Disease relevance of N-Desethyloxybutynin

• Lower N-desethyloxybutynin plasma concentration and greater saliva output during transdermal treatment correspond to the reported low incidence of dry mouth in patients with overactive bladder [1].

High impact information on N-Desethyloxybutynin

• Our results demonstrate that the CYP3A subfamily, and not CYP2D6, is involved in N-desethyloxybutynin formation [2].
• PURPOSE: To characterize the enantiomers of oxybutynin (OXY) and N-desethyloxybutynin (DEO) following transdermal and oral administration [3].
• Pharmacokinetics of the R- and S-enantiomers of oxybutynin and N-desethyloxybutynin following oral and transdermal administration of the racemate in healthy volunteers [3].
• Compared with IR-Oxy, Oxy-XL yielded higher (131% and 158% for the R- and S-isomer, respectively) oxybutynin and lower (62% and 78% for the R- and S-isomer, respectively) desethyloxybutynin bioavailability, suggesting reduced first-pass metabolism [4].
• The AUC, Cmax, tmax, t1/2 and MRT of oxybutynin and its active metabolite N-desethyloxybutynin were determined [5].

Associations of N-Desethyloxybutynin with other chemical compounds

• Oxybutynin is metabolized by oxidation to N-desethyloxybutynin, a stable and toxic metabolite, and previous results in vivo have suggested that cytochrome P450 2D6 (CYP2D6) may be involved in this pathway of metabolism [2].
• Salivary secretion was induced by pilocarpine (0.1 mg/kg, i.v.). Oxybutynin was administered at 15 mg/animal, and the plasma concentrations of oxybutynin and N-desethyloxybutynin were measured by high-performance liquid chromatography to clarify the effective concentration [6].

Gene context of N-Desethyloxybutynin

• Side effects induced by cytochrome P450 metabolism of oxybutynin into the primary metabolite desethyloxybutynin within the gut wall substantially affect the tolerability of the compound within the individual [7].

References