HDAC-IN-98

HDAC-IN-98 (compound 5d) selectively inhibits class I HDAC enzymes (HDAC1, HDAC2, HDAC3) with sub-nanomolar to low-nanomolar IC₅₀ values and weak or no activity against other HDAC isoforms (IC₅₀: HDAC1 = 41.2 nM, HDAC2 = 52.5 nM, HDAC3 = 74.3 nM, HDAC10 = 4261 nM, HDAC5/8/11 >10000 nM)^[1].
HDAC-IN-98 (1 μM; up to 60 min) inhibits total HDAC activity in a complex nuclear extract system^[1].
HDAC-IN-98 (0.1-100 μM; 48 h) selectively reduces viability of CRC cells with IC₅₀ values ranging from 14 μM and minimal toxicity to normal colon cells (IC₅₀: HCT116 = 1 μM, HT29 = 4 μM, DLD1 = 4 μM, HCEC >100 μM)^[1].
HDAC-IN-98 (1-4 μM; 48 h) modulates epigenetic markers (H₃K₉ acetylation) and apoptotic pathways (PARP cleavage) in CRC cells without inhibiting class II HDACs^[1].
HDAC-IN-98 (1-4 μM; 48 h) disrupts cell cycle progression, inducing subG₁ accumulation (apoptosis) in HCT116 and G₁ arrest in HT29/DLD1 cells^[1].
HDAC-IN-98 (1-4 μM; 48 h) triggers apoptosis selectively in HCT116 cells without inducing necrosis^[1].
HDAC-IN-98 (up to 10 μM) shows minimal hERG liability at concentrations relevant to its anticancer activity^[1].
HDAC-IN-98 (1 μM; in vitro pretreatment; 48 h) exhibits potent antitumor efficacy in chicken embryos with colorectal cancer chorioallantoic membrane model (CAM) models independent of p21 status. In the HCT116 p21 wildtype CAM model, HDAC-IN-98 confirmes a robust upregulation of p21. In the HCT116 p21^−/− CAM model, HDAC-IN-98 significantly reduces the vessel area, the vessel length, and the number of branching points whereas the vessel thickness is not affected^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.