Bromodomain Inhibitor, (+)-JQ1
|BET bromodomain inhibitor|
we offer trial solution enough for 3-5 experiments.
Quality Control & MSDS
- View current batch:
|IC50||77 nM/33 nM|
|Cas No.||1268524-70-4||SDF||Download SDF|
|Chemical Name||Bromodomain Inhibitor, (+)-JQ1|
|Solubility||Soluble in DMSO||Storage||Store at -20°C|
View Related Products By Research Topics
JQ1 induces 3/7-mediated apoptosis and DNA damage response in p53-wild-type (OCI)-AML3 cell lines where it possibly sensitizes AML cells to p53-mediated cell death. A mechanism has been proposed that JQ1 is activated in OCI-AML3 cells preventing BRD4-mediated recruitment of p53 to chromatin targets and eventually leading to cell cycle arrest and apoptosis in a c-MYC-independent manner.
The affinities of acetylated histone tails and JQ1 to ten different BRD4 BD1 mutants were analyzed by several complementary biochemical and biophysical methods, in which W81, Y97, N140 and M149 play similarly important roles in the recognition of both.
JQ1, an inhibitor of MYC expression, exhibits different inhibition in tumor cells where it decreased ~90% MYC transcription in BL cells and exhibited lesser inhibition in several non-BL cells possibly due to requirements of Brd4, transcription factors (such as Gdown1 and MED26) and other unknown cell specific factors.
The critical role of BET proteins in macrophage inflammatory responses has been demonstrated in studies using small interfering RNA knockdown and JQ1 where Brad2 and brd4 doesn’t physically associated with the promoters of inflammatory cytokine genes in macrophages following the inhibition of BET by JQ1. JQ1 reduces the production of cytokine in vitro and weakens the “cytokine storm” in endotoxemic mice through decreasing IL-6 and TNF-α levels while rescuing mice from LPS-induced death.
JQ1 dissociates Brd4 from the HIV promoter, synergizes with another latency activator prostratin and activates viral latency without inducing global T cell activation, which allow it and other closely related compounds as well as their antagonization of Brd4 to be used as effective agents/strategies to eliminating latent HIV in further investigations.
Bromodomain Inhibitor, (+)-JQ1 is a potent and highly specific inhibitor for the BET (bromodomain and extra-terminal) family of bromodomains. (+)-JQ1 binds to BRD4 bromodomains 1 and 2 with Kd values of ~ 50 and 90 nM, respectively. The binding is competitive with acetyl lysine. (+)-JQ1 can be a useful chemical probe to investigate the role of BET bromodomains in the transcriptional regulation of oncogenesis.
JQ1 exhibited strong dose-and time- dependent inhibition of BRDT and could significantly diminish the activity of a close structural relative of BRDT. A close look at JQ1 bound BRDT confirmed that the acetyl-lysine recognition site of BRDT was blocked. 
JQ1 does not produce sedative or anxiolytic effects and is instead a potent and selective inhibitor of the bromodomain testis-specific protein BRDT , which is essential for chromatin remodeling during spermatogenesis. By blocking BRDT, JQ1 effectively blocks the production of sperm in the testes and consequently produces effective contraception, without the negative side effects associated with previously researched hormonal contraceptives for men.
1. Matzuk, Martin M., et al. "Small-molecule inhibition of BRDT for male contraception." Cell 150.4 (2012): 673-684. 2. Filippakopoulos, P.; Qi, J.; Picaud, S.; Shen, Y.; Smith, W. B.; Fedorov, O.; Morse, E. M.; Keates, T. et al. (2010). "Selective inhibition of BET bromodomains". Nature 468 (7327): 1067–1073.