HDAC2 Inhibitor

HDAC-IN-43 is a potent HDAC 1/3/6 inhibitor with IC₅₀ values of 82, 45, and 24 nM, respectively. HDAC-IN-43 is a weak PI3K/mTOR inhibitors with IC₅₀ values of 3.6 and 3.7 μM, respectively. HDAC-IN-43 shows broad anti-proliferative activity .

HDAC-IN-105 is a histone deacetylase (HDAC) inhibitor with binding to HDAC2 and HDAC4 isoforms. HDAC-IN-105 suppresses HDAC activity via binding within conserved HDAC catalytic pockets. HDAC-IN-105 induces G2/M phase cell cycle arrest. HDAC-IN-105 triggers mitochondrial dysfunction marked by loss of mitochondrial membrane potential. HDAC-IN-105 exhibits growth inhibition in triple-negative breast cancer cells and low toxicity toward normal cells. HDAC-IN-105 can be used for the research of triple-negative breast cancer.

MC2590 is a potent pyridine-containing histone deacetylase (HDAC) inhibitor. MC2590 is a inhibitor of HDAC1-3, -6, -8, and -10 (class I/IIb-selective inhibitor) with IC₅₀s of 0.015 μM-0.156 μM. MC2590 also inhibits HDAC isoforms HDAC4, HDAC5, HDAC7, HDAC9, HDAC11 with IC₅₀s of 1.35 μM-3.98 μM. MC2625 induces G2/M cell cycle arrest and modulates pro- and anti-apoptotic microRNAs towards apoptosis induction.

HDAC-IN-94 is a potent, selective HDAC6 inhibitor (IC₅₀ = 4.5 nM). HDAC-IN-94 shows >1000-fold selectivity over HDAC8 and shows minimal activity against other isoforms (HDAC1-3/10). HDAC-IN-94 induces α-tubulin hyperacetylation, apoptosis, and G2/M cell cycle arrest, exhibiting potent anti-tumor efficacy with low cytotoxicity. HDAC-IN-94 can be used for neuroblastoma and glioblastoma research.

(R)-HDAC-IN-102 is a HDAC2 inhibitor and the isomer of HDAC-IN-102 (HY-185554). HDAC-IN-102 inhibits total HDAC with an IC₅₀ of 58 μM and exhibits partial subtype selectivity. Specifically, (R)-HDAC-IN-102 targets HDAC2, while (S)-HDAC-IN-102 (HY-185554A) targets HDAC8. HDAC-IN-102 exerts antioxidant effects via scavenging DPPH free radicals and can be used in cancer-related research.

CDK/HDAC-IN-2 is a potent HDAC/CDK dual inhibitor with IC₅₀ of 6.4, 0.25, 45, >1000, 8.63, 0.30, >1000 nM for HDAC1, HDAC2, HDAC3, HDAC6,8, CDK1, CDK2, CDK4,6,7, respectively. CDK/HDAC-IN-2 shows excellent antiproliferative activities. CDK/HDAC-IN-2 induces apoptosis and cell cycle arrest at G2/M phase. CDK/HDAC-IN-2 shows potent antitumor efficacy.

HDAC3/6-IN-2 (compound 15) is a potent HDAC6 and HDAC3 inhibitor, with IC₅₀ values of 0.368 and 0.635 μM, respectively. HDAC3/6-IN-2 shows antitumor activity, and induces cancer cell apoptosis. HDAC3/6-IN-2 decreases the levels of HDAC6 and HDAC3, associated with upregulation of acetylated H3 and α-tubulin.

HDAC-IN-71 (Compound 17q) is a potent HDAC inhibitor with IC₅₀ values of 12.6, 14.1, 20, 3, and 72 nM for HDAC1, HDAC2, HDAC3, HDAC6, and HDAC10, respectively. HDAC-IN-71 induces apoptosis and can be used in cancer research.

C1A is a class I/II HDACs and sirtuin inhibitor with an IC₅₀ of 479 nM for HDAC6. C1A induces sustained acetylation of HDAC6 substrates, α-tubulin and HSP90. C1A shows srtong anticancer effcts, and induces apoptosis in cancer cells.

HDAC-IN-41 (Compound 7c) is a selective, orally active class I HDAC inhibitor with IC₅₀ values of 0.62, 1.46 and 0.62 μM against HDAC1, HDAC2 and HDAC3, respectively. HDAC-IN-41 shows NO releasing activity.

HDAC-IN-9 is a potent and selective tubulin and HDAC dual inhibitor. HDAC-IN-9 inhibits the invasion and migration of A549 cells. HDAC-IN-9 shows potent antitumor and antiangiogenic effect in vitro and in vivo.

Top/HDAC-IN-2 (45b), a Top and HDAC dual inhibitor, exhibits potent antitumor activities and induces apoptosis.

HDAC3-IN-8 is a selective inhibitor targeting HDAC1, HDAC2 and HDAC3, with IC₅₀ values of 3.52 nM for HDAC1, 15.14 nM for HDAC2 and 0.38 nM for HDAC3. HDAC3-IN-8 shows high selectivity for HDAC3 and exerts its effect by inhibiting histone deacetylase activity. HDAC3-IN-8 can be used to construct HDAC3-targeted PROTAC degrader (HY-181767) and is suitable for the research of acute myeloid leukemia (AML).

HDAC6-IN-45 (Compound 15) is a selective inhibitor for HDAC6 with IC₅₀ of 15.2 nM. HDAC6-IN-45 exhibits neurotrophic through the upregulation of GAP43 and Beta-3 tubulin markers. HDAC6-IN-45 activates the Nrf2 signaling pathway, reduces H₂O₂-induced ROS production, inhibits apoptosis in PC12, and exhibits neuroprotective efficacy in SCOP-induced zebrafish Alzheimer's Disease models. HDAC6-IN-45 exhibits antioxidant activity and good blood-brain barrier (BBB) permeability.

sEH/HDAC6-IN-1 (compound M9) is a selective, orally active dual inhibitor for sEH and HDAC6, with IC₅₀s of 2 nM, 0.72 nM and 5 nM, for human sEH, murine sEH and HDAC6, respectively. sEH/HDAC6-IN-1 reveals analgesic and anti-inflammatory effects.

HDAC/Top-IN-1 is an orally active and pan HDAC/Top dual inhibitor with IC₅₀s of 0.036 μM, 0.14 μM, 0.059 μM, 0.089 μM and 9.8 μM for HDAC1, HDAC2, HDAC3, HDAC6 and HDAC8. HDAC/Top-IN-1 efficiently induces apoptosis with S cell-cycle arrest in HEL cells. HDAC/Top-IN-1 has exhibits excellent in vivo antitumor efficacy.

HDAC6-IN-51 (Compound 7e) is a selective HDAC6 inhibitor with an IC₅₀ value of 42.9 nM. HDAC6-IN-51 exhibits good anti-lung fibrosis activity.

KTT-1 is a kinetically selective and orally active HDAC2 inhibitor. KTT-1 exhibits high HDAC2-selectivity over HDAC1. KTT-1 inhibits osteoclast differentiation at an early stage by downregulating c-Fos expression. KTT-1 effectively suppresses arthritis symptoms in the collagen-induced arthritis (CIA) mouse model. KTT-1 can be used for the research of rheumatoid arthritis and neurodegenerative diseases.

sEH/HDAC6-IN-2 is a potent dual soluble epoxide hydrolase (sEH) and HDAC6 inhibitor with IC₅₀s of 0.9 nM, 46.8 nM, and 8 nM for human sEH, mouse sEH, and HDAC6, respectively. sEH/HDAC6-IN-2 can be used for the study of inflammatory pain.

Nanatinostat (CHR-3996) TFA is a potent, class I selective and orally active HDAC inhibitor with IC₅₀s of 3 nM, 4 nM, and 7 nM for HDAC1, HDAC2, and HDAC3, respectively. Nanatinostat TFA has low activity against HDAC5 (IC₅₀ of 200 nM) and HDAC6 (IC₅₀ of 2100 nM). Nanatinostat TFA induces apoptosis in myeloma cells. Nanatinostat TFA has potent anticancer effects, such as myeloma, advanced solid tumours and colorectal cancer.