 |
Template documentationTo transclude this template, use:
{{ Bicalutamide metabolism | caption = | align = }}
- Optional parameters
- The parameter
| caption =may be used to add an image caption. - The parameter
| align =may be set as left, right, or center. Center is the default image alignment when this parameter is not set as one of the two alternatives (i.e., left or right).
The image's
alternative text (i.e., the |alt= parameter) is "Graphic of bicalutamide metabolism in humans". The alt parameter can't be changed when transcluding this template.
- Reflist for template header
References
-
^ Cockshott ID (2004). "Bicalutamide: clinical pharmacokinetics and metabolism". Clinical Pharmacokinetics. 43 (13): 855–878.
doi:
10.2165/00003088-200443130-00003.
PMID
15509184.
S2CID
29912565.
These data indicate that direct glucuronidation is the main metabolic pathway for the rapidly cleared (S)-bicalutamide, whereas hydroxylation followed by glucuronidation is a major metabolic pathway for the slowly cleared (R)-bicalutamide.
- ^ Grosse L, Campeau AS, Caron S, Morin FA, Meunier K, Trottier J, Caron P, Verreault M, Barbier O (August 2013). "Enantiomer selective glucuronidation of the non-steroidal pure anti-androgen bicalutamide by human liver and kidney: role of the human UDP-glucuronosyltransferase (UGT)1A9 enzyme". Basic & Clinical Pharmacology & Toxicology. 113 (2): 92–102. doi: 10.1111/bcpt.12071. PMC 3815647. PMID 23527766.