bet in 2

BET-IN-2 is a BET inhibitor with an IC50 of 52 nM for BRD4-BD1.

BET bromodomain inhibitor 2 is a potent inhibitor of the BET-type bromodomain with an IC50 of 14.1 μM.

PROTAC BET-binding moiety 2 is an inhibitor of the BET bromodomain.

BET BD2-IN-1 (compound 45) is a potent and selective BET BD2 inhibitor with an IC50 value of 1.6 nM. It suppresses Th17 cell differentiation by reducing the activation of STAT3 and NF-κB, making it relevant for psoriasis and inflammatory bowel disease (IBD) research [1].

PROTAC BET degrader-2 is a highly potent degrader of Bromodomain and Extra-Terminal (BET) proteins, with an IC50 of 9.6 nM.

ARV-771 is a potent BET degrader based on PROTAC technology, with Kds of 34 nM for BRD2(1), 4.7 nM for BRD2(2), 8.3 nM for BRD3(1), 7.6 nM for BRD3(2), 9.6 nM for BRD4(1), and 7.6 nM for BRD4(2), respectively[1].

CF53 is a highly potent, selective, and orally active inhibitor of BET protein, with a Ki of <1 nM, Kd of 2.2 nM, and an IC50 of 2 nM for BRD4 BD1. CF53 binds to both the BD1 and BD2 domains of BRD2, BRD3, BRD4, and BRDT BET proteins with high affinities, being very selective over non-BET bromodomain-containing proteins. CF53 exhibits potent anti-tumor activity both in vitro and in vivo.

Ethyl Caffeate (ETHYL 3,4-DIHYDROXYCINNAMATE) suppressed the differentiation of naive CD4+ T cells into Th1 in vitro. Furthermore, Ethyl Caffeate intensely blocked the transcriptional expression in interferon-γ-related signaling, including IFN-γ, T-bet, STAT1, and STAT4.

(S,R,S)-AHPC-Me hydrochloride (VHL ligand 2 hydrochloride) is utilized in the synthesis of ARV-771, a potent BET protein degrader. It selectively degrades BET protein in castration-resistant cells with a DC50 <1 nM. Recognized as VHL ligand 2 hydrochloride, it serves as the VHL ligand from (S,R,S)-AHPC for recruiting von Hippel-Lindau (VHL) protein.

(R)-(-)-JQ1 Enantiomer is the stereoisomer of (+)-JQ1, a BET bromodomain inhibitor, which acts on BRD4(1 2) with IC50 values of 77 nM and 33 nM in a cell-free assay.

(S,R,S)-AHPC-Me (E3 ligase Ligand 1A) (VHL ligand 2) is an (S,R,S)-AHPC-based VHL ligand used to recruit the von Hippel-Lindau (VHL) protein. It is utilized in the synthesis of ARV-771, a VHL E3 ligase-based BET PROTAC degrader that effectively degrades BET proteins in castration-resistant prostate cancer (CRPC) cells with a DC50 <1 nM.

AZD5153 6-Hydroxy-2-naphthoic acid (AZD5153) is a potent triazolopyridazine-based Bromodomain (BRD4) and Extraterminal (BET) inhibitor utilized in cancer treatments.

Jaceosidin has anti-oxidative activity. Jaceosidin has anti-inflammatory activity, also a microglial inhibitor with anti-neuroinflammation activity. aceosidin has anticancer activity, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cd

(S,R,S)-AHPC-Me dihydrochloride, also known as VHL ligand 2 dihydrochloride, is a chemical compound used in the synthesis of ARV-771. ARV-771 is a BET PROTAC degrader that relies on von Hippel-Landau (VHL) E3 ligase and exhibits potent degradation of BET proteins in castration-resistant prostate cancer (CRPC) cells, with a DC50 of less than 1 nM. This compound acts as the VHL ligand, specifically the (S,R,S)-AHPC-based VHL ligand, facilitating the recruitment of von Hippel-Lindau (VHL) protein.

JQ1-TCO (JQ1-trans-cyclooctene), a derivative of the BET inhibitor JQ1, is designed for click chemistry applications, enabling its use as molecular probes both in vitro and in vivo [1] [2].

TW9 is a dual inhibitor of bromodomain 2 (BD2) in bromodomain-containing protein 4 (BRD4) and histone deacetylase 1 (HDAC1; IC50s = 0.074 and 0.29 μM, respectively).1It is selective for BD2 over BD1 in BRD4 (IC50= 0.72 μM) and for HDAC1 over HDAC2 (IC50= 2.5 μM). TW9 (50 nM) induces apoptosis in, and inhibits proliferation of, MIA PaCa-2 pancreatic cancer cells. It induces cell cycle arrest at the G1phase in HPAC pancreatic cancer cells when used at a concentration of 2 μM. TW9 acts synergistically with gemcitabine to reduce the viability of HPAC cells. 1.Zhang, X., Zegar, T., Weiser, T., et al.Characterization of a dual BET/HDAC inhibitor for treatment of pancreatic ductal adenocarcinomaInt. J. Cancer147(10)2847-2861(2020)