Catalog # Availability Size / Price Qty
(+)-JQ1 | CAS No. 1268524-70-4 | Bromodomain Inhibitors
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Description: Potent and selective BET bromodomain inhibitor; cell permeable

Chemical Name: (6S)-4-(4-Chlorophenyl)-2,3,9-trimethyl-6H-thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine-6-acetic acid 1,1-dimethylethyl ester

Purity: ≥98%

Product Details
Citations (12)

Biological Activity

(+)-JQ1 is a potent, high affinity, selective BET bromodomain inhibitor (IC50 values are 17.7, 32.6, 76.9 and 12942 nM for BRD2 (N-terminal (N)), BRD4 (C-terminal (C)), BRD4 (N) and CREBBP respectively; Kd values are 49, 59.5, 82, 90.1, 128 and 190 nM for BRD4 (N), BRD3 (N), BRD3 (C), BRD4 (C), BRD2 (N) and BRDT (N) respectively). (+)-JQ1 induces squamous differentiation in NUT midline carcinoma (NMC) cell lines and inhibits tumor growth in NMC xenograft models in vivo. (+)-JQ1 inhibits proliferation and induces autophagy in bladder cancer cells in vitro and in vivo. It also suppresses MYC gene expression and inhibits proliferation of lymphoma and leukemia cell lines. In human pulmonary microvasular endothelial cells (HPMEC), NF-κB activation, IL-6 and IL-8 expression and proliferation are inhibited by (+)-JQ1. The compound also inhibits transcription of ACE2 and TMPRSS2 genes in mouse lung tissue and prevents infection by SARS-CoV-2. In germ cells from male mice, (+)-JQ1 exhibits reversible contraceptive effects. (+)-JQ1 inhibits the BRD4-JUN-CCL2-TNF-α axis in pancreatic cancer cells and improves survival by reducing macrophage recruitment.

Inactive Analog also available.

Carboxylic acid-functionalized (Cat. No. 6588) and click-activated (alkyne) (Cat. No. 6589) versions for PROTAC development also available.

External Portal Information

Chemicalprobes.org is a portal that offers independent guidance on the selection and/or application of small molecules for research. The use of (+)-JQ1 is reviewed on the chemical probes website.

Technical Data

Soluble to 100 mM in DMSO and to 100 mM in ethanol
Store at -20°C

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.

Additional Information

Licensing Caveats:
This probe is supplied in conjunction with the Structural Genomics Consortium. For further characterization details, please visit the (+)-JQ1 probe summary on the SGC website.
Other Product-Specific Information:

Background References

  1. Targeting MYC dependence in cancer by inhibiting BET bromodomains.
    Mertz JA, Conery AR, Bryant BM et al.
    Proc Natl Acad Sci U S A
  2. Selective inhibition of BET bromodomains.
    Filippakopoulos et al.
    Nature, 2010;468:1067
  3. Small-molecule inhibition of BRD4 as a new potent approach to eliminate leukemic stem- and progenitor cells in acute myeloid leukemia AML.
    Herrmann et al.
    Oncotarget. [Epub ahead of print], 2012;3:1588
  4. Small-molecule inhibition of BRDT for male contraception.
    Matzuk et al.
    Cell, 2012;150:673

Product Datasheets

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Citations for (+)-JQ1

The citations listed below are publications that use Tocris products. Selected citations for (+)-JQ1 include:

12 Citations: Showing 1 - 10

  1. BET protein targeting suppresses the PD-1/PD-L1 pathway in triple-negative breast cancer and elicits anti-tumor immune response.
    Authors: Andrieu Et al.
    Cancer Lett  2019;465:45
  2. Activity of BET-proteolysis targeting chimeric (PROTAC) compounds in triple negative breast cancer.
    Authors: Noblejas-Lopez Et al.
    J Exp Clin Cancer Res  2019;38:383
  3. Super-Enhancer-Associated LncRNA UCA1 Interacts Directly with AMOT to Activate YAP Target Genes in Epithelial Ovarian Cancer.
    Authors: Lin Et al.
    iScience  2019;17:242
  4. Bromodomain protein BRD4 inhibitor JQ1 regulates potential prognostic molecules in advanced renal cell carcinoma.
    Authors: Sakaguchi
    Oncotarget  2018;9(33):23003
  5. PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells.
    Authors: Georgilis Et al.
    Cancer Cell  2018;34:85
  6. IRE1α RNase-dependent lipid homeostasis promotes survival in Myc-transformed cancers.
    Authors: Xie Et al.
    J Clin Invest  2018;128:1300
  7. VEGF amplifies transcription through ETS1 acetylation to enable angiogenesis.
    Authors: Chen
    Nat Commun  2017;8(1):383
  8. AMPK-ULK1-Mediated Autophagy Confers Resistance to BET Inhibitor JQ1 in Acute Myeloid Leukemia Stem Cells.
    Authors: Jang Et al.
    Clin Cancer Res  2017;23:2781
  9. MYCL is a target of a BET bromodomain inhibitor, JQ1, on growth suppression efficacy in small cell lung cancer cells.
    Authors: Kato Et al.
    Oncotarget  2016;7:77378
  10. Reprogramming by De-bookmarking the Somatic Transcriptional Program through Targeting of BET Bromodomains.
    Authors: Shao Et al.
    Cell Rep  2016;16:3138


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