BTB06584F1F0 ATP synthases CAS# 219793-45-0 |
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Quality Control & MSDS
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Chemical structure
3D structure
| Cas No. | 219793-45-0 | SDF | Download SDF |
| PubChem ID | 2799764 | Appearance | Powder |
| Formula | C19H12ClNO6S | M.Wt | 417.82 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 47 mg/mL (112.49 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | [5-(benzenesulfonyl)-2-nitrophenyl] 4-chlorobenzoate | ||
| SMILES | C1=CC=C(C=C1)S(=O)(=O)C2=CC(=C(C=C2)[N+](=O)[O-])OC(=O)C3=CC=C(C=C3)Cl | ||
| Standard InChIKey | WNDWKKPBLAKXMI-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C19H12ClNO6S/c20-14-8-6-13(7-9-14)19(22)27-18-12-16(10-11-17(18)21(23)24)28(25,26)15-4-2-1-3-5-15/h1-12H | ||
| 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 | BTB06584 is an IF1-dependent selective inhibitor of the mitochondrial F1Fo-ATPase.
Target: ATPase
in vitro: BTB06584 inhibits F1Fo-ATPase activity with no effect on ΔΨm or O2 consumption. ATP consumption was decreased following inhibition of respiration, and ischaemic cell death was reduced. BTB06584 efficiency was increased by IF1 overexpression and reduced by silencing the protein. BTB06584 may represent a valuable tool to selectively inhibit mitochondrial F1Fo-ATPase activity without compromising ATP synthesis and to limit ischaemia-induced injury caused by reversal of the mitochondrial F1Fo-ATPsynthase.
in vivo: BTB06584 rescues defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost. References: | |||||
BTB06584 Dilution Calculator
BTB06584 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.3934 mL | 11.9669 mL | 23.9338 mL | 47.8675 mL | 59.8344 mL |
| 5 mM | 0.4787 mL | 2.3934 mL | 4.7868 mL | 9.5735 mL | 11.9669 mL |
| 10 mM | 0.2393 mL | 1.1967 mL | 2.3934 mL | 4.7868 mL | 5.9834 mL |
| 50 mM | 0.0479 mL | 0.2393 mL | 0.4787 mL | 0.9574 mL | 1.1967 mL |
| 100 mM | 0.0239 mL | 0.1197 mL | 0.2393 mL | 0.4787 mL | 0.5983 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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Ischaemia compromises mitochondrial respiration. Consequently, the mitochondrial 1Fo-ATP synthase reverses and plays as a proton-pumping ATPase, so maintaining the mitochondrial membrane potential (ΔΨm), while accelerating ATP depletion and cell death. BTB06584 is an IF1-dependent selective inhibitor of the mitochondrial F1Fo-ATPase.
In vitro: BTB inhibited F1Fo-ATPase activity with no effect on the mitochondrial membrane potential (ΔΨm) or O2 consumption. ATP consumption decreased via inhibition of respiration, and ischaemic cell death was reduced. BTB efficiency increased by IF1 overexpression and reduced by silencing this protein. In addition, BTB rescued defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost [1].
In vivo: The BTB-mediated protection was further tested in neurons. Primary cultured cortical neurons of mice were exposed to OGD, treated or not with BTB, followed by RX. The resulting cell death was significantly reduced by BTB, as scored by PI staining, compared with cells left untreated during OGD [1].
Clinical trials: Currenlty no clinical data are available.
Reference:
[1] Ivanes F, Faccenda D, Gatliff J, Ahmed AA, Cocco S, Cheng CH, Allan E, Russell C, Duchen MR, Campanella M. The compound BTB06584 is an IF1-dependent selective inhibitor of the mitochondrial F1 Fo-ATPase. Br J Pharmacol. 2014;171(18):4193-206.
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The compound BTB06584 is an IF1 -dependent selective inhibitor of the mitochondrial F1 Fo-ATPase.[Pubmed:24641180]
Br J Pharmacol. 2014 Sep;171(18):4193-206.
BACKGROUND AND PURPOSE: Ischaemia compromises mitochondrial respiration. Consequently, the mitochondrial F1 Fo-ATPsynthase reverses and acts as a proton-pumping ATPase, so maintaining the mitochondrial membrane potential (DeltaPsim ), while accelerating ATP depletion and cell death. Here we have looked for a molecule that can selectively inhibit this activity without affecting ATP synthesis, preserve ATP and delay ischaemic cell death. EXPERIMENTAL APPROACH: We developed a chemoinformatic screen based on the structure of BMS199264, which is reported to selectively inhibit F1 Fo-ATPase activity and which is cardioprotective. Results suggested the molecule BTB06584 (hereafter referred to as BTB). Fluorescence microscopy was used to study its effects on DeltaPsim and on the rate of ATP consumption following inhibition of respiration in several cell types. The effect of BTB on oxygen (O2 ) consumption was explored and protective potential determined using ischaemia/reperfusion assays. We also investigated a potential mechanism of action through its interaction with inhibitor protein of F1 subunit (IF1 ), the endogenous inhibitor of the F1 Fo-ATPase. KEY RESULTS: BTB inhibited F1 Fo-ATPase activity with no effect on DeltaPsim or O2 consumption. ATP consumption was decreased following inhibition of respiration, and ischaemic cell death was reduced. BTB efficiency was increased by IF1 overexpression and reduced by silencing the protein. In addition, BTB rescued defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost. CONCLUSIONS AND IMPLICATIONS: BTB may represent a valuable tool to selectively inhibit mitochondrial F1 Fo-ATPase activity without compromising ATP synthesis and to limit ischaemia-induced injury caused by reversal of the mitochondrial F1 Fo-ATPsynthase.
