Participants who was one dose Bay 43-9006 Sorafenib of study medication and attended all the data safety of the treatment period, defined as the time of initial exposure to a drug test up to n Chsten performed. All adverse events were of Medical Dictionary for Regulatory activity Th terminology. The incidence of adverse events was calculated and summarized by treatment and organ system. For vital signs, ECG, laboratory safety parameters and summary statistics were calculated by the treatment. Results Participants A total of 28 participants were enrolled in the study. One participant withdrew consent, and 3 participants broke due kardiovaskul Rer events. Twenty-four participants completed the study and were included in the PK analysis. The demographic characteristics of these participants are summarized in Table I. The pharmacokinetic parameters of plasma concentration versus time curves for asenapine, M, N and gluc, in both the absence and presence of valproate, are shown in Figures 1-3. The mean plasma pharmacokinetic parameters are summarized in Table II summarize, t, and the results of the statistical analysis of tests for interactions with other drugs are summarized in Table III. As shown in Figure 1, the plasma concentration profiles asenapine time Similar for both treatments. The mean pharmacokinetic parameters asenapine during43 bpm to treatment A, approximately 3 hours after treatment with asenapine alone. The other was a neutral mediation reflex bradycardia for 8 minutes in the supine position, which was defined as bradycardia with significant reductions in blood pressure and a vasovagal response to treatment B, about 4 hours after treatment with asenapine the day of combined treatment. Descriptive statistical analysis of vital signs, ECG and laboratory parameters showed no clinically significant differences or discrepancies between asenapine asenapine and combined, and valproate. Discussion This study shows that co-administration of valproate on asenapine has no control over exposure to asenapine. The lack of effect of valproate concentration asenapine is compatible with a pharmacokinetic analysis of pooled patients with schizophrenia or bipolar disorder.21 In this analysis, treatment with valproate as a covariate Asenapine exposure potential, but only age included as essential to VER Change asenapine PK .21 Although the concomitant administration of valproate reduces the N-glucuronidation was identified, it had no effect on the exposure of the parent compound asenapine, plasma concentrations of which may need during the simultaneous administration remained stable with valproate. A m Possible explanation Tion for this observation is that asenapine will be extensively degraded in various ways, with the three major axes to be glucuronidation, demethylation, and asenapine hydroxylation.11 metabolism by other pathways k Can therefore compensate for the high content of asenapine from inhibition of glucuronidation. The main metabolic pathways are direct glucuronidation, which in the main Gemcitabine metabolite N asenapine glucuronide, demethylation and N, N desmethyl products asenapine. Other metabolic pathways include hydroxylation to 11-hydroxy and dihydroxy asenapine asenapine 10.11 followed by further conjugation. In this study, only the big s meta.