Bosentan

Bosentan
Clinical data
Trade names Tracleer
AHFS/Drugs.com Monograph
MedlinePlus a605001
Pregnancy
category
  • X
Routes of
administration		 Oral
ATC code C02KX01 (WHO)
Legal status
Legal status
  • ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 50%
Protein binding >98%
Metabolism Hepatic
Biological half-life 5 hours
Identifiers
CAS Number 147536-97-8 YesY
PubChem (CID) 104865
IUPHAR/BPS 3494
DrugBank DB00559 YesY
ChemSpider 94651 YesY
UNII XUL93R30K2 YesY
KEGG D01227 N
ChEBI CHEBI:51450 YesY
ChEMBL CHEMBL957 YesY
ECHA InfoCard 100.171.206
Chemical and physical data
Formula C27H29N5O6S
Molar mass 551.614 g/mol
3D model (Jmol) Interactive image
 NYesY (what is this?)  (verify)

Bosentan is a dual endothelin receptor antagonist used in the treatment of pulmonary artery hypertension (PAH). It is licensed in the United States, the European Union and other countries by Actelion Pharmaceuticals for the management of PAH under the trade name Tracleer.

Medical uses

Bosentan is indicated mainly for the treatment of pulmonary hypertension. In 2007, Bosentan was also approved in the European Union for reducing the number of new digital ulcers in patients with systemic sclerosis and ongoing digital ulcer disease.

In the United States, Bosentan is indicated for the treatment of pulmonary arterial hypertension (WHO Group I) in patients with WHO Class II-IV symptoms, to improve exercise capacity and decrease the rate of clinical worsening.[1]

Side effects

Due to potential hepatotoxicity, the FDA requires monthly monitoring of liver function tests while taking Bosentan.

Bosentan use requires hematocrit monitoring due to potential onset of anemia.[2]

Hormone-based contraception is not possible in women taking Bosentan, due to a pharmacokinetic interaction.[3] Therefore, other highly reliable forms of contraception should be used instead.

Bosentan is contraindicated in pregnancy because of its teratogenicity (Pregnancy Category X).[4][5]

Mechanism of action

Bosentan is a competitive antagonist of endothelin-1 at the endothelin-A (ET-A) and endothelin-B (ET-B) receptors. Under normal conditions, endothelin-1 binding of ET-A or ET-B receptors causes constriction of the pulmonary blood vessels. By blocking this interaction, bosentan decreases pulmonary vascular resistance. Bosentan has a slightly higher affinity for ET-A than ET-B.[6]

See also

References

  1. ↑ http://www.tracleer.com/pdf/09%20276%2001%2000%200809_Tra%20PI_4%20Pg_081409pdf.pdf
  2. ↑ http://www.ionchannels.org/showabstract.php?pmid=15875338
  3. ↑ http://www.ionchannels.org/showabstract.php?pmid=15875338
  4. ↑ http://www.medicinescomplete.com/mc/bnf/current/PHP1044-bosentan.htm?q=bosentan&t=search&ss=text&p=1#_hit
  5. ↑ http://www.nzf.org.nz/nzf_1183.html
  6. ↑ Funke C, Farr M, Werner B, Dittmann S, Uberla K, Piper C, Niehaus K, Horstkotte D (Apr 2010). "Antiviral effect of Bosentan and Valsartan during coxsackievirus B3 infection of human endothelial cells.". Journal of General Virology. 91 (8): 1959–1570. doi:10.1099/vir.0.020065-0. PMID 20392896.
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