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Fig. 1 · Structure
Cat. No.
A12729
CAS No.
1268524-70-4
Formula
C23H25ClN4O2S
Mol. Weight
456.99

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(+)-JQ1

BET Inhibitor

(+)-JQ1 is a potent, high affinity, selective BET bromodomain inhibitor.

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Publications for (+)-JQ1

16 publications citing this product

  1. Yoshimi Yasukawa, .et al. , Cancer Science, 2026, 117(7): 1894-1906 PMID: 42070972
  2. Stephanie Tanis, .et al. , Proc Natl Acad Sci U S A, 2026, Apr 14;123(15):e2517498123 PMID: 41945432
  3. Yuichiro Hara, .et al. , bioRxiv, 2025, Dec 05
  4. Jiang Zhou, .et al. , Neoplasia, 2025, Oct:68:101223 PMID: 40850308
  5. Kei Taga, .et al. , Microbiol Immunol, 2024, Mar;68(3):90-99 PMID: 38244193
  6. Deeksha Sharma, .et al. , Breast Cancer Res, 2023, Nov 15;25(1):144 PMID: 37968653
  7. Adriana K Alexander, .et al. , Nat Commun, 2023, Mar 29;14(1):1753 PMID: 36990976
  8. Haruki Kitamura, .et al. , Biochem Biophys Res Commun, 2023, Jan 22;641:139-147 PMID: 36527748
  9. Gerald Thiel, .et al. , Pharmaceuticals (Basel), 2022, Jul 10;15(7):846 PMID: 35890145
  10. Selase D Deletsu, .et al. , Biochem Biophys Res Commun, 2021, Aug 27;567:106-111 PMID: 34146904
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Biological Activity

Bioactivity / Mechanism

(+)-JQ1 competitively disrupts acetyl-lysine recognition by BET bromodomains. Its BRD4 peptide-displacement activity is stereospecific, and experiments in BRD4-NUT-dependent NMC 797 cells link exposure to differentiation-associated gene expression and G1 arrest. These results describe the active (+) enantiomer rather than racemic JQ1. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Cellular Effect

Cell Line Activity Value Description Reference
697 EC50 0.09 μM Cytotoxicity against human 697 cells assessed as reduction in cell viability after 5 days by CellTiter-Glo assay [PMID: 29170024]
A-375 IC50 7.5 μM Antiproliferative activity against human A375 cells assessed as reduction in cell growth measured after 48 hrs by MTT assay [PMID: 30926312]
A549 IC50 1.67 μM Antiproliferative activity against human A549 cells treated at 12 hrs post cell seeding measured at 72 to 144 hrs post cell seeding by Cell-Titer Glo assay [PMID: 29758518]
A549 IC50 13.1 μM Antiproliferative activity against human A549 cells assessed as reduction in cell growth measured after 48 hrs by MTT assay [PMID: 30926312]
A549 EC50 17 μM Cytotoxicity against human A549 cells assessed as viable cells incubated for 23 hrs by alamar blue assay [PMID: 35007061]
ASPC1 IC50 3.39 μM Antiproliferative activity against human ASPC1 cells assessed as cell growth inhibition incubated for 6 days by MTS assay [PMID: 35500243]
CAPAN-1 IC50 0.45 μM Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 7 days by MTT assay [PMID: 35091172]
CAPAN-1 IC50 0.58 μM Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 5 days by MTT assay [PMID: 35091172]
CAPAN-1 IC50 2.44 μM Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 4 days by MTT assay [PMID: 35091172]
CAPAN-1 IC50 2.44 μM Antiproliferative activity against human CAPAN-1 cells assessed as reduction in cell viability after 4 days by MTT assay [PMID: 34813314]
CAPAN-1 IC50 24.1 μM Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 3 days by MTT assay [PMID: 35091172]
CFPAC-1 IC50 0.35 μM Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 7 days by MTT assay [PMID: 35091172]
CFPAC-1 IC50 1.56 μM Antiproliferative activity against human CFPAC-1 cells assessed as reduction in cell viability after 4 days by MTT assay [PMID: 34813314]
CFPAC-1 IC50 1.56 μM Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 5 days by MTT assay [PMID: 35091172]
CFPAC-1 IC50 1.86 μM Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 4 days by MTT assay [PMID: 35091172]
CFPAC-1 IC50 13.9 μM Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 3 days by MTT assay [PMID: 35091172]
CT26 IC50 28.67 μM Antiproliferative activity against human CT26 cells assessed as inhibition of cell proliferation incubated for 48 hrs by MTT assay [PMID: 33862375]
CWR22R IC50 0.033 μM Antiproliferative activity against human 22Rv1 cells assessed as inhibition of cell growth incubated for 96 to 120 hrs by celltiter glo assay [PMID: 34999525]
CWR22R IC50 0.071 μM Antiproliferative activity against human 22Rv1 cells treated at 12 hrs post cell seeding measured at 72 to 144 hrs post cell seeding by Cell-Titer Glo assay [PMID: 29758518]

19 records · Scroll to view more

In Vitro Studies

Displacement of acetylated histone H4 from BRD4

Biochemical assay · Recombinant human BRD4 first and second bromodomains [1]

The active (+) enantiomer displaced acetylated histone H4 from both BRD4 bromodomains. The inactive enantiomer provided a stereochemical comparison; these assay-specific IC50 values are not cellular treatment concentrations.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
BRD4 first bromodomain / acetylated H4 bindingIC50 77 nM[1]
BRD4 second bromodomain / acetylated H4 bindingIC50 33 nM[1]

Literature-Reported Treatment Conditions

Method
Bead-based luminescence proximity assay using tetra-acetylated histone H4; comparison with (−)-JQ1 and CREBBP. Recombinant protein expression is not a drug-treated cell model.
Reported limits
Detailed assay incubation and buffer conditions in supplementary methods were not retrieved for this batch.
Methods and source locations

Compound reported in the paper: (+)-JQ1

Evidence specifically concerns the (+) enantiomer, not (−)-JQ1 or a racemic product.

A selective and potent inhibitor for the BET sub-family of bromodomains; Figure 1e

BRD4 first bromodomain / acetylated H4 binding: ALPHA-screen peptide-displacement assay — Figure 1e and biochemical Results

BRD4 second bromodomain / acetylated H4 binding: ALPHA-screen peptide-displacement assay — Figure 1e and biochemical Results

Differentiation and cell-cycle responses in NMC 797 cells

Cell-based study · BRD4-NUT-dependent NMC 797 carcinoma cells [1]

(+)-JQ1 induced a squamous differentiation-associated expression pattern and G1 arrest. The matched (−) enantiomer did not reproduce these responses, supporting a stereospecific effect in this BRD4-NUT model.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Keratin-14 expressionReported induction 30-fold[1]
DNA-content distributionQualitative response G1 arrest relative to vehicle and (−)-JQ1[1]

Literature-Reported Treatment Conditions

Treatment concentration
250 nM (+)-JQ1; separate comparator: 250 nM (−)-JQ1
Exposure duration
48 h
Method
RT-PCR and flow cytometry with vehicle and inactive-enantiomer controls. Figure 4f reports mean ± s.d., n = 3; no precision beyond the stated 30-fold induction is inferred.
Reported limits
Vehicle composition for these particular panels is not specified in the reviewed main-text caption.
Methods and source locations

Compound reported in the paper: (+)-JQ1

Evidence specifically concerns (+)-JQ1 in this BRD4-NUT-dependent cell model.

Figure 4f,h and captions; JQ1 induces squamous differentiation and growth arrest in BRD4-dependent carcinoma

Keratin-14 expression: Quantitative RT-PCR relative to vehicle — Figure 4f; Results: JQ1 induces squamous differentiation

DNA-content distribution: Flow cytometry — Figure 4h and caption

MYC suppression in MM.1S myeloma cells

Cell-based study · Human MM.1S multiple myeloma cells [2]

The active JQ1 enantiomer reduced MYC transcript and c-Myc protein in MM.1S cells. The matched inactive enantiomer did not reproduce the protein response, linking this result to stereospecific BET inhibition rather than direct binding to c-Myc.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
MYC transcript in MM.1SQualitative time course Rapid reduction over the reported 0.5–8 h time course[2]
c-Myc protein in MM.1SQualitative response Reduced with (+)-JQ1 but not the matched (−)-JQ1 treatment[2]

Literature-Reported Treatment Conditions

Treatment concentration
500 nM (+)-JQ1; 500 nM (−)-JQ1 comparator in the protein experiment
Exposure duration
MYC qRT-PCR: 0, 0.5, 1, 4 and 8 h; protein comparison: 24 h
Method
qRT-PCR relative to baseline expression; c-Myc immunoblot with GAPDH loading control; vehicle and inactive-enantiomer comparators.
Reported limits
No exact fold reduction is inferred from the expression bars. Supplementary extended methods for this paper were not retrieved.
Methods and source locations

Compound reported in the paper: (+)-JQ1

Evidence is for the active (+) enantiomer; (−)-JQ1 is a separate comparator.

Downregulation of MYC; Figure 3B–C; Gene expression analysis

MYC transcript in MM.1S: qRT-PCR — Figure 3B

c-Myc protein in MM.1S: Immunoblotting — Figure 3C

In Vivo Studies

Tumor growth in NMC 11060 and Per403 xenografts

Animal study · NMC 11060 and Per403 xenografts in NCr nude mice [1]

Daily (+)-JQ1 reduced tumor burden relative to vehicle in both NMC models at the reported day-10 assessment. The active enantiomer used here is distinct from the racemic JQ1 used in a separate NMC 797 imaging experiment.

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Daily
Treatment course
Study planned for 30 days; tumor-volume comparison at day 10
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
NMC 11060 vehicleVehicle comparatorLarger tumor volumes than in the (+)-JQ1 cohort at day 10.[1]
NMC 11060 (+)-JQ1
50 mg/kg		Vehicle in the same tumor modelReduced tumor burden at day 10; P < 0.0001 reported. No exact volume or percentage reduction is estimated from the bars.[1]
NMC Per403 vehicleVehicle comparatorLarger tumor volumes than in the (+)-JQ1 cohort at day 10.[1]
NMC Per403 (+)-JQ1
50 mg/kg		Vehicle in the same tumor modelReduced tumor burden at day 10; P < 0.0001 reported. No exact volume or percentage reduction is estimated from the bars.[1]
NMC 11060 vehicle
Model: NMC 11060
NMC 11060 (+)-JQ1
Model: NMC 11060
NMC Per403 vehicle
Model: NMC Per403
NMC Per403 (+)-JQ1
Model: NMC Per403
Methods and source locations

Compound reported in the paper: (+)-JQ1

Evidence is specifically for the (+) enantiomer in these NMC xenograft models.

Publisher Supplementary Figure 15a,c (page 15); Primary NMC Xenograft Studies (pages 30–31)

NMC 11060 vehicle · Publisher Supplementary Figure 15a,c (page 15); Primary NMC Xenograft Studies (pages 30–31)

NMC 11060 (+)-JQ1 · Publisher Supplementary Figure 15a,c (page 15); Primary NMC Xenograft Studies (pages 30–31)

NMC Per403 vehicle · Publisher Supplementary Figure 15a,c (page 15); Primary NMC Xenograft Studies (pages 30–31)

NMC Per403 (+)-JQ1 · Publisher Supplementary Figure 15a,c (page 15); Primary NMC Xenograft Studies (pages 30–31)

Independent MM.1S-luc xenograft replication with enantiomer controls

Animal study · Orthotopic MM.1S-luc disease in female SCID-beige mice [3]

The replication study found longer survival with (+)-JQ1 than vehicle, but the day-22 tumor-burden comparison was not statistically significant. Survival also did not differ significantly between the two enantiomer groups. These results qualify, rather than uniformly reproduce, the earlier myeloma findings.

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Daily
Treatment course
36 days
Vehicle
Reported vehicle: 10% hydroxypropyl-β-cyclodextrin with 8% DMSO; formulation prepared by adding 920 μL 10% HP-β-CD to 80 μL DMSO per 5 mg compound
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
VehicleVehicle comparatorMedian survival 24.5 days during treatment.[3]
(+)-JQ1
50 mg/kg		Vehicle and separately administered (−)-JQ1Survival longer than vehicle; median not reached by day 36. Day-22 tumor burden lower in direction but not statistically significant; survival comparison with (−)-JQ1 not significant.[3]
(−)-JQ1 comparator
50 mg/kg (−)-JQ1		Separate enantiomer controlMedian survival 29 days. These data are not attributed to the (+)-JQ1 product.[3]
Vehicle
Model: Orthotopic MM.1S-luc disease in female SCID-beige mice
(+)-JQ1
Model: Orthotopic MM.1S-luc disease in female SCID-beige mice
(−)-JQ1 comparator
Model: Orthotopic MM.1S-luc disease in female SCID-beige mice
Methods and source locations

Compound reported in the paper: (+)-JQ1

Evidence concerns (+)-JQ1; (−)-JQ1 is retained only as a distinct comparator. The replication does not establish a significant difference between the enantiomer survival distributions.

MM.1S inoculation; JQ1 administration; individual survival/tumor-burden Results; Figures 2–3

Vehicle · MM.1S inoculation; JQ1 administration; individual survival/tumor-burden Results; Figures 2–3

(+)-JQ1 · MM.1S inoculation; JQ1 administration; individual survival/tumor-burden Results; Figures 2–3

(−)-JQ1 comparator · MM.1S inoculation; JQ1 administration; individual survival/tumor-burden Results; Figures 2–3

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1268524-70-4
Applications BET Inhibitor
Formula C23H25ClN4O2S
Molecular Weight 456.99
SMILES
CC1=C(SC2=C1C(=N[C@H](C3=NN=C(N32)C)CC(=O)OC(C)(C)C)C4=CC=C(C=C4)Cl)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 90 mg/mL (196.93 mM)
Water Insoluble
Ethanol 90 mg/mL

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
4 mg/mL
Vehicle
2% DMSO+30% PEG 300+5% Tween 80+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Filippakopoulos P, Qi J, Picaud S, et al. Selective inhibition of BET bromodomains. Nature (2010). PMID: 20871596 DOI: 10.1038/nature09504 Source material
  2. [2] Delmore JE, Issa GC, Lemieux ME, et al. BET bromodomain inhibition as a therapeutic strategy to target c-Myc. Cell (2011). PMID: 21889194 DOI: 10.1016/j.cell.2011.08.017 Source material
  3. [3] Aird F, Kandela I, Mantis C, et al. Replication Study: BET bromodomain inhibition as a therapeutic strategy to target c-Myc. eLife (2017). PMID: 28100400 DOI: 10.7554/elife.21253 Source material

Publications

16 publications citing this product

  1. Yoshimi Yasukawa, .et al. , Cancer Science, 2026, 117(7): 1894-1906 PMID: 42070972
  2. Stephanie Tanis, .et al. , Proc Natl Acad Sci U S A, 2026, Apr 14;123(15):e2517498123 PMID: 41945432
  3. Yuichiro Hara, .et al. , bioRxiv, 2025, Dec 05
  4. Jiang Zhou, .et al. , Neoplasia, 2025, Oct:68:101223 PMID: 40850308
  5. Kei Taga, .et al. , Microbiol Immunol, 2024, Mar;68(3):90-99 PMID: 38244193
  6. Deeksha Sharma, .et al. , Breast Cancer Res, 2023, Nov 15;25(1):144 PMID: 37968653
  7. Adriana K Alexander, .et al. , Nat Commun, 2023, Mar 29;14(1):1753 PMID: 36990976
  8. Haruki Kitamura, .et al. , Biochem Biophys Res Commun, 2023, Jan 22;641:139-147 PMID: 36527748
  9. Gerald Thiel, .et al. , Pharmaceuticals (Basel), 2022, Jul 10;15(7):846 PMID: 35890145
  10. Selase D Deletsu, .et al. , Biochem Biophys Res Commun, 2021, Aug 27;567:106-111 PMID: 34146904
  11. Cole Schonhofer, .et al. , Biochem Pharmacol, 2021, Apr;186:114462 PMID: 33577894
  12. Nandini Verma, .et al. , Sci Adv, 2020, 6 : eaba8968 PMID: 32937365
  13. Kuo MT, .et al. , Transl Oncol, 2020, 13(2):355-364 PMID: 31887630
  14. Rao Z, .et al. , J Immunol, 2019, Aug 15;203(4):1031-1043 PMID: 31300512
  15. A Carrer, .et al. , Cancer Discov, 2019, Jan 9. pii: CD-18-0567 PMID: 30626590
  16. Clocchiatti A, .et al. , J Clin Invest, 2018, Dec 3;128(12):5531-5548 PMID: 30395538

Showing 10 of 16 publications

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