CR8 - CAS 294646-77-8
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Not Intended for Therapeutic Use. For research use only.
CR8 is a potent and selective inhibitor of CDK. CR8 is a more potent pyridyl analogue of roscovitine. In comparison to roscovirtine, the compound gains in potency toward CK1, which is involved in amyloid-β formation. The R-CR8 enantiomer is slightly more potent than S. CR8 is around 30 times more potent at cellular assay then roscovitine.
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1.Antitumoral effects of cyclin-dependent kinases inhibitors CR8 and MR4 on chronic myeloid leukemia cell lines.
Troadec S1,2, Blairvacq M3, Oumata N4, Galons H5, Meijer L6, Berthou C7. J Biomed Sci. 2015 Jul 17;22:57. doi: 10.1186/s12929-015-0163-x.
BACKGROUND: Although Imatinib mesylate has revolutionized the treatment of chronic myeloid leukemia, some patients develop resistance with progression of leukemia. Alternative or additional targeting of signalling pathways deregulated in Bcr-Abl-driven chronic myeloid leukemia may provide a feasible option for improving clinical response and overcoming resistance.
2.Studies of a Large Odd-Numbered Odd-Electron Metal Ring: Inelastic Neutron Scattering and Muon Spin Relaxation Spectroscopy of Cr8 Mn.
Baker ML1,2, Lancaster T3, Chiesa A4, Amoretti G4, Baker PJ5, Barker C6, Blundell SJ7, Carretta S4, Collison D6, Güdel HU8, Guidi T5, McInnes EJ6, Möller JS9, Mutka H10, Ollivier J10, Pratt FL5, Santini P4, Tuna F6, Tregenna-Piggott PL8, Vitorica-Yrezabal Chemistry. 2016 Jan;22(5):1779-88. doi: 10.1002/chem.201503431. Epub 2016 Jan 8.
The spin dynamics of Cr8 Mn, a nine-membered antiferromagnetic (AF) molecular nanomagnet, are investigated. Cr8 Mn is a rare example of a large odd-membered AF ring, and has an odd-number of 3d-electrons present. Odd-membered AF rings are unusual and of interest due to the presence of competing exchange interactions that result in frustrated-spin ground states. The chemical synthesis and structures of two Cr8 Mn variants that differ only in their crystal packing are reported. Evidence of spin frustration is investigated by inelastic neutron scattering (INS) and muon spin relaxation spectroscopy (μSR). From INS studies we accurately determine an appropriate microscopic spin Hamiltonian and we show that μSR is sensitive to the ground-spin-state crossing from S=1/2 to S=3/2 in Cr8 Mn. The estimated width of the muon asymmetry resonance is consistent with the presence of an avoided crossing. The investigation of the internal spin structure of the ground state, through the analysis of spin-pair correlations and scalar-spin chirality, shows a non-collinear spin structure that fluctuates between non-planar states of opposite chiralities.
3.E2F1-CDK1 pathway activation in kanamycin-induced spiral ganglion cell apoptosis and the protective effect of CR8.
Liu YY1, Wang GP2, Peng Z2, Guo JY2, Wu Q2, Xie J2, Gong SS3. Neurosci Lett. 2016 Mar 23;617:247-53. doi: 10.1016/j.neulet.2016.02.034. Epub 2016 Feb 22.
Cochlear hair cell loss results in the secondary loss of spiral ganglion cells (SGCs). The death of these SGCs is due to apoptosis. The E2F1-cyclin dependent kinase 1 (CDK1) pathway is believed to represent an important mechanism of neuronal cell death. However, the role of this pathway in spiral ganglion neuronal apoptosis has not yet been reported. In this study, we deafened guinea pigs with a subcutaneous injection of kanamycin followed by an intravenous infusion of furosemide and then assayed the expression levels of cleaved caspase-3, E2F1, CDK1 and cleaved caspase-9 during the induced SGC apoptosis. Our results revealed that co-administration of kanamycin and furosemide rapidly induced hair cell loss in the guinea pigs and then resulted in a progressive loss of SGCs. Expression levels of E2F1 and CDK1 were obviously up-regulated at 1 and 3 days after deafening. Cleaved caspase-9 also increased robustly 1 or 2 weeks after the deafening procedure.
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