7ACC1CAS# 50995-74-9 |
- PI 828
Catalog No.:BCC7494
CAS No.:942289-87-4
Quality Control & MSDS
3D structure
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Number of papers citing our products
| Cas No. | 50995-74-9 | SDF | Download SDF |
| PubChem ID | 659294 | Appearance | Powder |
| Formula | C14H15NO4 | M.Wt | 261.27 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | DEAC; Coumarin D 1421; D 1421 | ||
| Solubility | DMSO : 33.33 mg/mL (127.57 mM; Need ultrasonic) | ||
| Chemical Name | 7-(diethylamino)-2-oxochromene-3-carboxylic acid | ||
| SMILES | CCN(CC)C1=CC2=C(C=C1)C=C(C(=O)O2)C(=O)O | ||
| Standard InChIKey | WHCPTFFIERCDSB-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C14H15NO4/c1-3-15(4-2)10-6-5-9-7-11(13(16)17)14(18)19-12(9)8-10/h5-8H,3-4H2,1-2H3,(H,16,17) | ||
| 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. | ||
7ACC1 Dilution Calculator
7ACC1 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.8275 mL | 19.1373 mL | 38.2746 mL | 76.5492 mL | 95.6865 mL |
| 5 mM | 0.7655 mL | 3.8275 mL | 7.6549 mL | 15.3098 mL | 19.1373 mL |
| 10 mM | 0.3827 mL | 1.9137 mL | 3.8275 mL | 7.6549 mL | 9.5686 mL |
| 50 mM | 0.0765 mL | 0.3827 mL | 0.7655 mL | 1.531 mL | 1.9137 mL |
| 100 mM | 0.0383 mL | 0.1914 mL | 0.3827 mL | 0.7655 mL | 0.9569 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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7ACC1(DEAC; Coumarin D 1421; D 1421) selectively interfere with lactate fluxes in the lactate-rich tumor microenvironment; inhibits lactate influx but not efflux in tumor cells expressing MCT1 and MCT4 transporters. IC50 value: 0.86 uM(Lactate uptake inhibition) [1] Target: MCT inhibitor; lactate transport inhibitor Contrary to the reference MCT1 inhibitor AR-C155858, 7ACC unexpectedly inhibited lactate influx but not efflux in tumor cells expressing MCT1 and MCT4 transporters. 7ACC delayed the growth of cervix SiHa tumors, colorectal HCT116 tumors, and orthoptopic MCF-7 breast tumors. MCT target engagement was confirmed by the lack of activity of 7ACC on bladder UM-UC-3 carcinoma that does not express functional MCT. 7ACC also inhibited SiHa tumor relapse after treatment with cisplatin. Finally, we found that contrary to AR-C155858, 7ACC did not prevent the cell entry of the substrate-mimetic drug 3-bromopyruvate (3BP) through MCT1, and contributed to the inhibition of tumor relapse after 3BP treatment.
References:
[1]. Draoui N, et al. Antitumor activity of 7-aminocarboxycoumarin derivatives, a new class of potent inhibitors of lactate influx but not efflux. Mol Cancer Ther. 2014 Jun;13(6):1410-8.
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Downregulation of MCT4 for lactate exchange promotes the cytotoxicity of NK cells in breast carcinoma.[Pubmed:30051648]
Cancer Med. 2018 Sep;7(9):4690-4700.
Monocarboxylate transporter-4 (MCT4), a monocarboxylic acid transporter, demonstrates significantly increased expression in the majority of malignancies. We performed an experiment using BALB/C mice, and our results showed that ShMCT4 transfection or the pharmaceutic inhibition of MCT4 with 7ACC1 strengthens the activity of NK cells. The results of a calcein assay revealed that the cytotoxicity of NK cells was strengthened via inhibition of MCT4. In addition, ELISA testing showed that the content of perforin and CD107a was increased, and PCR amplification and immunoblotting revealed that the expression of NKG2D and H60 was upregulated after the inhibition of MCT4. Further, we observed an elevated pH value, decreased extracellular lactate flow, and attenuated tumor growth. Therefore, we concluded that the inhibition of MCT4 enhanced the cytotoxicity of NK cells by blocking lactate flux and reversing the acidified tumor microenvironment. In addition to these findings, we also discovered that MCT4 depletion may have a pronounced impact on autophagy, which was surmised by observing that the inhibition of autophagy (3MA) pulled the enhanced cytotoxicity of NK cells downwards. Together, these data suggest that the key effect of MCT4 depletion on NK cells probably utilizes inductive autophagy as a compensatory metabolic mechanism to minimize the acidic extracellular microenvironment associated with lactate export in tumors.
