jq1

(+)-JQ-1 (JQ1) is a BET bromine domain inhibitor that inhibits BRD4 (1/2) (IC50=77/33 nM) with specificity and reversibility. (+)-JQ-1 induces cell autophagy and inhibits cell proliferation.

β-NF-JQ1 is a PROTAC that recruits aryl hydrocarbon receptor E3 (AhR E3) ligase to target proteins. β-NF-JQ1 uses β-NF as an AhR ligand to target bromodomain (BRD)-containing proteins and induce AhR and BRD protein interactions. β-NF-JQ1 shows potent anticancer activity associated with protein knockdown activity. .

(+)-JQ-1 carboxylic acid is a potent bromodomain and extra terminal domain (BET) inhibitor. (+)-JQ-1 carboxylic has potential to be used as a precursor to synthesize PROTACs and other conjugates.

KB02-JQ1 is a potent and specific proteolysis targeting chimera (PROTAC) that specifically degrades BRD4, acting as a molecular glue. It does not degrade BRD2 or BRD3. The mechanism of action involves covalent modification of the E3 ligase DCAF16, thereby promoting BRD4 degradation. Importantly, KB02-JQ1 demonstrates enhanced stability and durability in facilitating protein degradation within biological systems. The compound forms a complex with the ubiquitin E3 ligase ligand KB02 through a linker, resulting in the formation of KB02-JQ1[1].

(+)-JQ1 maleimide, featuring a cysteine-reactive maleimide linked to the BRD4 ligand, JQ1, via a PEG2 linker, serves as a probe suitable for the COFFEE method (COvalent Functionalization Followed by E3 Electroporation). This approach facilitates the covalent attachment of (+)-JQ1 maleimide to VHL, followed by electroporation into live cells, where the E3 ligase complexes with intracellular BRD4 to prompt its degradation.

JQ-1 (carboxylic acid) is a cell-permeable BRD4 inhibitor with IC50s of 77 nM for BRD4(1) and 33 nM for BRD4(2)

β-Naphthoflavone-CH2-OH (β-NF-CH2-OH) serves as an AhR E3 ligase ligand, forming chimeric molecules when connected to a protein ligand through a linker, resulting in PROTACs or SNIPERs (e.g., β-naphthoflavone-JQ1). These chimeric molecules recruit the AhR E3 ligase complex by incorporating AhR ligands. By inducing ubiquitination-mediated degradation, PROTACs effectively target and degrade cancer-promoting proteins [1].

NH2-PEG3 (PROTAC Linker 35) is a polyethylene glycol (PEG) linker utilized in the synthesis of PROTAC (β-NF-JQ1)[1].

KB02-COOH is a synthetic fragment derived from ubiquitin E3 ligase ligand KB02, which possesses potential utility in the synthesis of PROTAC compounds. Notably, KB02-COOH can be employed in the generation of PROTAC constructs like KB02-JQ1 and KB02-SLF.

TD-428 is a highly specific degrader of BRD4(DC50 of 0.32 nM). TD-428 is a BET PROTAC, which comprises TD-106 (a CRBN ligand) linked to JQ1 (a BET inhibitor). TD-428 efficiently induce BET protein degradation.

VH032 thiol (VHL ligand 6) is a VHL ligand that interacts with pan-BET inhibitor JQ1 through a linker to create a PROTAC[1] compound.

BI01826025 (pArg-JQ1), a PROTAC degrader targeting the bromodomain 1 of BRDT (BRDT BD1), proves useful in exploring the regulatory impact of ClpC2 on the ClpC1P1P2 protease complex [1].

β-Naphthoflavone-CH2-Br is an arylhydrocarbon receptor (AhR) ligand. β-Naphthoflavone-CH2-Br used to synthesize the PROTAC β-NF-JQ1.

SRG-II-19F (dCym-JQ1), a BRDT BD1 (bromodomain1 of BRDT) degrader, is utilized to examine the regulatory influence of ClpC2 on the ClpC1P1P2 protease [1].

dBET1 is a hybrid molecule that combines (+)-JQ1 and thalidomide. It induces cereblon-dependent BET protein degradation in vitro (EC50: 430 nM) and induces apoptosis.