04 ng/mL and 76.09 ng·h/mL for the Cmax and AUC∞, respectively, of risperidone, and 11.02 ng/mL and 246.02 ng·h/mL for the Cmax and AUC∞, respectively, of 9-hydroxy-risperidone [11]. In the present study, the Cmax values (15.78 and 11.69 ng/mL for risperidone and 9-hydroxy-risperidone, respectively) and the AUC∞ values (97.89 and 332.55 ng·h/mL for risperidone and

9-hydroxy-risperidone, respectively) were both higher than those reported RXDX-106 ic50 by Cánovas et al. [11] In another randomized, open-label, two-way crossover study by van Schaick et al. [10], 37 healthy volunteers of both sexes were administered a single dose of two 0.5 mg tablets of risperidone, with the last sample collection point being 96 hours after administration. For the parent drug, risperidone, the reported Cmax was 9.3 ng/mL (18.6 ng/mL as normalized to a 2 mg dose), the tmax was 1.2 hours, and the t½ was 3.6 hours. In our study, the Cmax (14.66 ng/mL), tmax (1.09 hours), and t½ (4.94 hours) of risperidone

were all numerically lower than those reported by Schaick et al. Although the differences between the values reported in the present study and those reported in the aforementioned studies may represent a race effect, the previously reported studies did not specify the races of their subjects. On the other hand, pharmacogenetic variables may also be involved. As mentioned previously, CYP2D6 is the major enzyme responsible for the metabolism of risperidone www.selleckchem.com/products/PLX-4032.html [8]. Thus, genetic polymorphism or other gene variations may have influenced the pharmacokinetics and bioavailability of risperidone in our population. In accordance with the FDA guidelines [20], our study was designed to administer a single dose of each formulation, with a 2-week washout period between Amobarbital the two treatments. The individual t½ values of the parent drug, risperidone, and the active metabolite, 9-hydroxy-risperidone, ranged from 1.97 to 12.59 hours and from 15.98 to 33.62 hours, respectively, so the 2-week washout period was sufficient to clear the residual compound from the previous period, which represents undetectable plasma concentrations at baseline

of the second period in all subjects. All AEs that occurred were expected events in healthy subjects [9]. There were no significant differences in the incidence of AEs between the test and the reference formulations, and there were no serious AEs with either formulation. Like any clinical trial, the current study had several limitations that should be considered. Because the data were obtained only from healthy men who were administered a single dose, and the participants were studied only in the fasted state, the pharmacokinetic characteristic of risperidone might differ in target populations. These formulations are yet to be tested in patients with schizophrenia and other psychiatric illnesses. A larger study including subjects in the fed state is also necessary.