Chromatin/Epigenetic Epigenetic Reader Domain (+)-JQ-1


Catalog No. T2110   CAS 1268524-70-4
Synonyms: JQ1

(+)-JQ1 is a BET bromodomain inhibitor (IC50: 77 nM/33 nM for BRD4 (1/2)).

(+)-JQ-1, CAS 1268524-70-4
Pack Size Availability Price/USD Quantity
2 mg In stock 40.00
5 mg In stock 56.00
10 mg In stock 80.00
25 mg In stock 118.00
50 mg In stock 165.00
100 mg In stock 230.00
1 mL * 10 mM (in DMSO) In stock 56.00
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Biological Description
Chemical Properties
Storage & Solubility Information
Description (+)-JQ1 is a BET bromodomain inhibitor (IC50: 77 nM/33 nM for BRD4 (1/2)).
Targets&IC50 BRD4 (1) : ic50 77nM,   BRD4 (2) : ic50 33nM,  
In vitro Binding of a tetra-acetylated Histone H4 peptide to BRD4 was strongly inhibited by (+)-JQ1, with IC50 values of 77 nM and 33 nM for the first and second bromodomain, respectively. Compared to vehicle control, JQ1 (500 nM) markedly accelerated time to half fluorescence recovery in photobleached regions of cells transfected with GFP-BRD4-NUT. Treatment of the patient-derived 797 NMC cell line for 48 hours with JQ1 (500 nM) effaces nuclear foci, producing diffuse nuclear NUT staining by IHC [1]. MM cell proliferation was uniformly inhibited by JQ1, including several MM cell lines selected for resistance to FDA-approved agents (dexamethasone-resistant MM.1R and melaphalan-resistant LR5) [2].
In vivo A marked reduction in 18F-fluorodeoxyglucose (FDG) uptake was observed with JQ1 treatment (50 mg/kg), whereas vehicle-treated animals demonstrated progressive disease. A reduction in tumor growth with JQ1 treatment [1]. Treatment of mice with JQ1 reduced seminiferous tubule area, testis size, and spermatozoa number and motility without affecting hormone levels. Although JQ1-treated males mate normally, inhibitory effects of JQ1 evident at the spermatocyte and round spermatid stages cause a complete and reversible contraceptive effect [3]. Raji BL tumors grew significantly slower in (+)-JQ1-treated (twice a day at 30 mg/kg or once a day at 50 mg/kg, i.p.) mice compared with vehicle-treated controls. In this model, the average tumor volume was 45% smaller in the compound-treated group at day 14 [4].
Cell Research
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). (Only for Reference)
Cell lines: MC 11060 cells
Animal Research
Animal Model: Mice bearing NMC 797 xenografts
Synonyms JQ1
Purity 99.97%
Molecular Weight 456.99
Formula C23H25ClN4O2S
CAS No. 1268524-70-4


0-4℃ for short term (days to weeks), or -20℃ for long term (months).

Solubility Information

DMSO: 45.7 mg/mL (100 mM)

Ethanol: 45.7 mg/mL (100 mM)

( < 1 mg/ml refers to the product slightly soluble or insoluble )


References and Literature
1. Filippakopoulos P, et al. Selective inhibition of BET bromodomains. Nature. 2010 Dec 23;468(7327):1067-73. 2. Delmore JE, et al. BET bromodomain inhibition as a therapeutic strategy to target c-Myc. Cell. 2011 Sep 16;146(6):904-17. 3. Matzuk MM, et al. Small-molecule inhibition of BRDT for male contraception. Cell. 2012 Aug 17;150(4):673-84. 4. Mertz JA, et al. Targeting MYC dependence in cancer by inhibiting BET bromodomains. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16669-74. 5. Wang M, Zhao L, Tong D, et al. BET bromodomain inhibitor JQ1 promotes immunogenic cell death in tongue squamous cell carcinoma[J]. International Immunopharmacology. 2019, 76: 105921.

Related compound libraries

This product is contained In the following compound libraries:
Bioactive Compound Library Inhibitor Library Anti-cancer Compound Library Clinical Compound Library Autophagy Compound Library Epigenetics Compound Library Anti-cancer Clinical Compound Library Preclinical Compound Library Histone Modification Research Compound Library

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