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Home   »   Product Pathways  »  PIKfyve  »  YM-201636

Products are for research use only. Not for human use. We do not sell to patients.


CS-0592 YM-201636


(YM 201636;YM201636)
Structure Price and Availability of    YM-201636
United States
Size Price Stock
2mg $55 In-stock Inquiry
5mg $95 In-stock
10mg $170 In-stock
50mg $640 In-stock
100mg $1100 In-stock
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 Distributor In Japan:  フナコシ株式会社 www.funakoshi.co.jp    電話番号:81-3-5684-1620   
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YM-201636  M.Wt:  467.48
YM-201636  Formula: C25H21N7O3
YM-201636  Solubility: DMSO ≥33mg/mL Water <1.2mg/mL Ethanol <1.2mg/mL
YM-201636  Purity: >98%
YM-201636  Storage:  Please store the product under the recommended conditions in the Certificate of Analysis.
CAS: 371942-69-7

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YM201636 is a selective PIKfyve inhibitor with IC50 of 33 nM, less potent to p110α. IC50 value: 33 nM [1] Target: PIKfyve in vitro: 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)P2 production, 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].

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