TriflusalCAS# 322-79-2 |
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Quality Control & MSDS
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Chemical structure
3D structure
Cas No. | 322-79-2 | SDF | Download SDF |
PubChem ID | 9458 | Appearance | Powder |
Formula | C10H7F3O4 | M.Wt | 248.16 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 100 mg/mL (402.97 mM; Need ultrasonic) | ||
Chemical Name | 2-acetyloxy-4-(trifluoromethyl)benzoic acid | ||
SMILES | CC(=O)OC1=C(C=CC(=C1)C(F)(F)F)C(=O)O | ||
Standard InChIKey | RMWVZGDJPAKBDE-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C10H7F3O4/c1-5(14)17-8-4-6(10(11,12)13)2-3-7(8)9(15)16/h2-4H,1H3,(H,15,16) | ||
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 | Triflusal irreversibly inhibits the production of thromboxane-B2 in platelets by acetylating cycloxygenase-1.
Target: COX
Triflusal at 10 mM, 100 mM and 1 M decreases LDH efflux in rat brain slices after anoxia/reoxygenation by 24%, 35% and 49% respectively. Triflusal also reduces inducible NO synthase activity by 18%, 21% and 30% [1].
Triflusal (10 mg/kg i.v.) reduces platelet deposition on subendothelium-induced primary thrombus by about 68% in rabbits. Triflusal (10 mg/kg i.v.) reduces platelet deposition on a fresh thrombus formed over tunica media by about 48% in rabbits. Triflusal (40 mg/kg p.o.) reduces platelet deposition on a primary thrombus triggered by subendothelium and tunica media by 53% in rabbits. Triflusal (40 mg/kg p.o.) significantly reduces Cox-2 mRNA levels and protein levels without influence Cox-1 mRNA levels on the vascular wall in rabbits [2]. Triflusal (600 mg/day for 5 days) results in an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils in healthy volunteers [3]. References: |
Triflusal Dilution Calculator
Triflusal Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.0297 mL | 20.1483 mL | 40.2966 mL | 80.5932 mL | 100.7415 mL |
5 mM | 0.8059 mL | 4.0297 mL | 8.0593 mL | 16.1186 mL | 20.1483 mL |
10 mM | 0.403 mL | 2.0148 mL | 4.0297 mL | 8.0593 mL | 10.0741 mL |
50 mM | 0.0806 mL | 0.403 mL | 0.8059 mL | 1.6119 mL | 2.0148 mL |
100 mM | 0.0403 mL | 0.2015 mL | 0.403 mL | 0.8059 mL | 1.0074 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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Triflusal irreversibly inhibits the production of thromboxane-B2 in platelets by acetylating cycloxygenase-1.
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Neuroprotective effect of triflusal and its main metabolite, 2-hydroxy-4-trifluoromethylbenzoic acid (HTB), in the postischemic brain.[Pubmed:28189746]
Neurosci Lett. 2017 Mar 16;643:59-64.
2-Hydroxy-4-trifluoromethylbenzoic acid (HTB) is a metabolite of Triflusal (TF), and has been reported to exert anti-inflammatory effect. In this study, the authors investigated whether HTB has a neuroprotective effect against ischemic brain injuries. We showed that intravenous administration of HTB (5mg/kg) 30min before or 1, 3, or 6h after middle cerebral artery occlusion (MCAO) reduced brain infarct to 10.4+/-3.3%, 16.9+/-2.3%, 22.2+/-1.5% and 40.7+/-7.5%, respectively, of that of treatment-naive MCAO controls, and the therapeutic time window extended to 9h after MCAO (40.7+/-7.5%). Furthermore, HTB suppressed infarct formation, protected motor activities, and ameliorated neurological deficits more effectively than by TF or salicylic acid (SA). HTB markedly suppressed microglial activation and proinflammatory cytokines expressions in the postischemic brain and in BV2 cells and suppressed LPS-induced nitrite production by inhibiting IkB degradation. In addition, HTB suppressed NMDA-induced neuronal cell death more effectively than TF or SA in primary cortical neuron cultures. Together, these results indicate that HTB has multi-modal protective effects against ischemic brain damage that encompass anti-inflammatory, anti-excitotoxicity, and anti-Zn(2+)-toxicity effects.
Photosensitivity to Triflusal: Formation of a Photoadduct with Ubiquitin Demonstrated by Photophysical and Proteomic Techniques.[Pubmed:27621705]
Front Pharmacol. 2016 Aug 29;7:277.
Triflusal is a platelet aggregation inhibitor chemically related to acetylsalicylic acid, which is used for the prevention and/or treatment of vascular thromboembolisms, which acts as a prodrug. Actually, after oral administration it is absorbed primarily in the small intestine, binds to plasma proteins (99%) and is rapidly biotransformed in the liver into its deacetylated active metabolite 2-hydroxy-4-trifluoromethylbenzoic acid (HTB). In healthy humans, the half-life of Triflusal is ca. 0.5 h, whereas for HTB it is ca. 35 h. From a pharmacological point of view, it is interesting to note that HTB is itself highly active as a platelet anti-aggregant agent. Indeed, studies on the clinical profile of both drug and metabolite have shown no significant differences between them. It has been evidenced that HTB displays ability to induce photoallergy in humans. This phenomenon involves a cell-mediated immune response, which is initiated by covalent binding of a light-activated photosensitizer (or a species derived therefrom) to a protein. In this context, small proteins like ubiquitin could be appropriate models for investigating covalent binding by means of MS/MS and peptide fingerprint analysis. In previous work, it was shown that HTB forms covalent photoadducts with isolated lysine. Interestingly, ubiquitin contains seven lysine residues that could be modified by a similar reaction. With this background, the aim of the present work is to explore adduct formation between the Triflusal metabolite and ubiquitin as model protein upon sunlight irradiation, combining proteomic and photophysical (fluorescence and laser flash photolysis) techniques. Photophysical and proteomic analysis demonstrates monoadduct formation as the major outcome of the reaction. Interestingly, addition can take place at any of the epsilon-amino groups of the lysine residues of the protein and involves replacement of the trifluoromethyl moiety with a new amide function. This process can in principle occur with other trifluoroaromatic compounds and may be responsible for the appearance of undesired photoallergic side effects.
Protocol for the comparison of triflusal and clopidogrel in secondary prevention of stroke based on cytochrome P450 2C19 genotyping (MASETRO study): A multicenter, randomized, open-label, parallel-group trial.[Pubmed:26763917]
Int J Stroke. 2016 Jun;11(4):485-91.
RATIONALE AND AIM: The antiplatelet effect of clopidogrel is reportedly influenced by cytochrome P450 2C19 (CYP2C19) polymorphisms. However, there is no data concerning the relationship between stroke recurrence and CYP2C19 polymorphisms in patients treated with clopidogrel for secondary prevention of ischemic stroke. Triflusal may be an alternative therapy for clopidogrel in patients with poor genotype. The Comparison of Triflusal and Clopidogrel Effects in Secondary Prevention of Stroke Based on Cytochrome P450 2C19 Genotyping (MAESTRO) study will investigate the effect of antiplatelet agents based on CYP2C19 polymorphisms in secondary prevention of ischemic stroke. SAMPLE SIZE AND DESIGN: Assuming that 55% of patients belong to the poor genotype group, the required sample size is 1080 patients with at least 24 months of follow-up. This study is designed as a prospective, multicenter, randomized, parallel-group, open-label, and blind genotype trial. Patients who experience their first non-cardiogenic ischemic stroke within 30 days prior to screening are eligible. Patients received 300 mg Triflusal twice a day or 75 mg clopidogrel once daily during the trial. The study is registered with ClinicalTrials.gov (NCT01174693). STUDY OUTCOME: The primary outcome is recurrent ischemic stroke or hemorrhagic stroke. Secondary outcomes consist of composite major vascular events including stroke, myocardial infarction, coronary revascularization, or vascular death. DISCUSSION: Personalized medicine may be essential for patients according to individual drug metabolism abilities. MAESTRO is the first prospective study designed to evaluate the effect of CYP2C19 polymorphism in secondary stroke prevention and will resolve several questions regarding preventive antiplatelet agents for recurrent stroke.