BRD4770CAS# 1374601-40-7 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 1374601-40-7 | SDF | Download SDF |
| PubChem ID | 72193870 | Appearance | Powder |
| Formula | C25H23N3O3 | M.Wt | 413.47 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : 5.56 mg/mL (13.45 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
| Chemical Name | methyl 2-benzamido-1-(3-phenylpropyl)benzimidazole-5-carboxylate | ||
| SMILES | COC(=O)C1=CC2=C(C=C1)N(C(=N2)NC(=O)C3=CC=CC=C3)CCCC4=CC=CC=C4 | ||
| Standard InChIKey | UCGWYCMPZXDHNR-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C25H23N3O3/c1-31-24(30)20-14-15-22-21(17-20)26-25(27-23(29)19-12-6-3-7-13-19)28(22)16-8-11-18-9-4-2-5-10-18/h2-7,9-10,12-15,17H,8,11,16H2,1H3,(H,26,27,29) | ||
| 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. | ||
| Description | G9a inhibitor and S-adenosyl methionine (SAM) mimetic. Inhibits methylation of H3K9 (EC50 ~ 5 μM) and induces senescence in PANC-1 cells. Induces ATM activation without DNA damage. Cell permeable. |
BRD4770 Dilution Calculator
BRD4770 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4186 mL | 12.0928 mL | 24.1856 mL | 48.3711 mL | 60.4639 mL |
| 5 mM | 0.4837 mL | 2.4186 mL | 4.8371 mL | 9.6742 mL | 12.0928 mL |
| 10 mM | 0.2419 mL | 1.2093 mL | 2.4186 mL | 4.8371 mL | 6.0464 mL |
| 50 mM | 0.0484 mL | 0.2419 mL | 0.4837 mL | 0.9674 mL | 1.2093 mL |
| 100 mM | 0.0242 mL | 0.1209 mL | 0.2419 mL | 0.4837 mL | 0.6046 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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Modulation of the Fanconi anemia pathway via chemically induced changes in chromatin structure.[Pubmed:29100324]
Oncotarget. 2017 Jul 22;8(44):76443-76457.
Fanconi anemia (FA) is a rare disease characterized by congenital defects, bone marrow failure, and atypically early-onset cancers. The FA proteins function cooperatively to repair DNA interstrand crosslinks. A major step in the activation of the pathway is the monoubiquitination of the FANCD2 and FANCI proteins, and their recruitment to chromatin-associated nuclear foci. The regulation and function of FANCD2 and FANCI, however, is poorly understood. In addition, how chromatin state impacts pathway activation is also unknown. In this study, we have examined the influence of chromatin state on the activation of the FA pathway. We describe potent activation of FANCD2 and FANCI monoubiquitination and nuclear foci formation following treatment of cells with the histone methyltransferase inhibitor BRD4770. BRD4770-induced activation of the pathway does not occur via the direct induction of DNA damage or via the inhibition of the G9a histone methyltransferase, a mechanism previously proposed for this molecule. Instead, we show that BRD4770-inducible FANCD2 and FANCI monoubiquitination and nuclear foci formation may be a consequence of inhibition of the PRC2/EZH2 chromatin-modifying complex. In addition, we show that inhibition of the class I and II histone deacetylases leads to attenuated FANCD2 and FANCI monoubiquitination and nuclear foci formation. Our studies establish that chromatin state is a major determinant of the activation of the FA pathway and suggest an important role for the PRC2/EZH2 complex in the regulation of this critical tumor suppressor pathway.
Arsenic silences hepatic PDK4 expression through activation of histone H3K9 methylatransferase G9a.[Pubmed:27217333]
Toxicol Appl Pharmacol. 2016 Aug 1;304:42-7.
It is well established that increased liver cancer incidence is strongly associated with epigenetic silencing of tumor suppressor genes; the latter is contributed by the environmental exposure to arsenic. Pyruvate dehydrogenase kinase 4 (PDK4) is a mitochondrial protein that regulates the TCA cycle. However, the epigenetic mechanisms mediated by arsenic to control PDK4 expression remain elusive. In the present study, we showed that histone methyltransferase G9a- and Suv39H-mediated histone H3 lysine 9 (H3K9) methylations contributed to PDK4 silencing in hepatic cells. The PDK4 expression was induced by G9a inhibitor BRD4770 (BRD) and Suv39H inhibitor Chaetocin (CHA). In contrast, arsenic exposure decreased PDK4 expression by inducing G9a and increasing H3K9 di- and tri-methylations levels (H3K9me2/3). In addition, arsenic exposure antagonizes the effect of BRD by enhancing the enrichment of H3K9me2/3 in the PKD4 promoter. Moreover, knockdown of G9a using siRNA induced PDK4 expression in HCC cells. Furthermore, arsenic decreased hepatic PDK4 expression as well as diminished the induction of PDK4 by BRD in mouse liver and hepatocytes. Overall, the results suggest that arsenic causes aberrant repressive histone modification to silence PDK4 in both HCC cells and in mouse liver.
Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells.[Pubmed:23807219]
Cell Death Dis. 2013 Jun 27;4:e690.
The histone methyltransferase G9a is overexpressed in a variety of cancer types, including pancreatic adenocarcinoma, and promotes tumor invasiveness and metastasis. We recently reported the discovery of BRD4770, a small-molecule inhibitor of G9a that induces senescence in PANC-1 cells. We observed that the cytotoxic effects of BRD4770 were dependent on genetic background, with cell lines lacking functional p53 being relatively resistant to compound treatment. To understand the mechanism of genetic selectivity, we used two complementary screening approaches to identify enhancers of BRD4770. The natural product and putative BH3 mimetic gossypol enhanced the cytotoxicity of BRD4770 in a synergistic manner in p53-mutant PANC-1 cells but not in immortalized non-tumorigenic pancreatic cells. The combination of gossypol and BRD4770 increased LC3-II levels and the autophagosome number in PANC-1 cells, and the compound combination appears to act in a BNIP3 (B-cell lymphoma 2 19-kDa interacting protein)-dependent manner, suggesting that these compounds act together to induce autophagy-related cell death in pancreatic cancer cells.
A small-molecule probe of the histone methyltransferase G9a induces cellular senescence in pancreatic adenocarcinoma.[Pubmed:22536950]
ACS Chem Biol. 2012 Jul 20;7(7):1152-7.
Post-translational modifications of histones alter chromatin structure and play key roles in gene expression and specification of cell states. Small molecules that target chromatin-modifying enzymes selectively are useful as probes and have promise as therapeutics, although very few are currently available. G9a (also named euchromatin histone methyltransferase 2 (EHMT2)) catalyzes methylation of lysine 9 on histone H3 (H3K9), a modification linked to aberrant silencing of tumor-suppressor genes, among others. Here, we report the discovery of a novel histone methyltransferase inhibitor, BRD4770. This compound reduced cellular levels of di- and trimethylated H3K9 without inducing apoptosis, induced senescence, and inhibited both anchorage-dependent and -independent proliferation in the pancreatic cancer cell line PANC-1. ATM-pathway activation, caused by either genetic or small-molecule inhibition of G9a, may mediate BRD4770-induced cell senescence. BRD4770 may be a useful tool to study G9a and its role in senescence and cancer cell biology.
