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Signaling Pathway



(JQ-1; JQ1)


(+)-JQ-1 Chemical Structure

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

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Product name: (+)-JQ-1
Cat. No.: HY-13030

(+)-JQ-1 Data Sheet

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    Purity: 99.78% ee.:97.57%

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Related Compound Libraries

Biological Activity of (+)-JQ-1

(+)-JQ1 is a BET bromodomain inhibitor, with IC50 of 77 nM/33 nM for BRD4(1/2).
IC50 Value: 77 nM(for BRD4(1)); 33 nM( for BRD4(2))
Target: BRD4
in vitro: (+)-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.
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.

Protocol (Extracted from published papers and Only for reference)


Chemical Information

M.Wt 456.99 Storage Please store the product under the recommended conditions in the Certificate of Analysis.
Formula C₂₃H₂₅ClN₄O₂S
CAS No 1268524-70-4
Solvent & Solubility

DMSO: ≥ 45 mg/mL

Preparing Stock Solutions

1 mg 5 mg 10 mg
1 mM 2.1882 mL 10.9412 mL 21.8823 mL
5 mM 0.4376 mL 2.1882 mL 4.3765 mL
10 mM 0.2188 mL 1.0941 mL 2.1882 mL

References on (+)-JQ-1

[1]. Selective inhibition of BET bromodomains By Filippakopoulos, Panagis; Qi, Jun; Picaud, Sarah; Shen, Yao; Smith, William B.; Fedorov, Oleg; Morse, Elizabeth M.; Keates, Tracey; Hickman, Tyler T.; Felletar, Ildiko; et al From Nature. 2010 Dec 23;468(7327):1067-73. Epub 2010 Sep 24.
Epigenetic proteins are intently pursued targets in ligand discovery. So far, successful efforts have been limited to chromatin modifying enzymes, or so-called epigenetic 'writers' and 'erasers'. Potent inhibitors of histone binding modules have not yet been described. Here we report a cell-permeable small molecule (JQ1) that binds competitively to acetyl-lysine recognition motifs, or bromodomains. High potency and specificity towards a subset of human bromodomains is explained by co-crystal structures with bromodomain and extra-terminal (BET) family member BRD4, revealing excellent shape complementarity with the acetyl-lysine binding cavity. Recurrent translocation of BRD4 is observed in a genetically-defined, incurable subtype of human squamous carcinoma. Competitive binding by JQ1 displaces the BRD4 fusion oncoprotein from chromatin, prompting squamous differentiation and specific antiproliferative effects in BRD4-dependent cell lines and patient-derived xenograft models. ...

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