hdac-in-3

HDAC-IN-3 (GSK3117391A) is a potent histone deacetylase (HDAC) inhibitor, and treatment chronic inflammatory disorders.

CDK HDAC-IN-3 is an orally active dual inhibitor of HDACs and CDKs, offering potent and selective inhibition of CDK9, CDK12, CDK13, HDAC1, HDAC2, and HDAC3, with IC50 values of 98.32 nM, 98.85 nM, 100 nM, 62.12 nM, 93.28 nM, and 82.87 nM, respectively, and is applicable in the treatment of acute myeloid leukemia (AML) [1].

Tubulin HDAC-IN-3 (compound 12a) is a potent dual inhibitor of tubulin polymerization and HDAC1 8, with IC50 values of 5.4 μM for tubulin polymerization, and 0.155 and 0.177 μM for HDAC1 and HDAC8, respectively. It obstructs the cell cycle, triggers apoptosis, and suppresses colony formation [1].

c-Met/HDAC-IN-3, a dual inhibitor targeting both c-Met and HDAC, exhibits potent inhibitory activity with IC50 values of 12.50 nM for c-Met and 26.97 nM for HDAC1. It induces apoptosis and causes cell cycle arrest in the G2/M phase.

PI3K HDAC-IN-3 (36) acts as a dual inhibitor targeting PI3K and HDAC, exhibiting respective IC50 concentrations of 0.23 nM for PI3Kα and 172 nM for HDAC1. In MV4-11 cells, it inhibits AKT phosphorylation while enhancing H3 acetylation. Furthermore, PI3K HDAC-IN-3 (36) demonstrates substantial, dose-dependent anticancer effects in an MV4-11 xenograft model [1].

HDAC/HSP90-IN-3 is a selective and potent dual inhibitor of fungal Hsp90 (IC50: 0.83 μM) and HDAC (IC50: 0.91 μM), exhibiting antifungal effects against azole-resistant Candida albicans. HDAC/HSP90-IN-3 exhibits inhibitory effects on important virulence factors and is able to downregulate the resistance genes ERG11 and CDR1.

JAK HDAC-IN-3 (13a), a dual inhibitor of JAK and HDAC, exhibits IC50 values of 25.36 nM for JAK2, 0.2 μM for HDAC, and 0.43 μM for HDAC1, respectively [1].

HDAC-IN-7 (HBI-8000) (Chidamide impurity) is an impurity of Chidamide, a potent and orally bioavailable inhibitor of HDAC enzymes class I (HDAC1 2 3) and class IIb [HDAC10].

mTOR HDAC-IN-1 (Compound 50) is a dual inhibitor of mTOR and HDAC, with IC50 values of 0.49 nM and 0.91 nM, respectively, holding potential as an anti-cancer agent [1].

MI-192 is a selective HDAC2 and HDAC3 inhibitor with IC50 values of 30 nM and 16 nM, respectively. It exhibits greater selectivity for HDAC2 3 over other HDAC isomers and induces apoptosis in myeloid leukemic cells, indicating potential therapeutic use in leukemia and as an anti-stroke agent [1] [2].

Fimepinostat (CUDC 907) is an orally bioavailable inhibitor of both phosphoinositide 3-kinase (PI3K) class I and pan-histone deacetylase (HDAC) enzymes, with potential antineoplastic activity. Upon oral administration, CUDC-907 inhibits the activity of both PI3K class I isoforms and HDAC, thereby preventing the activation of the PI3K-AKT-mTOR signal transduction pathway that is often overactivated in many cancer cell types.

AES-350 is a potent and orally active HDAC6 inhibitor (IC50 and Ki of 0.0244 μM and 0.035 μM, respectively), also exhibiting activity against HDAC-3, -8, and -11 in an enzymatic assay with IC50 values of 0.187 μM, 0.245 μM, and >1 μM, respectively. AES-350 triggers apoptosis in AML cells through HDAC inhibition and can be used for acute myeloid leukemia (AML) research.

Quisinostat dihydrochloride (JNJ26854165(Quisinostat) 2HCl) is a novel second-generation HDAC inhibitor with highest potency for HDAC1 with IC50 of 0.11 nM in a cell-free assay, modest potent to HDACs 2, 4, 10, and 11; greater than 30-fold selectivity against HDACs 3, 5, 8, and 9 and lowest potency to HDACs 6 and 7. Phase 2.

HDAC CD13-IN-1 (Compound 12) is an inhibitor of both HDAC and CD13, with IC50 values of 0.34 μM for hCD13, 0.53 μM for porcine CD13, and 0.03, 0.06, and 0.02 μM for HDAC1, HDAC2, and HDAC3, respectively. This compound effectively suppresses proliferation and induces apoptosis in MV4-11, K562, Jeko-1, and HL60 cancer cells, with IC50 ranges of 0.25-2.04 μM, and demonstrates capabilities in hindering metastasis and invasion [1].

CAY10722 is an inhibitor of sirtuin 3 (SIRT3), a class III HDAC (71% inhibition at 200 μM). SIRT3 is involved in modulating metabolic homeostasis as a NAD+-dependent protein deacetylase in the mitochondria. SIRT3 functions as either an oncogene or tumor suppressor, depending on cancer cell type. High SIRT3 expression in patient-derived esophageal cancer tissues is associated with shorter survival and, in mice, downregulation leads to a lower tumor load. In contrast, low SIRT3 expression in patient-derived breast cancer cells is correlated with shorter survival.

Compound A5b, also known as JMJD3/HDAC-IN-1, is a dual inhibitor that targets both JMJD3 (Jumonji domain-containing protein demethylase 3) and HADC1 (histone deacetylase, IC50 = 16 nM). It induces hypermethylation of histone H3K27 and hyperacetylation of H3K9, while also promoting apoptosis through the cleavage of caspase-7 and PARP. This compound has demonstrated the ability to effectively inhibit cancer cell cloning, migration, and invasion [1].

HDAC-IN-27 is a potent and orally active inhibitor of HDAC Class I (0.43 nM - 3.01 nM for HDAC1-3). HDAC-IN-27 shows activity against anti-acute myeloid leukemia (AML).

Nampt-IN-3 simultaneously inhibit nicotinamide phosphoribosyltransferase (NAMPT) and HDAC (IC50s of 31 nM and 55 nM, respectively).

HDAC-IN-53 is an orally active, selective inhibitor of HDAC1-3, with IC50 values of 47 nM, 125 nM, and 450 nM, respectively. It exhibits no inhibitory effects on class II HDACs (HDAC4, 5, 6, 7, 9; IC50 >10 μM). The compound induces caspase-dependent apoptosis and significantly hampers the growth of human tumor xenografts in nude mice and murine tumor growth in immune-competent mice with MC38 colon cancer [1].

HDAC-IN-38 is a potent inhibitor of HDAC. HDAC-IN-38 has similar micromolar inhibitory effects on HDAC1, 2, 3, 5, 6 and 8, and also increases histone acetylation levels (H3K14 or H4K5). HDAC-IN-38 increases cerebral blood flow (CBF), reduces cognitive impairment and improves hippocampal atrophy.

HDAC3-IN-T326 is a potent and selective HDAC3 inhibitor that acts by increasing NF-κB acetylation and activating HIV gene expression in latent HIV-infected cells.

Givinostat (ITF-2357) is an HDAC inhibitor with IC50 values of 198 nM for HDAC1 and 157 nM for HDAC3.

HDAC1/2-IN-3 is an inhibitor of both HDAC1 and HDAC2, demonstrating IC50 values of 0-5 nM and 5-10 nM, respectively.

HDAC-IN-47 is an orally active histone deacetylase (HDAC) inhibitor, with IC50 values of 19.75 nM, 57.8 nM, 40.27 nM, 5.63 nM, and 302.73 nM for HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8, respectively. HDAC-IN-47 can block the cell cycle in the G2 M phase, inhibit autophagy, induce apoptosis via the Bax Bcl-2 and caspase-3 pathways, and exhibits anti-cancer activity in vivo.

HDAC-IN-71 (Compound 17q), a potent HDAC inhibitor, exhibits IC 50 values of 12.6 nM for HDAC1, 14.1 nM for HDAC2, 20 nM for HDAC3, 3 nM for HDAC6, and 72 nM for HDAC10. This compound induces apoptosis and is utilized in cancer research [1].

HDAC3-IN-T247 (HDAC3 inhibitor T247) is a selective and potent histone deacetylase 3 (HDAC3) inhibitor with anticancer and antiviral activities.HDAC3-IN-T247 induces NF-κB acetylation in human colon cancer HCT116 cells in a dose-dependent manner.HDAC3-IN-T247 inhibits cancer cell proliferation. HDAC3-IN-T247 inhibits cancer cell proliferation.

Suberoylanilide hydroxamic acid (SAHA) is a class I and class II histone deacetylase (HDAC) inhibitor that binds directly to the catalytic site of the enzyme thereby blocking substrate access. SAHA-BPyne is a SAHA derivative with a benzophenone crosslinker and an alkyne tag intended to be used for profiling HDAC activities in proteomes and live cells. Such terminal alkyne groups can be used in linking reactions, known as click chemistry, characterized by high dependability and specificity of azide-alkyne bioconjugation reactions. SAHA-BPyne labels HDAC complex proteins both in proteomes at 100 nM and in live cells at 500 nM and demonstrates an IC50 value of ~3 μM for inhibition of HDAC activity in HeLa cell nuclear lysates in an HDAC activity assay.

HDAC-IN-43 is a potent HDAC 1 3 6 inhibitor with IC50 values of 82 nM for HDAC 1, 45 nM for HDAC 3, and 24 nM for HDAC 6, and a weak PI3K mTOR inhibitor with IC50 values of 3.6 μM for PI3K and 3.7 μM for mTOR, exhibiting a broad-spectrum anti-proliferative effect.

Theophylline (1,3-Dimethylxanthine) sodium glycinate is a potent phosphodiesterase (PDE) inhibitor that targets PDE3 to relax airway smooth muscle and is used in asthma and chronic obstructive pulmonary disease (COPD) research. It also functions as an adenosine receptor antagonist, histone deacetylase (HDAC) activator, and exhibits anti-inflammatory activity by increasing IL-10 levels and inhibiting NF-κB nuclear import, while inducing apoptosis [1] [2] [3] [4] [5].

MHY219 is a novel HDAC inhibitor. MHY219 induces apoptosis via up-regulation of androgen receptor expression in human prostate cancer cells. MHY219 was shown to enhance the cytotoxicity on DU145 cells (IC50, 0.36 μM) when compared with LNCaP (IC50, 0.97 μM) and PC3 cells (IC50, 5.12 μM). MHY219 showed a potent inhibition of total HDAC activity when compared with SAHA. MHY219 increased histone H3 hyperacetylation and reduced the expression of class I HDACs (1, 2 and 3) in prostate cancer cells. MHY219 effectively increased the sub-G1 fraction of cells through p21 and p27 dependent pathways in DU145 cells. MHY219 significantly induced a G2/M phase arrest in DU145 and PC3 cells and arrested the cell cycle at G0/G1 phase in LNCaP cells. Furthermore, MHY219 effectively increased apoptosis in DU145 and LNCaP cells, but not PC3 cells, according to Annexin V/PI staining and Western blot analysis. These results indicate that MHY219 is a potent HDAC inhibitor that targets regulating mu......

MPT0G211 mesylate is a powerful and selective HDAC6 inhibitor (IC50 = 0.291 nM), with high oral bioavailability. It exhibits remarkable selectivity for HDAC6 over other HDAC isoforms (>1000-fold selectivity). Additionally, MPT0G211 mesylate can effectively cross the blood-brain barrier. In preclinical studies using an Alzheimer's disease model, MPT0G211 mesylate has shown promising results in reducing tau phosphorylation and cognitive deficits. Furthermore, this compound exhibits anti-metastatic and neuroprotective effects, making it a potential candidate for anticancer interventions. [1] [2] [3].