Introduction of 1418033-25-6 :
LMK-235 is a potent and selective HDAC4/5 inhibitor, inhibits HDAC5, HDAC4, HDAC6, HDAC1, HDAC2, HDAC11 and HDAC8, with IC50s of 4.22 nM, 11.9 nM, 55.7 nM, 320 nM, 881 nM, 852 nM and 1278 nM, respectively, and is used in cancer research. IC50 & Target: IC50: 4.22 nM (HDAC5), 11.9 nM (HDAC4), 55.7 nM (HDAC6), 320 nM (HDAC1), 881 nM (HDAC2), 852 nM (HDAC11), 1278 nM (HDAC8)[1] In Vitro: LMK-235 shows cytotoxic activity against human ovarian cancer cell lines A2780 and A2780 CisR, with IC50s of 0.49 μM and 0.32 μM, respectively. LMK-235 inhibits HDAC in A2780 and A2780 CisR cell lines, with IC50s of 0.65 μM and 0.32 μM, respectively. LMK-235 produces a higher reduction in cell viability in comparison to the combination of cisplatin and vorinostat in all cell lines[1]. LMK-235 (0, 0.625, 1.25, 2.5, 5, 10, and 20 μM) reduces the proliferation of BC cells in a dose- and time-dependent manner. LMK-235 (0-800 nM) also inhibits the growth of BC cells. Moreover, LMK-235 synergizes with bortezomib in BC cell lines[2]. LMK235 (2, 20 nM) decreases in HDAC4 nuclear accumulation in Cdkl5 -/Y NPCs, completely restores the reduced number of neurons generated from Cdkl5 -/Y NPCs. LMK235 also restores histone 3 acetylation in Cdkl5 -/Y NPCs. LMK235 causes a notable increase in the isoform IV, but does not affect BDNF isoforms I or II[3]. In Vivo: LMK235 (5 and 20 mg/kg) restores survival and maturation of postmitotic granule neurons in Cdkl5 -/Y mice. LMK235 also restores synapse development in the dentate gyrus and hippocampus of Cdkl5 -/Y mice. Furthermore, LMK235 restores hippocampus-dependent learning and memory in Cdkl5 -/Y mice[3].
