Vilazodone - CAS 163521-12-8
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CAS 163521-12-8 Vilazodone

Reference Reading

1. Antidepressant–placebo differences in 16 clinical trials over 10 years at a single site: role of baseline severity
Arif Khan & Amritha Bhat & James Faucett & Russell Kolts & Walter A. Brown. Psychopharmacology (2011) 214:961–965
Randomization codes were requested for trials of Food and Drug Administration (FDA)-approved antidepressants, as well as trials of antidepressants that were not ultimately approved by the FDA. We were able to present data from both the antidepressant and placebo arms of all medications that received approval from the FDA, as well as for one compound currently under FDA review (vilazodone). Drug arm data for compounds that were not eventually approved by the FDA remain proprietary to the pharmaceutical company, and therefore, only the placebo arm data from trials of unapproved compounds are presented. Each clinical trial for which we received randomization codes for patient HAM-D17 scores was included in the study.
2. Mechanism of action of the bimodal antidepressant vilazodone: evidence for serotonin1A-receptor-mediated auto-augmentation of extracellular serotonin output
Christoph van Amsterdam & Christoph A. Seyfried. Psychopharmacology (2014) 231:2547–2558
In spite of intensive animal and human research, the medical need for more effective antidepressants remains substantial. A great number of mechanistic approaches including monoaminergic and nonaminergic, e.g., petidergic, glutamatergic, GABAergic, hormonal, and intracellular messenger mechanisms, have been followed (for review, see Adell et al. 2005), with the goal of improving efficacy, onset of therapeutic action and tolerability. Likewise, polypharmacy concepts including at least five compounds combining 5-HT uptake inhibition plus a 5-HT1A component and compounds targeting the 5-HT reuptake transporter site plus four other 5-HT receptor subtypes (Mørk et al. 2012) are being developed. In a recent article (Khan 2009), 24 antidepressant candidates in late clinical stages were identified; among these, only vilazodone has been approved for major depressive disorder (MDD) at this time. In two Phase III clinical trials, the anti-depressant efficacy primary endpoint was statistically significant in favor of vilazodone compared with placebo (Khan et al. 2011; Rickels et al. 2009). According to the “serotonin augmentation” hypothesis of MDD which posits in its simplest guise that a net increase of 5-HT neuronal transmission should relieve depression and that 5-HT receptor desensitization is necessary for the onset of therapeutic action, vilazodone, a dual action molecule, might be a suitable candidate to examine these hypotheses.
3. Experimental Design Approach for Selective Separation of Vilazodone HCl and Its Degradants by LC‑PDA and Characterization of Major Degradants by LC/QTOF–MS/MS
Pradipbhai D. Kalariya • M. V. N. Kumar Talluri • Srinivas Ragampeta. Chromatographia (2014) 77:1299–1313
Vilazodone hydrochloride (VLZ), (5-(4-(4-(5-cyano-1H-indol-3-yl)butyl)piperazin-1-yl)benzofuran-2-carboxamide), is a benzofuran derivative. Vilazodone acts as a selective serotonin reuptake inhibitor (SSRI) and 5-HT1A receptor partial agonist. Therefore, it is used for the treatment of major depressive disorder (MDD) in adults. MDD is a devastating disease that affects patients’ overall health and quality of life. This disease affects subjects throughout their lifetime—those who are single, have a low income, or are unemployed or disabled. In contrast to other SSRIs, VLZ does not cause significant weight gain or decreased sexual function. Vilazodone (Viibryd®) was approved on 21 January 2011 by the Food and Drug Administration (FDA) for the treatment of MDD.
4. The Impact of Psychoactive Drugs on Seizures and Antiepileptic Drugs
Mitra Habibi & Felecia Hart & Jacquelyn Bainbridge. Curr Neurol Neurosci Rep.
Vilazodone Vilazodone is a major substrate of CYP3A4, and a minor substrate of CYP2C19 and CYP2D6 enzymes. It also moderately induces CYP2C19 and weakly inhibits CYP2C8 enzymes. When administered with carbamazepine, the AUC and Cmax at steady state were both decreased by 44.5 % and 40.8 %, respectively. This decrease is likely due to the induction of CYP3A4 by carbamazepine, and when administered with any drug that has the potential to induce CYP3A4, vilazodone doses may need to be increased by as much as 2-fold. Other AEDs that have the potential of decreasing vilazodone concentrations include other enzyme-inducing AEDs such as phenytoin and phenobarbital.