Bifeprunox

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Bifeprunox
Systematic (IUPAC) name
7-[4-[(3-Phenylphenyl)methyl]piperazin-1-yl]-3H-benzooxazol-2-one
Identifiers
CAS number  ?
ATC code  ?
PubChem 208951
Chemical data
Formula C24H23N3O2 
Mol. mass 385.458 g/mol
Pharmacokinetic data
Bioavailability  ?
Metabolism  ?
Half life  ?
Excretion  ?
Therapeutic considerations
Pregnancy cat.

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Legal status
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Bifeprunox is a novel atypical antipsychotic agent which, along with SLV313, aripiprazole and SSR-181507 combines minimal D2 receptor agonism with 5-HT receptor agonism.[1]

Bifeprunox has a novel mechanism of action. Conventional antipsychotics are classed into typical and atypical. The typical antipsychotics, such as chlorpromazine and haloperidol are potent D2 receptor antagonists. The atypical antipsychotics started with clozapine, these are classified as multireceptor interacting compounds, acting as an agonist towards 5-HT1A and an antagonist towards D2 receptors among other 5-HT and DA receptors. Bifeprunox and other novel atypical antipsychotics will instead of antagonizing D2 receptors, will act as partial agonists, as well as agonists towards 5-HT1A receptors. [2]

An NDA for Bifeprunox was filed by the US FDA in January, 2007. The FDA rejected the application in August, 2007.[3] In the EU, Bifeprunox is still in Phase III clinical trials.

References

  1. ^ Cuisiat S, Bourdiol N, Lacharme V, Newman-Tancredi A, Colpaert F, Vacher B (2007). "Towards a new generation of potential antipsychotic agents combining D2 and 5-HT1A receptor activities". J. Med. Chem. 50 (4): 865–76. doi:10.1021/jm061180b. PMID 17300168. 
  2. ^ Bardin L, Auclair A, Kleven MS, et al (2007). "Pharmacological profiles in rats of novel antipsychotics with combined dopamine D2/serotonin 5-HT1A activity: comparison with typical and atypical conventional antipsychotics". Behav Pharmacol 18 (2): 103–18. doi:10.1097/FBP.0b013e3280ae6c96. PMID 17351418. 
  3. ^ Wyeth and Solvay say FDA rejects application for antipsychotic drug bifeprunox. Thomson Financial, August 10, 2007.

Wikipedia content modification information:

  • This page was last modified on 30 January 2008, at 03:12.

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