Enzastaurin (LY317615) supplier|cas 170364-57-5 |DC Chemicals|Supplier|Price|Buy  

Enzastaurin (LY317615) supplier|cas 170364-57-5 |DC Chemicals|Supplier|Price|Buy

DC ChemicalsSupply: Enzastaurin (LY317615) supplier,cas 170364-57-5, Cat No. DC5057, In stock

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Product name: Enzastaurin (LY317615), Synonym:　3-(1-methyl-1H-indol-3-yl)-4-(1-(1-(pyridin-2-ylmethyl)piperidin-4-yl)-1H-indol-3-yl)-1H-pyrrole-2,5-dione, Cat No. DC5057, Cas: 170364-57-5, Chemical Name:N/A, Molecular Formula: C32H29N5O2, MW: 515.61

Enzastaurin (LY317615),cas 170364-57-5, Purity: >98%. Best Price and quality in the market,DC Chemicals,Primary Manufacturer, confirmed by HNMR and HPLC. Enzastaurin (LY317615) is a potent PKCβ selective inhibitor with IC50 of 6 nM, 6- to 20-fold selectivity against PKCα, PKCγ and PKCε. Phase 3.

Enzastaurin application results in a marked dose-dependent inhibition of growth in all MM cell lines investigated, including MM.1S, MM.1R, RPMI 8226 (RPMI), RPMI-Dox40 (Dox40), NCI-H929, KMS-11, OPM-2, and U266, with IC50 from 0.6-1.6 μM. Enzastaurin direct impacts human tumor cells, inducing apoptosis and suppressing proliferation in cultured tumor cells. Enzastaurin also suppresses the phosphorylation of GSK3βser9, ribosomal protein S6S240/244, and AKTThr308 while having no direct effect on VEGFR phosphorylation. [1] Enzastaurin increases apoptosis in malignant lymphocytes of CTCL. When combined with GSK3 inhibitors, enzastaurin demonstrated an enhancement of cytotoxicity levels. Treatment with a combination of enzastaurin and the GSK3 inhibitor AR-A014418 led to increased levels of β-catenin total protein and β-catenin-mediated transcription. Blocking of β-catenin-mediated transcription or small hairpin RNA (shRNA) knockdown of β-catenin induced the same cytotoxic effects as that of enzastaurin plus AR-A014418. Additionally, treatment with enzastaurin and AR-A014418 decreased the mRNA levels and surface expression of CD44. [2]Treatment of xenografts with Enzastaurin and radiation produced greater reductions in density of microvessels than either treatment alone. The decrease in microvessel density corresponded to delayed tumor growth. [3]