Other
CN
EU
USA
Description: (+)-JQ1 is a novel, potent and highly specific BET (Bromodomain and extra terminal domain) bromodomain inhibitor, with IC50 of 77 nM and 33 nM for BRD4(1/2) in enzymatic assays. It has high specificity for BET in that it only binds to bromodomains of the BET family, but not to any bromodomains of non-BET family. (+)-JQ1 has potential antineoplastic activity against various cancers such as MM (Multiple myeloma), pancreatic ductal adenocarcinoma and ovarian cancer etc. Its mechanism of action is to inhibit c-MYC and upregulate p21. (+)-JQ1 has been used as a chemical probe to investigate the role of BET bromodomains in the transcriptional regulation of oncogenesis.
References: Nature. 2010 Dec 23;468(7327):1067-73; Cell. 2011 Sep 16;146(6):904-17; Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74.
Related CAS: 1268524-71-5 [(-)-JQ-1]; 202592-23-2 [(+)-JQ1 carboxylic acid]; 2115701-93-2 [(+)-JQ1 PA];
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
In vitro activity: (+)-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.
Kinase Assay: (+)-JQ1 is a potent and highly specific BET (Bromodomain and extra terminal domain) bromodomain inhibitor, with IC50 of 77 nM and 33 nM for BRD4(1/2) in enzymatic assays.
Cell Assay: Cells are seeded into white, 384-well microtiter plates at 500 cells per well in a total volume of 50 μL media. The 797, TT and TE10 cells are grown in DMEM containing 1% penicillin/streptomycin and 10% FBS. The Per403 cells are grown in DMEM containing 1 % penicillin/streptomycin and 20% FBS. Patient-derived NMC 11060 cells are grown in RPMI with 10% FBS and 1% penicillin/streptomycin. (+)-JQ1 is delivered to microtiter assay plates by robotic pin transfer. Following a 48 hours incubation at 37℃, cells are lysed and wells are assessed for total ATP content using a commercial proliferation assay. Replicate measurements are analyzed with respect to dose and estimates of IC50 are calculated by logistic regression (GraphPad Prism).
Lot#: V041101, Purity ≥98%
COA
MSDS
NMR
HPLC
Lot#: V041102, Purity ≥98%
Lot#: V041103, Purity ≥98%
Lot#: V041104, Purity ≥98%
Leukemia and lymphoma cell lines are broadly sensitive to BET-bromodomain inhibition. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74.
Gene expression profiling of LP-1 and Raji cells treated with active or inactive BET inhibitors. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74.
Small molecule BET-bromodomain inhibition suppresses MYC transcription. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74.
MYC reconstitution significantly protects cells from BET-mediated effects. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74.
BET-bromodomain inhibition decreases tumor load in vivo. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74.
Integrated genomic rationale for BET bromodomains as therapeutic targets in MM. Cell. 2011 Sep 16;146(6):904-17.
Inhibition of Myc-dependent transcription by the JQ1 BET bromodomain inhibitor. Cell. 2011 Sep 16;146(6):904-17.
BET inhibition suppresses MYC transcription in MM. Cell. 2011 Sep 16;146(6):904-17.
Regulation of MYC transcription by BET bromodomains. Cell. 2011 Sep 16;146(6):904-17.
Anti-myeloma activity of JQ1 in vitro. Cell. 2011 Sep 16;146(6):904-17.
JQ1 induces cell cycle arrest and cellular senescence in MM cells. Cell. 2011 Sep 16;146(6):904-17.
Translational implications of BET bromodomain inhibition in MM. Cell. 2011 Sep 16;146(6):904-17.