LMK-235

Research use only, not for human use.

A selective HDAC5 and HDAC4 inhibitor with IC50 of 4.22 nM and 11.9 nM respectively.

A selective HDAC5 and HDAC4 inhibitor with IC50 of 4.22 nM and 11.9 nM respectively; less potent for HDAC1/11/2/8; demonstrates activity against chemoresistant cancer cell lines in an MTT assay for cytotoxicity using human ovarian cancer cell lines A2780 and cisplatin resistant A2780CisR (IC50 =0.49 and 0.32 uM respectively).

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. 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. LMK235 (2, 20nM) 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.

LMK235 (5 and 20mg/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.

LMK 235 | LMK 235

Cell Cycle/DNA Damage

HDAC

HDAC4|HDAC5

Cancer

——

1418033-25-6

294.3462

C15H22N2O4

>98% (HPLC)

DMSO: ≥ 30 mg/mL

O=C(NOCCCCCC(NO)=O)C1=CC(C)=CC(C)=C1

Benzamide, N-[[6-(hydroxyamino)-6-oxohexyl]oxy]-3,5-dimethyl-

(-20℃)

With Ice Pack

≥ 2 years