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Catalog No.
Product Name
Application
Product Information
Citations
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HDAC/ER stress inhibitor
Sodium phenylbutyrate is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research. -
HDAC6 inhibitor
Tubastatin A 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). -
HDAC inhibitor
CG-200745 is a potent HDAC inhibitor which has the hydroxamic acid moiety to bind zinc at the bottom of catalytic pocket. -
HDAC1 inhibitor
Domatinostat tosylate (4SC-202) is a selective class I HDAC inhibitor with IC50 of 1.20 μM, 1.12 μM, and 0.57 μM for HDAC1, HDAC2, and HDAC3, respectively. It also displays inhibitory activity against Lysine specific demethylase 1 (LSD1). -
HDAC inhibitor
Givinostat (ITF-2357) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively. -
HDAC inhibitor
Givinostat hydrochloride (ITF-2357 hydrochloride) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively. -
pan HDAC inhibitor
Tefinostat (CHR-2845) is a monocyte/macrophage-targeted pan HDAC inhibitor, cleaved into active acid CHR-2847 by the intracellular esterase human carboxylesterase-1 (hCE-1). Anti-monocytoid lineage leukaemias activity. -
HDAC inhibitor
Oxamflatin (Metacept-3) is a potent HDAC inhibitor with an IC50 of 15.7 nM. -
HDAC inhibitor
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. -
HDAC inhibitor
MPT0E028 is an orally active and selective HDAC inhibitor with IC50s of 53.0 nM, 106.2 nM, 29.5 nM for HDAC1, HDAC2 and HDAC6, respectively. -
HDAC inhibitor
Resminostat hydrochloride is a potent inhibitor of HDAC1/3/6(IC50=43-72 nM); less potent to HDAC8 with IC50 of 877 nM. -
HDAC Inhibitor
NCH 51 is a cell-permeable prodrug that is intracellularly converted to a potent HDAC inhibitor, with an IC50 of 48 nM. -
HDAC6 inhibitor
TCS HDAC6 20b, selective inhibitor of histone deacetylase 6 (HDAC6). Inhibits HCT116 growth in combination with taxol. Also inhibits growth of MCF-7 cells stimulated by estrogen. -
HDAC/ACE inhibitor
Sinapinic acid (Sinapic acid) is a phenolic compound isolated from Hydnophytum formicarum Jack. Rhizome, acts as an inhibitor of HDAC, with an IC50 of 2.27 mM, and also inhibits ACE-I activity. Sinapinic acid posssess potent anti-tumor activity, induces apoptosis of tumor cells. -
HDAC8 inhibitor
HDAC8-IN-1, is a HDAC8 inhibitor with an IC50 of 27.2 nM in cancer cell lines. -
HDAC inhibitor
Tucidinostat is a potent and orally bioavailable HDAC enzymes class I (HDAC1/2/3) and class IIb (HDAC10) inhibitor, with IC50s of 95, 160, 67 and 78 nM, less active on HDAC8 and HDAC11 (IC50s, 733 nM, 432 nM, respectively), and shows no effect on HDAC4/5/6/7/9. -
HDAC inhibitor
EDO-S101 is a pan HDAC inhibitor; inhibits HDAC1, HDAC2 and HDAC3 with IC50 values of 9, 9 and 25 nM, respectively. -
HDAC Inhibitor
DL-Sulforaphane N-acetyl-L-cysteine is an orally active inhibitor of histone deacetylases (HDACs) and a stable metabolite of sulforaphane. This compound enhances autophagy-mediated reduction of α-tubulin expression via the ERK signaling pathway, making it a valuable tool in cancer research. Its improved blood-brain barrier permeability and extended half-life support its potential in neurobiological studies and therapeutic applications. -
HDAC Inhibitor
Panobinostat lactate is a potent, orally active non-selective histone deacetylase (HDAC) inhibitor. It exhibits significant antineoplastic activity and has been shown to disrupt HIV latency effectively. Additionally, Panobinostat lactate induces apoptosis and autophagy in various cell types. This reagent is valuable for studying refractory or relapsed multiple myeloma and exploring HDAC inhibition in cancer research. -
HDAC Inhibitor
Purinostat mesylate is a selective inhibitor of histone deacetylases (HDACs), effectively targeting class I and class IIb HDACs with IC50 values ranging from 0.81 to 11.5 nM. This compound induces apoptosis and influences the cell cycle in LAMA84 and 188 BL-2 cell lines, demonstrating potent anti-leukemic effects in vivo. Purinostat mesylate serves as a valuable tool for researching lymphoblastic leukemia and its therapeutic potential. -
HDAC1/HDAC2 Inhibitor
MRLB-223 is a selective inhibitor of HDAC1 and HDAC2, demonstrating potent activity against tumor cells. It induces histone hyperacetylation and activates the intrinsic apoptotic pathway, leading to tumor cell apoptosis and degradation of Bcr-Abl in a caspase-dependent manner. Notably, MRLB-223 mediates p53-independent cell death in Bcr-Abl-expressing myeloid cells and shows efficacy in animal models of Eμ-myc lymphoma. This compound is valuable for research focusing on the mechanisms of lymphomagenesis and therapeutic strategies for Eμ-myc lymphoma. -
HDAC Inhibitor
HDAC-IN-37 is a potent inhibitor of histone deacetylases (HDACs), demonstrating IC50 values of 0.0551 μM for HDAC1, 1.24 μM for HDAC3, 0.948 μM for HDAC8, and 34.2 μM for HDAC6. This compound effectively increases histone acetylation through a slow-off binding mechanism. Additionally, HDAC-IN-37 disrupts the transition from the G1 phase to the S phase of the cell cycle and promotes early apoptosis in various cell types, making it a valuable tool for research in cancer biology and therapeutic development. -
c-Met/HDAC Inhibitor
c-Met/HDAC-IN-3 is a dual inhibitor targeting c-Met and histone deacetylase 1 (HDAC1), exhibiting IC50 values of 12.50 nM and 26.97 nM, respectively. This compound demonstrates significant biological activity by inducing apoptosis and causing cell cycle arrest at the G2/M phase. c-Met/HDAC-IN-3 serves as a valuable tool for research in cancer biology and therapeutic development, particularly in studies focused on synergistic inhibition of oncogenic pathways.
