2)
评论
文献 (1)

生物活性 for SU 6668

SU 6668 is an ATP-competitive PDGFR, VEGF and FGFR inhibitor (IC50 values are 0.06, 2.43, 3.04 and > 100 μM at PDGFRβ, VEGFR2, FGFR1 and EGFR respectively). Inhibits proliferation of HUVEC and NIH3T3 cells in vitro (IC50 values are 0.41, 9.3 and 16.5 μM for VEGF, FGF and PDGF-stimulated growth respectively) and induces > 75% growth inhibition against a broad range of tumor types in vivo. Exhibits antiangiogenic, anti-inflammatory, antimetastatic and proapoptotic activity and is orally active.

技术数据 for SU 6668

分子量 310.35
公式 C18H18N2O3
储存 Store at RT
纯度 ≥99% (HPLC)
CAS Number 252916-29-3
PubChem ID 5329099
InChI Key NHFDRBXTEDBWCZ-ZROIWOOFSA-N
Smiles O=C2NC1=CC=CC=C1/C2=C/C3=C(C)C(CCC(O)=O)=C(C)N3

上方提供的技术数据仅供参考。批次相关数据请参见分析证书。

Tocris products are intended for laboratory research use only, unless stated otherwise.

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关键词: SU 6668, SU 6668 supplier, FGFR, VEGFR, PDGFR, inhibitors, inhibits, Fibroblast, Growth, Factor, Receptors, Receptor, Tyrosine, Kinases, RTKs, Platelet, Derived, Vascular, Endothelial, KDR, Flt, SU6668, TSU68, Orantinib, 3335, Tocris Bioscience

2 篇 SU 6668 的引用文献

引用文献是使用了 Tocris 产品的出版物。 SU 6668 的部分引用包括:

Mathew et al (2015) Feedback circuitry between miR-218 repression and RTK activation in glioblastoma. Mol Biol Cell 8 ra42 PMID: 25943352

Yan et al (2017) Chemical inhibition reveals differential requirements of signaling pathways in krasV12- and Myc-induced liver tumors in transgenic zebrafish. Sci Rep 7 45796 PMID: 28378824


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该领域的文献

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!

*请注意,Tocris 仅会向正规科研企业/机构地址发送文献。


Angiogenesis in Cancer Poster

Angiogenesis in Cancer Poster

This poster summarizes the pathogenesis of angiogenesis in cancer, as well as some of the main angiogenesis therapeutic targets.