HDAC-IN-91 is a multiple inhibitor of HDAC (IC₅₀ = 134.22 nM for HDAC1, 66.29 nM for HDAC2), carbonic anhydrase (CA) (K_I = 72.03 nM for CA IX, 50.76 nM for XII), and tubulin polymerization ( IC₅₀ = 2.56 μM). HDAC-IN-91 inhibits PARP1 and increases the Bax/Bcl-2 ratio. HDAC-IN-91 blocks the cell cycle at the G2/M phase and induces apoptosis through a mitochondrial apoptosis activation mechanism. HDAC-IN-91 can exert potent cytotoxic activity through tubulin polymerization inhibition. HDAC-IN-91 can be used in breast, colorectal, cervical and lung cancer research^[1].

HDAC-IN-91 (Compounds 6e) shows cytotoxicity against MCF7, Hela, HCT116, A549 cells, with IC₅₀s of 1.40 μM, 2.22 μM, 1.57 μM, 2.54 μM, respectively^[1].

HDAC-IN-91 presents promising inhibitory activity against HDAC isoforms 3, 4, 6, and 8 with IC

50

HDAC-IN-91 (1.40 μM, 48 h) inhibits the growth of MCF-7 cells by interfering with cell mitosis and ultimately inducing cell apoptosis^[1].

HDAC-IN-91 (1.40 μM, 48 h) induces apoptosis by increasing the Bax/Bcl-2 ratio and caspase-9 and -7 levels in MCF-7 cells^[1].

HDAC-IN-91 (1.40 μM, 48 h) has potential PARP1 inhibitory activity in MCF-7 cells^[1].

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

517.39

C₂₃H₂₁BrN₂O₅S

BrC1=CC=C(C(/C=C/C2CC=C(OCC(NC3=CC=C(S(N)(=O)=O)C=C3)=O)C=C2)=O)C=C1

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Mohamed MFA, et al. Synthesis and apoptotic induction of sulfonamide-based chalcone hybrids as first-in-class dual histone deacetylase‑carbonic anhydrase inhibitors with potential anti-tubulin activity. Bioorg Chem. 2025 Jun 20;163:108694.  [Content Brief]