HDAC6-IN-89

HDAC6-IN-89 inhibits proliferation of A549, PC3, and CT26 cells with IC₅₀ values of 1.05, 0.28, and 4.47 µM, respectively^[1].

HDAC6-IN-89 (0.2-5 µM; 24 h) induces dose-dependent apoptosis in CT26 cells, reaching 41.41% at 5 µM^[1].
HDAC6-IN-89 induces apoptosis in A549 and PC3 cells^[1].

HDAC6-IN-89 blocks GLS1-mediated glutamine conversion and reduces glutamine-derived TCA-cycle intermediates in HCT116 cells^[1].

HDAC6-IN-89 (0.2-5 µM; 24 h) induces dose-dependent G0/G1 cell-cycle arrest in CT26 cells, with 82.03% of cells in G0/G1 at 5 µM^[1].
HDAC6-IN-89 modulates cell-cycle distribution in A549 and PC3 cells^[1].

HDAC6-IN-89 (1-10 µM) induces dose-dependent intracellular ROS accumulation in HCT116 cells^[1].

HDAC6-IN-89 (Compound 58) inhibits recombinant GLS1 with an IC₅₀ of 3.30 µM^[1].
HDAC6-IN-89 is a potent HDAC inhibitor with strongest potency against HDAC6 (IC₅₀ 0.003 µM) and selectivity over other HDAC isoforms^[1].
HDAC6-IN-89 shows no antiproliferative activity against L02 cells with an IC₅₀ > 100 µM^[1].
HDAC6-IN-89 (0.2-5 µM; 24 h) increases α-tubulin and histone H3 acetylation in CT26 cells without altering total α-tubulin or histone H3 expression^[1].
HDAC6-IN-89 (2 h) is relatively stable in human and mouse plasma, with 92.2% and 91.4% remaining after 2 h^[1].
HDAC6-IN-89 has moderate rat liver microsomal stability with a half-life of 1.04 h and CL_int of 22.11 µL/min/mg^[1].
HDAC6-IN-89 shows no reversible inhibition against CYP enzymes^[1].
HDAC6-IN-89 (10 µM) shows no obvious time-dependent inhibition of CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP2E1, with a measurable time-dependent inhibition tendency for CYP3A4^[1].