Molecular Weight(MW): 294.35
LMK-235 is a selective inhibitor of HDAC4 and HDAC5 with IC50 of 11.9 nM and 4.2 nM, respectively.
Cited by 8 Publications
6 Customer Reviews
Upper panel: qPCR analysis of CDX2-negative HT29 cells treated with increasing concentrations of the DNMTi decitabine (1.25 μM, 2.5 μM, 5 μM, 10 μM) for 48 h and increasing concentrations of the HDAC4/5i LMK-235 (5 nM, 10 nM, 20 nM, 40 nM, 80 nM). Data were normalized to the HMBS housekeeping gene and are shown as n-fold regulation compared with DMSO-treated cells. MWU: ***p < 0.001, (n = 4). Lower panel: CDX2 Western blot analysis of the three highest concentrations for both compounds of HT29 cells treated as above. Total protein is shown as a loading control. Percentage indicates amount of protein normalized to respective DMSO controls
Clin Epigenetics, 2018, 10(1):120. LMK-235 purchased from Selleck.
Cells were exposed to HDAC Class II selective inhibitors LMK-235 or Nexturastat A (NA) at the indicated concentrations for 48 hrs and analyzed by Western blotting. Rom, romidepsin; Bel, belinostat, Pano, panobinostat; SAHA, suberoylanilide hydroxamic acid.
Oncotarget, 2016, 7(39):63829-63838. LMK-235 purchased from Selleck.
MDA-MB-231 and Hs-578T cells were treated with DMSO or 50 nM, 500 nM, or 1 μM LMK-235 for 24 hours. The levels of acetyl-histone H3 and total histone H3 were examined by western blot. GAPDH was used as a loading control.
Oncotarget, 2016, 7(25):37966-37978. LMK-235 purchased from Selleck.
B, 5×106 293T, HeLa, A549, and H1299 cells were seeded in 10-cm dishes on day 0 and treated with dimethyl sulfoxide, 10 μM TMP269, 10 μM LMK-235, or butyrate as indicated for 12 h. Cell lysates were collected for Western blotting analysis of Apaf-1 and β-actin. D, 1×106 293T cells were plated in 10-cm dishes on day 0 and transfected with 2 μg of vector plasmids or plasmids encoding FLAG-HDAC1 as indicated on day 1. On day 3, the cells were treated with butyrate sodium solution for 12 h. Cell lysates were collected and subjected to Western blotting analysis of Apaf-1, HDAC1, FLAG, and GAPDH.
J Biol Chem, 2016, 291(14):7386-95.. LMK-235 purchased from Selleck.
LMK-235 effects on apoptosis induction in pNET cells. (A,B) BON-1 (A) and QGP-1 (B) were incubated for 8, 24, and 32 h with different LMK-235 concentrations (0.078–20 µM). Relative changes in caspase activity were measured as a parameter for treatment-induced apoptosis. Bars represent mean ± SEM for n = 4 experiments. (C,D) Flow cytometry results of Annexin V/7-AAD staining are shown for BON-1 (C) and QGP-1 (D). Bars represent the cumulative percentages (n = 3) for alive, early, or late apoptotic and necrotic cells when treated for 24 h with LMK-235 (0.078–20 µM). Asterisks indicate p-values of <0.05 (one) or <0.01 (two) versus corresponding untreated control. Abbreviations: p.i. = post incubation, UTC = untreated control.
Int J Mol Sci, 2018, 19(10). LMK-235 purchased from Selleck.
Effect of LMK-235 on DPCs. (A) Cell viability, OD value for 0 nM group was compared with the remaining groups. &P<0.05 vs. 250 nM; #P<0.05 vs. 500 nM; $P<0.05 vs. 1,000 nM. (B) ALP activity, and (C) ALP, (D) Runx2 and (E) DSPP mRNA expression levels in DPCs following treatment with LMK-235. *P<0.05, **P<0.01, ***P<0.001. Data are presented as the mean ± standard deviation. OD, optical density; DPCs, dental pulp cells; ALP, alkaline phosphatase; DSPP, dentin sialophosphoprotein; Runx2, runt-related transcription factor 2; MI, mineralized inductive.
Mol Med Rep, 2018, 17(1):1445-1452. LMK-235 purchased from Selleck.
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Choose Selective HDAC Inhibitors
|Description||LMK-235 is a selective inhibitor of HDAC4 and HDAC5 with IC50 of 11.9 nM and 4.2 nM, respectively.|
LMK-235 causes HDAC inhibition with IC50 of <1 μM in human cancer cell lines with different sensitivity towards cisplatin. In breast cancer cell line MDA-MB-231, tongue cancer cell line Cal27, and esophagus cell line Kyse510 cell line, LMK-235 displays a high cytotoxicity, and markedly enhances the cytotoxicity of cisplatin.  In addition, LMK-235 also shows nanomolar activity against multiple malaria parasite life cycle stages. 
HDAC IC50 Profiling:The in vitro inhibitory activity of compounds against seven human HDAC isoforms (1, 2, 4 C2A, 5 C2A, 6, 8, and 11) are performed with a fluorescent based assay according to the company’s standard operating procedure. The IC50 values are determined using 10 different concentrations with 3-fold serial dilution starting at 10 μM. TSA and vorinostat are used as reference compounds.
|In vitro||DMSO||58 mg/mL (197.04 mM)|
|Ethanol||58 mg/mL (197.04 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
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