Endostatin
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187888-07-9CN(CC(=O)c1ccccc1)N=OAAFYOVPTFNNVDN-UHFFFAOYSA-NRecombinant Human Endostatin is a recombinant human proteolytic fragment of the C-terminal end of type XVIII collagen. Endostatin induces microvascular endothelial cell apoptosis and inhibits endothelial proliferation and angiogenesis, which may result in a reduction in tumor burden. This agent also may decrease hepatic metastasis by inhibiting proinflammatory cytokines and vascular cell adhesion molecule (VCAM)-dependent cell attachment to the hepatic microvasculature. (NCI04)
187888-07-9、55984-52-6DTXSID10204557CHEMBL4297747安全情報は参考情報です。供給元の安全データシート(SDS)、適用法令、専門家による評価に代わるものではありません。
Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Agents and endogenous substances that antagonize or inhibit the development of new blood vessels.
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