BET bromodomain inhibitorPotent and selective inhibitor for BRD4 CAS# 1380087-89-7 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 1380087-89-7 | SDF | Download SDF |
| PubChem ID | 76534645 | Appearance | Powder |
| Formula | C20H16ClN3O2 | M.Wt | 365.81 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : 100 mg/mL (273.37 mM; Need ultrasonic) | ||
| Chemical Name | 2-[6-(4-chlorophenyl)-1-methyl-4H-[1,2]oxazolo[5,4-d][2]benzazepin-4-yl]acetamide | ||
| SMILES | CC1=NOC2=C1C3=CC=CC=C3C(=NC2CC(=O)N)C4=CC=C(C=C4)Cl | ||
| Standard InChIKey | GCWIQUVXWZWCLE-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C20H16ClN3O2/c1-11-18-14-4-2-3-5-15(14)19(12-6-8-13(21)9-7-12)23-16(10-17(22)25)20(18)26-24-11/h2-9,16H,10H2,1H3,(H2,22,25) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
BET bromodomain inhibitor Dilution Calculator
BET bromodomain inhibitor Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.7337 mL | 13.6683 mL | 27.3366 mL | 54.6732 mL | 68.3415 mL |
| 5 mM | 0.5467 mL | 2.7337 mL | 5.4673 mL | 10.9346 mL | 13.6683 mL |
| 10 mM | 0.2734 mL | 1.3668 mL | 2.7337 mL | 5.4673 mL | 6.8341 mL |
| 50 mM | 0.0547 mL | 0.2734 mL | 0.5467 mL | 1.0935 mL | 1.3668 mL |
| 100 mM | 0.0273 mL | 0.1367 mL | 0.2734 mL | 0.5467 mL | 0.6834 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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IC50: < 500 nM for BRD4
BET (bromodomain and extra-terminal) proteins regulate gene expression through their ability to bind to acetylated chromatin and subsequently activate RNA PolII-driven transcriptional elongation. The bromodomain (BRD) and extra-C terminal domain (BET) protein family consists of four members (BRD2, BRD3, BRD4 and BRDT).Small molecule BET inhibitors prevent binding of BET proteins to acetylated histones and inhibit transcriptional activation of BET target genes. BET inhibitors attenuate cell growth and survival in several hematologic cancer models, partially through the down-regulation of the critical oncogene, MYC. BET bromodomain inhibitor is a potent and selective inhibitor for BRD4.
In vitro: The most potent systhsized ompound presented is BET bromodomain inhibitor, which shows activity with IC50 < 500 nM against BRD4 [1].
In vivo: BET bromodomain inhibitor shows activity in vivo at < 10 mg/kg against BRD4 in rat [1].
Clinical trial: Up to now, BET bromodomain inhibitor is still in the preclinical development stage.
Reference:
[1] Garnier JM, Sharp PP, Burns CJ. BET bromodomain inhibitors: a patent review. Expert Opin Ther Pat. 2014 Feb;24(2):185-99.
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The BET bromodomain inhibitor JQ1 radiosensitizes non-small cell lung cancer cells by upregulating p21.[Pubmed:28143717]
Cancer Lett. 2017 Apr 10;391:141-151.
Radiotherapy is an important treatment modality in the management of locally advanced non-small cell lung cancer (NSCLC). However, radioresistance markedly impairs its efficacy in clinic. Bromodomain and extra-terminal (BET) bromodomain inhibitors have demonstrated dramatic antitumor activity in several preclinical human cancer models. In this study, we investigated for the first time the effect of JQ1, a novel BET bromodomain inhibitor, on tumor cell radiosensitivity of NSCLC in vitro and in vivo. Our results demonstrated that JQ1 significantly enhanced the effect of irradiation in NSCLC cell lines through a c-myc-independent mechanism. The notable findings in response to this combined treatment were prolonged delay in IR-induced DNA double-strand break (DSB) repair, induced robust G2/M checkpoint arrest and increased cell apoptosis. Additional investigations revealed that induction of p21 played an important role in its radiosensitizing effects. In conclusion, these results suggested that BET bromodomain inhibition might offer a potential strategy for enhancing the effects of radiotherapy and reducing radioresistance.
Gene expression profiling of patient-derived pancreatic cancer xenografts predicts sensitivity to the BET bromodomain inhibitor JQ1: implications for individualized medicine efforts.[Pubmed:28275007]
EMBO Mol Med. 2017 Apr;9(4):482-497.
c-MYC controls more than 15% of genes responsible for proliferation, differentiation, and cellular metabolism in pancreatic as well as other cancers making this transcription factor a prime target for treating patients. The transcriptome of 55 patient-derived xenografts show that 30% of them share an exacerbated expression profile of MYC transcriptional targets (MYC-high). This cohort is characterized by a high level of Ki67 staining, a lower differentiation state, and a shorter survival time compared to the MYC-low subgroup. To define classifier expression signature, we selected a group of 10 MYC target transcripts which expression is increased in the MYC-high group and six transcripts increased in the MYC-low group. We validated the ability of these markers panel to identify MYC-high patient-derived xenografts from both: discovery and validation cohorts as well as primary cell cultures from the same patients. We then showed that cells from MYC-high patients are more sensitive to JQ1 treatment compared to MYC-low cells, in monolayer, 3D cultured spheroids and in vivo xenografted tumors, due to cell cycle arrest followed by apoptosis. Therefore, these results provide new markers and potentially novel therapeutic modalities for distinct subgroups of pancreatic tumors and may find application to the future management of these patients within the setting of individualized medicine clinics.
The BET Bromodomain Inhibitor JQ1 Suppresses Chondrosarcoma Cell Growth via Regulation of YAP/p21/c-Myc Signaling.[Pubmed:28059436]
J Cell Biochem. 2017 Aug;118(8):2182-2192.
Chondrosarcoma, the second-most frequent primary bone malignancy, is generally more resistant to conventional chemotherapy and radiotherapy. Therefore, the development of an effective adjuvant therapy is necessary. Recently, targeting the epigenetic regulator such as bromodomain and extraterminal domain (BET) proteins has achieved great success. For instance, the bromodomain inhibitor JQ1 has been shown to inhibit the growth of several cancer cells both in vitro and in vivo. Herein, we demonstrated that JQ1 significantly inhibited chondrosarcoma cell growth and colony formation. JQ1 also induced marked G1-phase cell cycle arrest coincided with the up-regulation of p21(WAF1/CIP1) , p27(Kip1) , and Cyclin D1 expression, and the down-regulation of Cyclin E2 expression. Moreover, JQ1 induced the premature senescence of SW 1353 cells, and that prolong treatment of JQ1 caused cell apoptosis. Mechanistically, the JQ1-induced cell growth inhibition was correlated with the suppression of c-Myc and Bcl-xL, which are the prime genes for cell cycle control and anti-apoptosis. Furthermore, we demonstrated that p21 negatively regulated the expression of c-Myc and Bcl-xL upon JQ1 treatment, and that the growth inhibition of SW 1353 and Hs 819.T cells and induction of p21 were predominantly regulated by the LATS1/YAP signaling but not through a p53-dependent manner. In conclusion, we disclosed a novel mechanism that JQ1 inhibits cell proliferation, induces cell senescence and apoptosis of chondrosarcoma cells through the regulation of the YAP/p21/c-Myc/Bcl-xL signaling axis. J. Cell. Biochem. 118: 2182-2192, 2017. (c) 2017 Wiley Periodicals, Inc.
