YM201636|cas 371942-69-7| DC Chem|Supplier|Price|Buy  

YM201636|cas 371942-69-7| DC Chem|Supplier|Price|Buy

DC Chemicals Supply: YM201636|cas 371942-69-7,Purity: >98% ,Cat No. DC7343, In stock.

Contact: website: www.dcchemicals.com,

sales@dcchemicals.com,order@dcchemicals.com,info@dcchemicals.com,

Tel: +86-21-61454686;Fax:+86-21-61642812；

YM201636|cas 371942-69-7 ,Synonym: YM 201636; YM201636  ,Chemical name: 3-Pyridinecarboxamide,6-amino-N-[3-[4-(4-morpholinyl)pyrido[3',2':4,5]furo[3,2-d]pyrimidin-2-yl]phenyl]- ,Molecular Formula: C25H21N7O3 ,MW:467.48

YM201636, cas 371942-69-7,Purity: >98%, Best Price and quality from DC Chemicals. YM201636 is a selective PIKfyve inhibitor with IC50 of 33 nM, less potent to p110α.

YM201636 potently inhibits mammalian PIKfyve with an IC50 of 33 nM but not yeast orthologue Fab1 with an IC50 of >5 μM, exhibiting around 100-fold selectivity for PtdIns3P p110α with an IC50 of 3 μM. YM201636 (0.8 μM) significantly decreases the production of PtdIns(3,5)P2 by 80% in serum-starved NIH3T3 cells followed by serum stimulation with no effect on serum-stimulated protein kinase B (PKB) Ser 473 phosphorylation. YM-201636 reversibly impairs endosomal trafficking in NIH3T3 cells by blocking PIKfyve and PtdIns(3,5)P2production, mimicking the effect produced by depleting PIKfyve with siRNA. YM-201636 (0.8 μM) also significantly reduces retroviruses budding from cells by 80%, apparently through interfering with the endosomal sorting complex required for transport (ESCRT) machinery. [1] In 3T3L1 adipocytes, YM-201636 inhibits basal and insulin-activated 2-deoxyglucose uptake with an IC50 of 54 nM, with almost complete inhibition at doses as low as 160 nM. YM-201636 (0.1 μM) has also been shown to completely block insulin-dependent activation of class IA PI 3-kinase. [2] Although not involved in NPM-ALK-dependent proliferation and migration, YM201636 (0.4 μM) strongly reduces invasive capacities of NPM-ALK-expressing cells and their capacity to degrade the extracellular matrix. [3] YM201636 treatment blocks the continuous recycling of junctional proteins claudin-1 and claudin-2 in MDCK cells, leading to the intracellular accumulation and delay of epithelial barrier formation. [4]