(+)-Cevimeline hydrochloride hemihydrate ((+)-SNI-2011), a potent muscarinic receptor agonist, stands as a promising therapeutic candidate for treating xerostomia in Sjogren's syndrome. This compound has demonstrated a broad pharmacological profile across various systems including gastrointestinal, urinary, and reproductive, in animal models such as mice, rats, guinea pigs, rabbits, and dogs. Its metabolism was assessed in vitro using rat and dog liver microsomes, revealing that (+)-SNI-2011 is rapidly absorbed with peak plasma concentrations (Cmax) reached within one hour post-oral administration, followed by a decline with a half-life (t1/2) ranging from 0.4 to 1.1 hours. Bioavailability was recorded at 50% in rats and 30% in dogs. Metabolic analysis indicated species-specific differences, with rats producing both S- and N-oxidized metabolites and dogs only producing N-oxidized metabolites. Additionally, sex-based differences in pharmacokinetics were observed in rats but not in dogs. The in vitro study highlighted the involvement of cytochrome P450 (CYP) and flavin-containing monooxygenase (FMO) in the sulfoxidation and N-oxidation of SNI-2011, respectively, with CYP2D and CYP3A being primarily responsible for sulfoxidation in rat liver microsomes.