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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). Induces squamous differentiation in NUT midline carcinoma (NMC) cell lines; inhibits tumor growth in NMC xenograft models in vivo. Exhibits reversible contraceptive effects in germ cells from male mice.
Inactive Analog also available.
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.
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.
|Storage||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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 456.99. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.19 mL||10.94 mL||21.88 mL|
|5 mM||0.44 mL||2.19 mL||4.38 mL|
|10 mM||0.22 mL||1.09 mL||2.19 mL|
|50 mM||0.04 mL||0.22 mL||0.44 mL|
References are publications that support the biological activity of the product.
Filippakopoulos et al (2010) Selective inhibition of BET bromodomains. Nature 468 1067 PMID: 20871596
Herrmann et al (2012) Small-molecule inhibition of BRD4 as a new potent approach to eliminate leukemic stem- and progenitor cells in acute myeloid leukemia AML. Oncotarget. [Epub ahead of print] 3 1588 PMID: 23249862
Matzuk et al (2012) Small-molecule inhibition of BRDT for male contraception. Cell 150 673 PMID: 22901802
If you know of a relevant reference for (+)-JQ1, please let us know.
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Keywords: (+)-JQ1, (+)-JQ1 supplier, BET, bromodomains, inhibitors, inhibits, potent, selective, high, affinity, NUT, midline, carcinomas, antitumor, male, contraceptive, BRD2, BRD3, BRD4, BRDT, sgc, Bromodomains, 4499, Tocris Bioscience
12 Citations for (+)-JQ1
Citations are publications that use Tocris products. Selected citations for (+)-JQ1 include:
Sakaguchi (2018) Bromodomain protein BRD4 inhibitor JQ1 regulates potential prognostic molecules in advanced renal cell carcinoma. Oncotarget 9 23003 PMID: 29796168
Lin et al (2019) Super-Enhancer-Associated LncRNA UCA1 Interacts Directly with AMOT to Activate YAP Target Genes in Epithelial Ovarian Cancer. iScience 17 242 PMID: 31307004
Sartor et al (2015) Epigenetic Readers of Lysine Acetylation Regulate Cocaine-Induced Plasticity. J Neurosci 35 15062 PMID: 26558777
Noblejas-Lopez et al (2019) Activity of BET-proteolysis targeting chimeric (PROTAC) compounds in triple negative breast cancer. J Exp Clin Cancer Res 38 383 PMID: 31470872
Andrieu et al (2019) BET protein targeting suppresses the PD-1/PD-L1 pathway in triple-negative breast cancer and elicits anti-tumor immune response. Cancer Lett 465 45 PMID: 31473251
Chen (2017) VEGF amplifies transcription through ETS1 acetylation to enable angiogenesis. Nat Commun 8 383 PMID: 28851877
Perry et al (2015) BET bromodomains regulate transforming growth factor-β-induced proliferation and cytokine release in asthmatic airway smooth muscle. Nat Commun 290 9111 PMID: 25697361
Georgilis et al (2018) PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells. Cancer Cell 34 85 PMID: 29990503
Xie et al (2018) IRE1α RNase-dependent lipid homeostasis promotes survival in Myc-transformed cancers. J Clin Invest 128 1300 PMID: 29381485
Jang et al (2017) AMPK-ULK1-Mediated Autophagy Confers Resistance to BET Inhibitor JQ1 in Acute Myeloid Leukemia Stem Cells. Clin Cancer Res 23 2781 PMID: 27864418
Shao et al (2016) Reprogramming by De-bookmarking the Somatic Transcriptional Program through Targeting of BET Bromodomains. Cell Rep 16 3138 PMID: 27653680
Kato et al (2016) MYCL is a target of a BET bromodomain inhibitor, JQ1, on growth suppression efficacy in small cell lung cancer cells. Oncotarget 7 77378 PMID: 27764802
Do you know of a great paper that uses (+)-JQ1 from Tocris? Please let us know.
Reviews for (+)-JQ1
Average Rating: 5 (Based on 2 Reviews.)
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JQ1 (1 μM)
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Epigenetics Scientific Review
Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.
Epigenetics Research Bulletin
Produced by Tocris and updated in 2014, the epigenetics research bulletin gives an introduction into mechanisms of epigenetic regulation, and highlights key Tocris products for epigenetics targets including:
- DNA Methyltransferases
- Histone Deacetylases
- Histone Demethylases
- Histone Methyltransferases
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.