Name | triflusal |
Synonyms | ur1501 triflusal TRIFLUOROTRIMESICACID 4-trifluoromethylsalicylicacidacetate 2-acetoxy-4-trifluoromethylbenzoic acid 2-Acetoxy-4-trifluoromethylbenzoic acid 2-Acetyloxy-4-trifluoromethylbenzoic Acid 2-(acetyloxy)-4-(trifluoromethyl)benzoic acid 4-cresoticacid,alpha,alpha,alpha-trifluoro-acetate 3-acetoxy-alpha,alpha,alpha-trifluoro-p-toluic acid alpha,alpha,alpha-trifluoro-2,4-creosoticacidacetate |
CAS | 322-79-2 |
EINECS | 206-297-5 |
InChI | InChI=1/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) |
Molecular Formula | C10H7F3O4 |
Molar Mass | 248.16 |
Density | 1.433±0.06 g/cm3(Predicted) |
Melting Point | 120-122° (upon slow heating); 110-112° (upon quick heating) |
Boling Point | 316.0±42.0 °C(Predicted) |
Flash Point | 144.9°C |
Solubility | DMSO: >30mg/mL |
Vapor Presure | 0.000178mmHg at 25°C |
Appearance | powder |
Color | white to off-white |
Maximum wavelength(λmax) | ['297nm(H2O)(lit.)'] |
Merck | 14,9688 |
pKa | 2.97±0.10(Predicted) |
Storage Condition | Sealed in dry,2-8°C |
Refractive Index | 1.483 |
In vitro study | The main metabolite of Triflusal, HTB, maintains the synthesis of 6-keto-PGF1α in porcine aortic endothelial cells (PAEC), even at higher concentrations, it will not be significantly reduced within 24 hours. After hypoxia/reoxygenation in rat brain slices, triflusu reduced LDH efflux by 24%,35% and 49% at 10 mM,100 mM and 1 M, respectively. Triflusal also reduced inducible NO synthase activity by 18%,21%, and 30%, respectively. |
In vivo study | Triflosal (10 mg/kg I. v.) reduced the primary thrombus induced by platelet deposition in the endothelium by 68% in rabbits. Triflosal (10 mg/kg I. v.) reduced platelet deposition on newly formed media thrombi by approximately 48% in rabbits. In rabbits, triflosal (40 mg/kg p.o.) reduced by 53% the deposition of platelets in incipient thrombi arising from the subcutaneous intima and media. Triflosal (40 mg/kg p.o.) significantly reduced vascular wall Cox-2 mRNA levels and protein levels in rabbits, but did not affect Cox-1 mRNA levels. In healthy volunteers, triflosal (600 mg/day,5 days) increased NO production in neutrophils and increased expression of endothelial nitric oxide synthase (eNOS) protein in neutrophils. Triflusu (300 mg, oral, twice daily) significantly increased total walking distance and pain-free walking distance more than placebo, while improving symptoms of chronic peripheral arterial disease in patients with claudication. In patients with chronic peripheral arterial disease, triflosal (300 mg, oral, twice daily) increases the peak flow recorded by pressure measurement plethysmography. In rats, triflosal (30 mg/kg) strongly reduced the immunolabeling of iNOS, attenuated iNOS immunoreactivity in astrocytes and infiltrating neutrophils as determined by survival time. In rats, triflosal (30 mg/kg) reduces the expression of COX-2 in neurons and microglia 10 and 24 hours after the lesion, and the expression of IL-1beta and TNF-alpha in microglia and astrocytes was reduced 24 hours after the lesion. |
Hazard Symbols | Xn - Harmful |
Risk Codes | R22 - Harmful if swallowed R36/37/38 - Irritating to eyes, respiratory system and skin. R43 - May cause sensitization by skin contact |
Safety Description | S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S36/37 - Wear suitable protective clothing and gloves. |
WGK Germany | 3 |
RTECS | GP4250000 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 4.03 ml | 20.148 ml | 40.297 ml |
5 mM | 0.806 ml | 4.03 ml | 8.059 ml |
10 mM | 0.403 ml | 2.015 ml | 4.03 ml |
5 mM | 0.081 ml | 0.403 ml | 0.806 ml |
Biological activity | Triflusal (UR1501) is an antithrombotic agent that irreversibly inhibits thromboxane-B2 in platelets by acetylating cyclooxygenase-1 production. |
Target | Value |