For research use only. Not for therapeutic Use.
YM201636（Cat No.:I003368）is a potent and selective inhibitor of PIKfyve, a lipid kinase involved in the synthesis of phosphatidylinositol-3,5-bisphosphate (PI(3,5)P2), which is crucial for endosomal trafficking and lysosomal function. By inhibiting PIKfyve, YM201636 impairs the maturation of early endosomes into late endosomes and disrupts lysosomal homeostasis. It is widely used in cell biology research to study vesicular trafficking, endosome-lysosome dynamics, and autophagy. YM201636 is also used to investigate the role of PIKfyve in neurodegenerative diseases, cancer, and other conditions where intracellular trafficking plays a significant role.
| Catalog Number | I003368 |
| CAS Number | 371942-69-7 |
| Synonyms | 6-amino-N-[3-(4-morpholin-4-ylpyrido[2,3]furo[2,4-b]pyrimidin-2-yl)phenyl]pyridine-3-carboxamide |
| Molecular Formula | C₂₅H₂₁N₇O₃ |
| Purity | ≥95% |
| Target | PIKfyve |
| Solubility | DMSO ≥33mg/mL Water <1.2mg/mL Ethanol <1.2mg/mL |
| Storage | 3 years -20℃ powder |
| IC50 | 33 nM |
| IUPAC Name | 6-amino-N-[3-(6-morpholin-4-yl-8-oxa-3,5,10-triazatricyclo[7.4.0.02,7]trideca-1(9),2(7),3,5,10,12-hexaen-4-yl)phenyl]pyridine-3-carboxamide |
| InChI | InChI=1S/C25H21N7O3/c26-19-7-6-16(14-28-19)24(33)29-17-4-1-3-15(13-17)22-30-20-18-5-2-8-27-25(18)35-21(20)23(31-22)32-9-11-34-12-10-32/h1-8,13-14H,9-12H2,(H2,26,28)(H,29,33) |
| InChIKey | YBPIBGNBHHGLEB-UHFFFAOYSA-N |
| SMILES | C1COCCN1C2=NC(=NC3=C2OC4=C3C=CC=N4)C5=CC(=CC=C5)NC(=O)C6=CN=C(C=C6)N |
| Reference | 1:PLoS One. 2013;8(3):e60152. doi: 10.1371/journal.pone.0060152. Epub 2013 Mar 27. Inhibition of PIKfyve by YM-201636 dysregulates autophagy and leads to apoptosis-independent neuronal cell death.Martin S,Harper CB,May LM,Coulson EJ,Meunier FA,Osborne SL, PMID: 23544129 PMCID: PMC3609765 DOI: 10.1371/journal.pone.0060152 </br><span>Abstract:</span> The lipid phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P 2), synthesised by PIKfyve, regulates a number of intracellular membrane trafficking pathways. Genetic alteration of the PIKfyve complex, leading to even a mild reduction in PtdIns(3,5)P 2, results in marked neurodegeneration via an uncharacterised mechanism. In the present study we have shown that selectively inhibiting PIKfyve activity, using YM-201636, significantly reduces the survival of primary mouse hippocampal neurons in culture. YM-201636 treatment promoted vacuolation of endolysosomal membranes followed by apoptosis-independent cell death. Many vacuoles contained intravacuolar membranes and inclusions reminiscent of autolysosomes. Accordingly, YM-201636 treatment increased the level of the autophagosomal marker protein LC3-II, an effect that was potentiated by inhibition of lysosomal proteases, suggesting that alterations in autophagy could be a contributing factor to neuronal cell death. |
