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    InvivoChem Cat #: V3676
    CAS #: 1268524-71-5Purity ≥98%

    Description: (-)-JQ-1 is the (R)-Enantiomer of JQ1 or the stereoisomer of (+)-JQ1. While (+)-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. (−)-JQ1 shows no significant interaction with any bromodomain. Besides, (−)-JQ1 enantiomer is comparatively inactive in nuclear protein in testis (NUT) midline carcinoma (NMC). (+)-JQ1 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#:1268524-70-4 [(+)-JQ1]; 2115701-93-2 [(+)-JQ1 PA]; 202592-23-2 [(+)-JQ1 carboxylic acid]; 

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    Molecular Weight (MW)456.99
    CAS No.1268524-71-5 [(-)-JQ-1]; 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 91 mg/mL (199.1 mM)
    Water: <1 mg/mL
    Ethanol:  91 mg/mL (199.1 mM)
    Solubility (In vivo)2% DMSO+30% PEG 300+5% Tween 80+ddH2O: 5 mg/mL
    SynonymsBromodomain Inhibitor; (-)-JQ-1; (1)-JQ1; (1)-JQ 1; (R)-(-)-JQ1 Enantiomer 
    SMILES CodeO=C(C[[email protected]]1N=C(C2=C(N3C1=NN=C3C)SC(C)=C2C)C4=CC=C(C=C4)Cl)OC(C)(C)C
    Chemical Nametert-butyl (R)-2-(4-(4-chlorophenyl)-2,3,9-trimethyl-6H-thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepin-6-yl) acetate

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    In Vitro

    In vitro activity: while (+)-JQ1 enantiomer binds directly into the Kac binding site of BET bromodomains, (−)-JQ1 shows no significant interaction with any bromodomain. Besides, (−)-JQ1 enantiomer is comparatively inactive in nuclear protein in testis (NUT) midline carcinoma (NMC). (+)-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).

    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.
    Animal modelMice bearing NMC 797 xenografts
    Formulation & Dosage1. Dissolved in 5% dextrose; 50 mg/kg; i.p. injection; Nature. 2010 Dec 23;468(7327):1067-73;
    2. Dissolved in 10% DMSO and 90% of a 10% 2-hydroxypropyl-β-cyclodextrin solution; Leukemia. 2017 Oct;31(10):2037-2047.;
    3. Dissolved in 1% DMSO+5% Glucose+ddH2O; Cell. 2018 Sep 20;175(1):186-199.e19.;
    4. Dissolved in 20% hydroxypropyl-β-cyclodextrin, 5% DMSO, 0.2% Tween-80 in saline; Mol Cancer Ther. 2016 Jun;15(6):1217-26.;
    5. Dissolved in 1:1 propylene glycol:water; J Biol Chem. 2016 Nov 4;291(45):23756-23768.;
    6. Dissolved in 5% DMSO in 10% 2-hydroxypropyl-β-cyclodextrin solution; Cancer Lett. 2017 Aug 28;402:100-109.
    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.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Leukemia and lymphoma cell lines are broadly sensitive to BET-bromodomain inhibition.  2011 Oct 4;108(40):16669-74.


    Gene expression profiling of LP-1 and Raji cells treated with active or inactive BET inhibitors.  2011 Oct 4;108(40):16669-74.


    Small molecule BET-bromodomain inhibition suppresses MYC transcription.  2011 Oct 4;108(40):16669-74.


    MYC reconstitution significantly protects cells from BET-mediated effects.  2011 Oct 4;108(40):16669-74.


    BET-bromodomain inhibition decreases tumor load in vivo.  2011 Oct 4;108(40):16669-74.


    Integrated genomic rationale for BET bromodomains as therapeutic targets in MM.  2011 Sep 16;146(6):904-17.


    Inhibition of Myc-dependent transcription by the JQ1 BET bromodomain inhibitor.  2011 Sep 16;146(6):904-17.


    BET inhibition suppresses MYC transcription in MM.  2011 Sep 16;146(6):904-17.


    Regulation of MYC transcription by BET bromodomains.  2011 Sep 16;146(6):904-17.


    Anti-myeloma activity of JQ1 in vitro.  2011 Sep 16;146(6):904-17. 


    JQ1 induces cell cycle arrest and cellular senescence in MM cells.  2011 Sep 16;146(6):904-17.


    Translational implications of BET bromodomain inhibition in MM.  2011 Sep 16;146(6):904-17.


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