Molecular Weight(MW): 456.99
(+)-JQ1 is a BET bromodomain inhibitor, with IC50 of 77 nM/33 nM for BRD4(1/2) in cell-free assays, binding to all bromodomains of the BET family, but not to bromodomains outside the BET family.
Cited by 11 Publications
7 Customer Reviews
The BET protein inhibitor JQ1 reduces c-Myc expression and attenuates primary MCC cell proliferation. A, decreased c-Myc expression in MCC-3 and MCC-5 treated with JQ1 (800 nmol/L) for 72 hours by qRT-PCR and immunoblotting. The mRNA expression of target genes was normalized to that of MRPS2 and a value of 1.0 was assigned to the mRNA expression of target genes in the control group (means+SEM; **, P < 0.01 vs. control); b-actin was used as a loading control for immunoblotting.
Cancer Res 2014 74(23), 7090-102. (+)-JQ1 purchased from Selleck.
Immunohistochemical staining of xenograft tumor tissues. Immunohistochemical staining of xenograft tumor tissues with the indicated antibodies. p21-, p27-, p57-, and Ki67 positive cells (brown staining) were quantified at x400 magnification (meansSEM;**, P < 0.01;***, P < 0.001 vs. control); scale bars, 10 um.
Cancer Res 2014 74(23), 7090-102. (+)-JQ1 purchased from Selleck.
(D) Effect of JQ1 on alterations of actin cytoskeleton in VEGF-induced HUVECs. The cells were pretreated with DMSO or JQ1 (100 nM) for 6 h, and stimulated with VEGF (10 ng/mL) for 12 h. F-actin (red) and nuclei (blue) were stained with phalloidin and DAPI, respectively. Representative images from 3 independent experiments.
Sci Rep, 2016, 6:23770.. (+)-JQ1 purchased from Selleck.
B. Repressed MCC-3 xenograft tumor growth upon combined treatment with MLN0128 and JQ1. Tumor bearing mice were treated with MLN0128 or vehicle at 1 mg/kg/day by oral gavage and JQ1 or vehicle at 50 mg/kg/day by i.p. injection for a period of 30 days. C. A more effective reduction of MCC-3 xenograft tumor growth in the group treated with combined therapy. Fold-reduction of tumor growth was calculated as average tumor growth of control group divided by average tumor growth of treatment group. Tumor growth was calculated as final average tumor volume minus initial average tumor volume in each group.
Oncotarget, 2016, 7(6):6576-92.. (+)-JQ1 purchased from Selleck.
JQ1 induces cell cycle arrest and apoptosis in Cal27 cells. (C) Cal27 cells were treated with JQ1 for 24 h and whole cell lysates were tested by western blot assays for the expression of cleaved-caspase-3. GAPDH was used as a loading control. (D) Apoptosis of Cal27 cells treated with JQ1 at 0 and 0.5 µM JQ1; *P<0.05 vs. control (the DMSO group)
Oncol Rep, 2016, 36(4):1989-96.. (+)-JQ1 purchased from Selleck.
Effect of BET domain family inhibition on AMI damage in cardiomyocytes. (A) LDH and (B) CK-MB activity in the serum. #P<0.01 vs. sham group; @P<0.05 and &P<0.01 vs. AMI group. BET, bromodomain and extra-terminal; AMI, acute myocardial infarction; LDH, lactate dehydrogenase; CK-MB, creatine kinase MB isoenzyme.
Exp Ther Med, 2015, 10(6):2319-2324.. (+)-JQ1 purchased from Selleck.
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Choose Selective Epigenetic Reader Domain Inhibitors
|Description||(+)-JQ1 is a BET bromodomain inhibitor, with IC50 of 77 nM/33 nM for BRD4(1/2) in cell-free assays, binding to all bromodomains of the BET family, but not to bromodomains outside the BET family.|
|Features||(+)-JQ1 is more effective than (-)-JQ1.|
(+)-JQ1 enantiomer binds directly into the Kac binding site of BET bromodomains. (+)-JQ1 (500 nM) binds BRD4 competitively with chromatin resulting in differentiation and growth arrest of NMC cells. (+)-JQ1 (500 nM) attenuates rapid proliferation of NMC 797 and Per403 cell lines as demonstrated by reduced Ki67 staining. (+)-JQ1 (500 nM) potently decreases expression of both BRD4 target genes in NMC 797 cells. (+)-JQ1 inhibits cellular viability with IC50 of 4 nM in NMC 11060 cells.  (+)-JQ1 results in robust inhibition of MYC expression in MM cell lines. (+)-JQ1 inhibits proliferating of KMS-34 and LR5 with IC50 of 68 nM and 98 nM, respectively. (+)-JQ1 (500 nM)-treated MM.1S cells results in a pronounced decrease in the proportion of cells in S-phase, with a concomitant increase in cells arrested in G0/G1. (+)-JQ1 (500 nM) results in pronounced cellular senescence by beta-galactosidase staining. (+)-JQ1 (800 nM) exposure leads to a significant reduction in cell viability among the majority of CD138+ patient-derived MM samples tested.  (+)-JQ1 inhibits growth of LP-1 cells with GI50 of 98 nM. (+)-JQ1 (625 nM) results in an increase in the percentage of LP-1 cells in G0/G1. (+)-JQ1 (500 nM) suppresses the expression of MYC, BRD4 and CDK9 in LP-1 cells.  (+)-JQ1 (1 μM) activates HIV transcription in latently infected Jurkat T cells. (+)-JQ1 (50 μM) stimulates predominantly Tat-dependent HIV transcription in both Jurkat and HeLa cells. (+)-JQ1 (5 μM) induces Brd4 dissociation enables Tat to recruit SEC to HIV promoter and induce Pol II CTD phosphorylation and viral transcription in J-Lat A2 cells. JQ1 enables Tat to increase CDK9 T-loop phosphorylation and partially dissociates P-TEFb from 7SK snRNP in Jurkat T cells. 
|In vivo||(+)-JQ1 (50 mg/kg) inhibits tumors growth in mice with NMC 797 xenografts. (+)-JQ1 (50 mg/kg) results in effacement of NUT nuclear speckles in mice with NMC 797 xenografts, consistent with competitive binding to nuclear chromatin. (+)-JQ1 (50 mg/kg) induces strong (grade 31) keratin expression in NMC 797 xenografts. (+)-JQ1 (50 mg/kg) promotes differentiation, tumor regression and prolonged survival in mice models of NMC xenografts.  (+)-JQ1 (50 mg/kg) results in a significant prolongation in overall survival of SCID-beige mice orthotopically xenografted after intravenous injection with MM.1S-luc+ cells compared to vehicle-treated animals.  (+)-JQ1 (50 mg/kg i.p.) leads to a highly significant increase in survival of mice bearing Raji xenografts. |
|In vitro||DMSO||91 mg/mL warmed (199.12 mM)|
|Ethanol||91 mg/mL (199.12 mM)|
|Water||slightly soluble or insoluble|
|In vivo||Add solvents individually and in order:
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
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