Terutroban

Last updated
Terutroban
Terutroban acid skeletal.svg
Clinical data
Routes of
administration
Oral
ATC code
  • none
Legal status
Legal status
  • Investigational
Pharmacokinetic data
Elimination half-life 6–10 hours
Identifiers
  • 3-((6R)-6-{[(4-Chlorophenyl)sulfonyl]amido}-2-methyl-5,6,7,8-tetrahydronaphthalen-1-yl]propanoic acid
CAS Number
PubChem CID
ChemSpider
UNII
ECHA InfoCard 100.107.361 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C20H22ClNO4S
Molar mass 407.91 g·mol−1
3D model (JSmol)
  • CC1=C(C2=C(CC(CC2)NS(=O)(=O)C3=CC=C(C=C3)Cl)C=C1)CCC(=O)O
  • InChI=1S/C20H22ClNO4S/c1-13-2-3-14-12-16(6-9-19(14)18(13)10-11-20(23)24)22-27(25,26)17-7-4-15(21)5-8-17/h2-5,7-8,16,22H,6,9-12H2,1H3,(H,23,24)/t16-/m1/s1 X mark.svgN
  • Key:HWEOXFSBSQIWSY-MRXNPFEDSA-N X mark.svgN
 X mark.svgNYes check.svgY  (what is this?)    (verify)

Terutroban is an antiplatelet agent developed by Servier Laboratories. It is a selective thromboxane prostanoid (TP) antagonist and is an orally active drug in clinical development for the secondary prevention of acute thrombotic complications. [1]

It has been tested in the Phase III clinical trial PERFORM (Prevention of cerebrovascular and cardiovascular Events of ischemic origin with teRutroban in patients with a history oF ischemic strOke or tRansient ischeMic attack). [2] The study was prematurely stopped and it could not be determined whether terutroban has a better effect than aspirin. The 2011 clinical trial that studied the antiplatelet agent versus aspirin found that it was not superior in the prevention of cerebral and cardiovascular ischaemic events, although it was significantly better in patients who already suffered previous stroke to the qualifying event. [3]

Researchers from the University of Milan also found in a new research that terutroban can prevent the development of aorta hyperplasia and has beneficial effects on fibrotic processes, leading to the conclusion that it has beneficial effects in preventing or retarding atherogenesis. [4]

Method of action

Aside from its anti-inflammatory effect, terutroban is a selective antagonist of the thromboxane receptor. It blocks thromboxane induced platelet aggregation and vasoconstriction. [5] [6]

Related Research Articles

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A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. TIA causes the same symptoms associated with strokes, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.

An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in the arterial circulation where anticoagulants have little effect.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

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<span class="mw-page-title-main">Thromboxane</span>

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Anterior cerebral artery syndrome is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum.

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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 derivative of acetylsalicylic acid (ASA) in which a hydrogen atom on the benzene ring has been replaced by a trifluromethyl group. Trade names include Disgren, Grendis, Aflen and Triflux.

<span class="mw-page-title-main">Mechanism of action of aspirin</span>

Aspirin causes several different effects in the body, mainly the reduction of inflammation, analgesia, the prevention of clotting, and the reduction of fever. Much of this is believed to be due to decreased production of prostaglandins and TXA2. Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme. This makes aspirin different from other NSAIDs, which are reversible inhibitors. However, other effects of aspirin, such as uncoupling oxidative phosphorylation in mitochondria, and the modulation of signaling through NF-κB, are also being investigated. Some of its effects are like those of salicylic acid, which is not an acetylating agent.

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<span class="mw-page-title-main">Lubeluzole</span> Chemical compound

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<span class="mw-page-title-main">Ticagrelor</span> Coronary medication

Ticagrelor, sold under the brand name Brilinta among others, is a medication used for the prevention of stroke, heart attack and other events in people with acute coronary syndrome, meaning problems with blood supply in the coronary arteries. It acts as a platelet aggregation inhibitor by antagonising the P2Y12 receptor. The drug is produced by AstraZeneca.

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References

  1. Waksman R, Gurbel P, Gaglia M (2014). Antiplatelet Therapy in Cardiovascular Disease. Hoboken, NJ: John Wiley & Sons. ISBN   9781118494028.
  2. Hennerici MG, Bots ML, Ford I, Laurent S, Touboul PJ (April 2010). "Rationale, design and population baseline characteristics of the PERFORM vascular project: an ancillary study of the Prevention of cerebrovascular and cardiovascular Events of ischemic origin with teRutroban in patients with a history oF ischemic strOke or tRansient ischeMic attack (PERFORM) trial". Cardiovascular Drugs and Therapy. 24 (2): 175–80. doi:10.1007/s10557-010-6231-2. PMC   2887499 . PMID   20490906.
  3. Hennerici M, Binder J, Szabo K, Kern R (2012). Stroke. Oxford, UK: Oxford University Press. p. 155. ISBN   9780199582808.
  4. Acton A (2012). Advances in Prostaglandins E Research and Application. Atlanta, GA: Scholarly Editions. p. 8. ISBN   9781481640084.{{cite book}}: CS1 maint: date and year (link)
  5. Spreitzer H (January 29, 2007). "Neue Wirkstoffe - Terutroban". Österreichische Apothekerzeitung (in German) (3/2007): 116.
  6. Sorbera LA, Serradell, N, Bolos, J, Bayes, M (2006). "Terutroban sodium". Drugs of the Future. 31 (10): 867–873. doi:10.1358/dof.2006.031.10.1038241.