HDAC-IN-4 is a selective HDAC6 and HDAC10 inhibitor with pIC50s of 7.2 and 6.8 in BRET assay, respectively. Antitumoral activity[1].
Bocodepsin hydrochloride (OKI-179) is an orally active and selective HDAC inhibitor, with antitumor activity. Bocodepsin hydrochloride can be used for suppression on solid tumor and hematologic malignancies[1].
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 [1].
MI-192 is a selective HDAC2 and HDAC3 inhibitor with IC50s of 30 nM and 16 nM, respectively. MI-192 is more selective for HDAC2/3 than other HDAC isomers.MI-192 induces myeloid leukaemic cells apoptosis. Anticaner and neuroprotective activities[1][2].
Phenylbutyrate is a potent histone deacetylases (HDACs) inhibitor. Phenylbutyrate can be used for urea cycle disorder research[1][2].
Panobinostat is a non-selective histone deacetylase (HDAC) inhibitor.
JPS035 is a benzamide-based Von Hippel-Lindau (VHL) E3-ligase proteolysis targeting chimeras (PROTAC). JPS035 degrades class I histone deacetylase (HDAC). JPS035 is potent HDAC1/2 degrader correlated with greater total differentially expressed genes and enhanced apoptosis in HCT116 cells[1].
IHCH-3064 is a dual-acting compounds targeting Adenosine A2A Receptor and HDAC. IHCH-3064 exhibits potent binding to A2AR (Ki=2.2 nM) and selective inhibition of HDAC1 (IC50=80.2 nM), with good antiproliferative activity against tumor cell lines in vitro. IHCH-3064 is a tumor immunotherapeutic agent[1].
BChE/HDAC6-IN-2 (compound 29a) is a dual inhibitor of BChE and HDAC6 with IC50s of 1.8 nM and 71.0 nM, respectively. BChE/HDAC6-IN-2 has prominently neuroprotective effects and reactive oxygen species (ROS) scavenging activity. BChE/HDAC6-IN-2 is also an effective chelator of metal ion (Fe2+ and Cu2+). BChE/HDAC6-IN-2 inhibits phosphorylation of tau, and exhibits moderate immunomodulatory effect.
HDAC ligand-1 is a HDAC ligand that can be used to synthesize PROTAC HDAC degraders[1].
Bocodepsin (OKI-179) is an orally active and selective HDAC inhibitor, with antitumor activity. Bocodepsin can be used for suppression on solid tumor and hematologic malignancies[1].
HDAC-IN-28, a novel HDAC inhibitor, shows potent activities against tumor growth and metastasis
HDAC-IN-42 (compound 14f) is a potent and selective HDAC inhibitor with IC50 values of 0.19 and 4.98 µM for HDAC1 and HDAC6, respectively. HDAC-IN-42 shows anticancer and anti-proliferative activity. HDAC-IN-42 induces apoptosis and cell cycle arrest at G2/M phase[1].
CG347B is a selective HDAC6 inhibitor[1].
MOCPAC is an HDAC1 specific substrate[1].
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 ic50 of 0.098 μM, 0.156 μM, 0.039 μM, 0.015 μM, 0.047 μM, 0.071 μM, respectively. MC2590 also inhibits HDAC isoforms HDAC4 (IC50=2.73 μM), HDAC5 (IC50=1.35 μM), HDAC7 (IC50=2.06 μM), HDAC9 (IC50=2.79 μM), HDAC11 (IC50=3.98 μM). MC2625 induces G2/M cell cycle arrest and modulates pro- and anti-apoptotic microRNAs towards apoptosis induction[1].
Dihydrochlamydocin is a Putative HDAC inhibitor.
BRD9757 is a potent, capless and selective HDAC6 inhibitor with an IC50 of 30 nM. BRD9757 shows excellent selectivity toward HDAC6 versus the class I (>20-fold) and class II (>400-fold) HDACs[1].
Ac-Arg-Gly-Lys(Ac)-AMC is a substrate for HDAC[1].
NN-390 is a potent and selective HDAC6 inhibitor, with an IC50 of 9.8 nM. NN-390 penetrates the blood-brain barrier (BBB). NN-390 shows study potential in metastatic Group 3 MB (medulloblastoma)[1].
4-Phenylbutyric acid-d5 is the deuterium labeled 4-Phenylbutyric acid[1]. 4-Phenylbutyric acid (4-PBA) is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research[2][3][4].
Butyric acid-13C1 is the 13C labeled Butyric acid. Butyric acid is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers.
HDAC6-IN-10 is a highly selective HDAC6 inhibitor with the IC50 of 0.73 nM. HDAC6-IN-10 has 144~10941-fold selectivity over other HDAC isoforms. HDAC6-IN-10 shows anti-proliferative activities against multiple myeloma cells[1].
CHDI-390576, a potent, cell permeable and CNS penetrant class IIa histonedeacetylase (HDAC) inhibitor with IC50s of 54 nM, 60 nM, 31 nM, 50 nM for class IIa HDAC4, HDAC5, HDAC7, HDAC9, respectively, shows >500-fold selectivity over class I HDACs (1, 2, 3) and ~150-fold selectivity over HDAC8 and the class IIb HDAC6 isoform[1].
Depudecin ((-)-Depudecin) is a histone deacetylase (HDAC) inhibitor. Depudecin can be isolated from the fungus Alternaria brassicicola[1][2].
Tubastatin A (TSA) TFA is a potent and selective?HDAC6?inhibitor with?IC50?of 15 nM in a cell-free assay, and is selective (1000-fold more) against all other isozymes except HDAC8 (57-fold more). Tubastatin A TFA also inhibits HDAC10 and metallo-β-lactamase domain-containing protein?2 (MBLAC2).
Nullscript is a negative control for Scriptaid. Nullscript is a known inactive analog of Scriptaid[1]. Scriptaid is a representative HDAC inhibitor[2]. Nullscript inhibits Cryptosporidium (C. parvum) growth with the IC50 value of 2.1 μM[3].
4-Phenylbutyric acid-d2 is the deuterium labeled 4-Phenylbutyric acid[1]. 4-Phenylbutyric acid (4-PBA) is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.
JPS036 is a benzamide-based Von Hippel-Lindau (VHL) E3-ligase proteolysis targeting chimeras (PROTAC). JPS036 degrades class I histone deacetylase (HDAC). JPS036 is potent HDAC1/2 degrader correlated with greater total differentially expressed genes and enhanced apoptosis in HCT116 cells[1].
2-Hexyl-4-pentynoic acid ((±)-2-Hexyl-4-pentynoic acid), valproic acid (VPA) derivative, exhibits potential roles of HDAC inhibition (IC50=13 µM) and HSP70 induction. Potent neuroprotective effects. 2-Hexyl-4-pentynoic acid causes histone hyperacetylation and protect against glutamate-induced excitotoxicity in cultured neurons[1].