Triflusal: Difference between revisions

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Triflusal
Clinical data
ATC code	B01AC18 (WHO) ;
Identifiers
	IUPAC name 2-acetyloxy-4-(trifluoromethyl)benzoic acid;
PubChem CID	9458;
E number	{{#property:P628}}
ECHA InfoCard	{{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value).
Chemical and physical data
Formula	C10H7F3O4
Molar mass	248.155 g/mol

VisualWikitext

Latest revision as of 18:09, 27 July 2014

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Triflusal is a platelet aggregation inhibitor that was discovered and developed in the Uriach Laboratories, and commercialised in Spain since 1981. Currently, it is available in 25 countries in Europe, Asia, Africa and America. It is a drug of the salicylate family but it is not a derivative of acetylsalicylic acid (ASA). Trade names include Disgren, Grendis, Aflen and Triflux ^[1]

Mechanism of action

Triflusal is a selective platelet antiaggregant through;

blocks cyclooxygenase inhibiting thromboxane A2, preventing aggregation
preserves vascular prostacyclin, thus promoting anti-aggregant effect
blocks phosphodiesterase thereby increasing cAMP concentration, thereby promoting anti-aggregant effect due to inhibition of calcium mobilization

Indication

Triflusal is indicated for;

Prevention of cardiovascular events such as stroke
Acute treatment of cerebral infarction, myocardial infarction
Thromboprophylaxis due to atrial fibrillation

Prevention of Stroke

In the 2008 guidelines for stroke management from the European Stroke Organization, triflusal was for the first time recommended as lone therapy, as an alternative to acetylsalicylic acid plus dipyridamole, or clopidogrel alone for secondary prevention of atherothrombotic stroke. This recommendation was based on the double-blind, randomised TACIP and TAPIRSS trials, which found triflusal to be equally as effective as Aspirin in preventing post-stroke vascular events, while having a more favourable safety profile.^[2]^[3]^[4]

Pharmacokinetics

It is absorbed in the small intestine and its bio-availability ranges from 83% to 100%.^[5]^[6]

References

↑ Murdoch D, et al. Triflusal: a review of its use in cerebral infarction and myocardial infarction, and as thromboprophylaxis in atrial fibrillation.Drugs 2006; 66(5):671-92
↑ Matías-Guiu J, Ferro JM, Alvarez J, et al; for the TACIP Investigators. Comparison of triflusal and aspirin for prevention of vascular events in patients after cerebral infarction. The TACIP study: a randomized, double-blind, multicenter trial. Stroke 2003; 34; 840-848
↑ Culebras A, Rotta-Escalante R, Vila J, et al; and the TAPIRSS investigators. Triflusal vs. aspirin for prevention of cerebral infarction.A randomized stroke study. Neurology. 2004; 62:1073-1080
↑ Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. The European Stroke Organization(ESO) Executive Committee and the ESO Writing Committee.Cerebrovasc Dis. 2008; 25: 57-507
↑ Ramis J, Mis R, Conte L, Forn J. Rat and human plasma protein binding of the main metabolite of triflusal. Eur J Pharmacol.1990; 183: 1867-1868
↑ Ramis J, Mis R, Forn J, Torrent J, Gorina E, Jané F. Pharmacokinetics of triflusal and its main metabolite HTB in healthy subjects following a single oral dose. Eur J Drug Metab Pharmacokinet.1991; 16: 169-273.37,38

[1] Murdoch D, et al. Triflusal: a review of its use in cerebral infarction and myocardial infarction, and as thromboprophylaxis in atrial fibrillation.Drugs 2006; 66(5):671-92

[2] Matías-Guiu J, Ferro JM, Alvarez J, et al; for the TACIP Investigators. Comparison of triflusal and aspirin for prevention of vascular events in patients after cerebral infarction. The TACIP study: a randomized, double-blind, multicenter trial. Stroke 2003; 34; 840-848

[3] Culebras A, Rotta-Escalante R, Vila J, et al; and the TAPIRSS investigators. Triflusal vs. aspirin for prevention of cerebral infarction.A randomized stroke study. Neurology. 2004; 62:1073-1080

[4] Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. The European Stroke Organization(ESO) Executive Committee and the ESO Writing Committee.Cerebrovasc Dis. 2008; 25: 57-507

[5] Ramis J, Mis R, Conte L, Forn J. Rat and human plasma protein binding of the main metabolite of triflusal. Eur J Pharmacol.1990; 183: 1867-1868

[6] Ramis J, Mis R, Forn J, Torrent J, Gorina E, Jané F. Pharmacokinetics of triflusal and its main metabolite HTB in healthy subjects following a single oral dose. Eur J Drug Metab Pharmacokinet.1991; 16: 169-273.37,38

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@@ Line 24: / Line 24: @@
 | routes_of_administration =
 }}
+__NOTOC__
+{{SI}}
+{{CMG}}
+==Overview==
+'''Triflusal''' is a [[platelet aggregation inhibitor]] that was discovered and developed in the Uriach Laboratories, and commercialised in Spain since 1981. Currently, it is available in 25 countries in Europe, Asia, Africa and America. It is a drug of the [[salicylate]] family but it is not a derivative of [[acetylsalicylic acid]] (ASA). Trade names include '''Disgren''', '''Grendis''', '''Aflen''' and '''Triflux''' <ref>Murdoch D, et al. Triflusal: a review of its use in cerebral infarction and myocardial infarction, and as thromboprophylaxis in atrial fibrillation.Drugs 2006; 66(5):671-92</ref>
+==Mechanism of action==
+Triflusal is a selective platelet antiaggregant through;
+* blocks [[cyclooxygenase]] inhibiting [[thromboxane A2]], preventing aggregation
+* preserves vascular [[prostacyclin]], thus promoting anti-aggregant effect
+* blocks [[phosphodiesterase]] thereby increasing [[cyclic AMP|cAMP]] concentration, thereby promoting anti-aggregant effect due to inhibition of calcium mobilization
-{{CMG}}
+==Indication==
+Triflusal is indicated for;
+* Prevention of [[cardiovascular events]] such as stroke
+* Acute treatment of [[cerebral infarction]], [[myocardial infarction]]
+* [[Thromboprophylaxis]] due to [[atrial fibrillation]]
-{{Editor Join}}
+==Prevention of Stroke==
+In the 2008 guidelines for stroke management from the European Stroke Organization, triflusal was for the first time recommended as lone therapy, as an alternative to acetylsalicylic acid plus [[dipyridamole]], or [[clopidogrel]] alone for secondary prevention of [[atherothrombosis|atherothrombotic]] stroke. This recommendation was based on the double-blind, randomised TACIP and TAPIRSS trials, which found triflusal to be equally as effective as Aspirin in preventing post-stroke vascular events, while having a more favourable safety profile.<ref>Matías-Guiu J, Ferro JM, Alvarez J, et al; for the TACIP Investigators. Comparison of triflusal and aspirin for prevention of vascular events in patients after cerebral infarction. The TACIP study: a randomized, double-blind, multicenter trial. Stroke 2003; 34; 840-848</ref><ref>Culebras A, Rotta-Escalante R, Vila J, et al; and the TAPIRSS investigators. Triflusal vs. aspirin for prevention of cerebral infarction.A randomized stroke study. Neurology. 2004; 62:1073-1080</ref><ref>Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. The European Stroke Organization(ESO) Executive Committee and the ESO Writing Committee.Cerebrovasc Dis. 2008; 25: 57-507</ref>
-==Overview==
+==Pharmacokinetics==
-'''Triflusal''' is a platelet aggregation inhibitor.
+It is absorbed in the small intestine and its [[bio-availability]] ranges from 83% to 100%.<ref>Ramis J, Mis R, Conte L, Forn J. Rat and human plasma protein binding of the main metabolite of triflusal. Eur J Pharmacol.1990; 183: 1867-1868</ref><ref>Ramis J, Mis R, Forn J, Torrent J, Gorina E, Jané F. Pharmacokinetics of triflusal and its main metabolite HTB in healthy subjects following a single oral dose. Eur J Drug Metab Pharmacokinet.1991; 16: 169-273.37,38</ref>
+==References==
+{{reflist|2}}
 {{Antithrombotics}}
-[[Category:Benzoic acids]]
+[[Category:Drug]]
-[[Category:Drugs]]
+[[Category:Cardiovascular Drugs]]
-{{WikiDoc Help Menu}}
+[[Category:Antiplatelet drugs]]
-{{WikiDoc Sources}}

Clinical data

ATC code	B01AC18 (WHO)
Identifiers
IUPAC name 2-acetyloxy-4-(trifluoromethyl)benzoic acid
PubChem CID	9458
E number	{{#property:P628}}
ECHA InfoCard	{{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value).
Chemical and physical data
Formula	C₁₀H₇F₃O₄
Molar mass	248.155 g/mol