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Triflusal

Triflusal ??? ???
?? ??:
322-79-2
???:
Triflusal
???(??):
ur1501;Drisgen;Disgren;TRIFLUSAL;Triflusal-d3;Triflusal CRS;Triflusal (UR1501);TRIFLUOROTRIMESICACID;Triflusal, 10 mM in DMSO;4-trifluoromethylsalicylicacidacetate
CBNumber:
CB9446472
???:
C10H7F3O4
??? ??:
248.16
MOL ??:
322-79-2.mol
MSDS ??:
SDS

Triflusal ??

???
120-122° (upon slow heating); 110-112° (upon quick heating)
?? ?
316.0±42.0 °C(Predicted)
??
1.433±0.06 g/cm3(Predicted)
?? ??
Sealed in dry,2-8°C
???
DMSO: >30mg/mL
?? ?? (pKa)
2.97±0.10(Predicted)
??? ??
??
??
???? ?????
?? ??(λmax)
297nm(H2O)(lit.)
Merck
14,9688
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)
InChIKey
RMWVZGDJPAKBDE-UHFFFAOYSA-N
SMILES
FC(F)(F)c1cc(c(cc1)C(=O)O)OC(=O)C
CAS ??????
322-79-2(CAS DataBase Reference)
??
  • ?? ? ?? ??
  • ?? ? ???? ?? (GHS)
??? ?? Xn
?? ???? ?? 22-36/37/38-43
????? 26-36/37
WGK ?? 3
RTECS ?? GP4250000
HS ?? 2918.29.7500
???? ??? 11 - Combustible Solids
Hazard Classifications Acute Tox. 4 Oral
Eye Irrit. 2
Skin Irrit. 2
Skin Sens. 1
STOT SE 3
????(GHS): Exclamation Mark (GHS07)
?? ?: Warning
??·?? ??:
?? ??·?? ?? ?? ?? ?? ?? ? ?? ?? P- ??
H302 ??? ??? ?? ?? ?? - ?? ?? 4 ?? P264, P270, P301+P312, P330, P501
H315 ??? ??? ??? ????? ?? ????? ?? 2 ?? P264, P280, P302+P352, P321,P332+P313, P362
H317 ????? ?? ??? ??? ? ?? ?? ??? ?? ?? 1 ?? P261, P272, P280, P302+P352,P333+P313, P321, P363, P501
H319 ?? ?? ??? ??? ?? ? ?? ?? ??? ?? ?? 2A ?? P264, P280, P305+P351+P338,P337+P313P
H335 ?? ???? ??? ? ?? ?? ???? ?? - 1? ??;???? ?? ?? 3 ??
??????:
P261 ??·?·??·???·??·...·????? ??? ????.
P264 ?? ??? ?? ??? ????.
P264 ?? ??? ?? ??? ????.
P280 ????/???/???/?????? ?????.
P333+P313 ????? ?? ??? ???? ???? ??·??? ????.
NFPA 704
0
2 0

Triflusal C??? ??, ??, ??

??? ??

White to Off-White Solid

??

An analog of Aspirin; inhibits platelet aggregation. Antithrombotic.

Mechanism of action

2-hydroxy-4-trifluoromethylbenzoic acid (HTB), the deacetylated metabolite of triflusal, retains significant antiplatelet activity. Triflusal is rapidly absorbed and metabolized. The area under the concentration–time curve for triflusal is 20.26 mg/L/hour after a 900-mg dose, whereas that for HTB is 42.27 mg/L/hour. Much of the pharmacokinetic data for triflusal activity is associated with HTB. The inhibition of COX, as measured by reduced production of thromboxane B2, is 25% after 2 hours and 85% after 7 days with triflusal, whereas the effects of aspirin on thromboxane B2 is more than 90% reduction after 2 hours and is maintained at this level after 7 days. It would appear that the presence of a 4-trifluoromethyl group also greatly enhances triflusal's ability to inhibit the activation of nuclear factor κB, which in turn regulates the expression of the mRNA of vascular cell adhesion molecule-1 needed for platelet aggregation. In addition, triflusal increases nitric oxide synthesis in neutrophils, which results in an increased vasodilatory potential. Finally, an additional site of action for triflusal/HTB is the inhibition of cAMP phosphodiesterase, leading to increased levels of cAMP. Elevated cAMP levels decrease platelet aggregation through decreased mobilization of calcium. Aspirin and salicylic acid do not significantly increase cAMP levels.

Clinical Use

Triflusal (2-acetoxy-4-trifluoromethyl benzoic acid) is an antiplatelet drug that despite its structural similarity to aspirin exhibits quite different pharmacological and pharmacokinetic properties.

Triflusal ?? ?? ? ???

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Triflusal ?? ??

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Triflusal ?? ??:

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