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Clinical Data, Inc is a pharmaceutical company.It has developed an antidepressant called vilazodone and marketed it as Viibryd.Clinical Data was acquired by Forest Laboratories on April 14, 2011. Wikipedia.

Maas J.E.,Medical College of Wisconsin | Wan T.C.,Medical College of Wisconsin | Figler R.A.,Clinical Data Inc. | Gross G.J.,Medical College of Wisconsin | Auchampach J.A.,Medical College of Wisconsin
Journal of Molecular and Cellular Cardiology | Year: 2010

Ischemic preconditioning (IPC) is a protective phenomenon in which brief ischemia renders the myocardium resistant to subsequent ischemic insults. Here, we used A2BAR gene knock-out (A2BKO)/β-galactosidase reporter gene knock-in mice and the A2BAR antagonist ATL-801 to investigate the potential involvement of the A2BAR in IPC, focusing on the acute phase of protection. Cardioprotection provided by acute IPC elicited by two 3-min occlusion/3-min reperfusion cycles was readily apparent in an isolated, Langendorff-perfused mouse heart model in studies using hearts from A2BKO mice. IPC equivalently improved the recovery of contractile function following 20min of global ischemia and 45min of reperfusion in both WT and A2BKO hearts by ~30-40%, and equivalently decreased the release of cardiac troponin I during the reperfusion period (from 5969±925 to 1595±674ng/g and 4376±739 to 2278±462ng/g using WT and A2BKO hearts, respectively). Similarly, the infarct size-reducing capacity of acute IPC in an in vivo model of infarction was fully manifested in experiments using A2BKO mice, as well as in experiments using rats pretreated with ATL-801. We did observe, however, a marked reduction in infarct size in rats following administration of the selective A2BAR agonist BAY 60-6583 (~25% reduction at a dose of 1.0mg/kg). While supportive of its concept as a cardioprotective receptor, these experiments indicate that the mechanism of the early phase of IPC is not dependent on signaling by the A2BAR. We present the idea that the A2BAR may contribute to the later stages of IPC dependent on the induction of stress-responsive genes. © 2010 Elsevier Ltd.

Pierz K.A.,Clinical Data Inc. | Thase M.E.,University of Pennsylvania
Primary Care Companion to the Journal of Clinical Psychiatry | Year: 2014

Objective: To review the mechanism of selective serotonin reuptake inhibitor (SSRI)-mediated serotonergic neurotransmission, focusing on serotonin 1A (5-HT1A) autoreceptors, which are proposed to be involved in delaying therapeutic efficacy. Vilazodone was specifically designed to function both as an SSRI and a partial agonist at 5-HT1A receptors. This combined mechanism is proposed to decrease time to efficacy, minimize sexual side effects, and provide concomitant anxiolytic properties. Data Sources: A PubMed search of all English-language articles from January 1990 to January 2013 was conducted using the search termsdepression and 5-HT1A, depressionand buspirone, depression andpindolol, and vilazodone. Study Selection: We found 47 articles and abstracts that were selected for inclusion on the basis of information about the pharmacology of 5-HT1A receptors and the clinical data on pindolol, buspirone, and vilazodone in depression. Data Extraction: This review summarizes current literature involving antidepressant activity, the role of 5-HT1A autoreceptors, and clinical trials involving serotonin reuptake inhibition in conjunction with 5-HT1A agonists and partial agonists, with a focus on vilazodone. Results: Vilazodone has demonstrated efficacy in 2 large, randomized, double-blind, placebo-controlled trials in major depressive disorder. Results suggest that vilazodone has a low incidence of sexual side effects and is effective in patients with high levels of anxiety. A pooled analysis shows evidence of significant symptom reduction after only 1 week of therapy. Conclusions: If future studies corroborate the clinical benefits attributed to its mechanism of action, vilazodone may show potential advantages in terms of onset of action, sexual side effects, and anxiolytic activity in patients with major depressive disorder. © 2014 Physicians Postgraduate Press, Inc.

Callis T.E.,Clinical Data Inc. | Jensen B.C.,University of North Carolina at Chapel Hill | Weck K.E.,University of North Carolina at Chapel Hill | Willis M.S.,University of North Carolina at Chapel Hill
Expert Review of Molecular Diagnostics | Year: 2010

Cardiomyopathies are an important and heterogeneous group of common cardiac diseases. An increasing number of cardiomyopathies are now recognized to have familial forms, which result from single-gene mutations that render a Mendelian inheritance pattern, including hypertrophic cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and left ventricular noncompaction cardiomyopathy. Recently, clinical genetic tests for familial cardiomyopathies have become available for clinicians evaluating and treating patients with these diseases, making it necessary to understand the current progress and challenges in cardiomyopathy genetics and diagnostics. In this review, we summarize the genetic basis of selected cardiomyopathies, describe the clinical utility of genetic testing for cardiomyopathies and outline the current challenges and emerging developments. © 2010 Expert Reviews Ltd.

Edwards J.,Forest Research Institute | Sperry V.,Forest Research Institute | Sperry V.,PGxHealth LLC | Adams M.H.,MH Adams and Associates Inc. | And 5 more authors.
International Journal of Clinical Pharmacology and Therapeutics | Year: 2013

Objective: Vilazodone is a potent serotonin reuptake inhibitor and 5-HT1A receptor partial agonist approved for the treatment of major depressive disorder (MDD) in adults. The effect of clinical and supratherapeutic doses of vilazodone on cardiac repolarization was determined in healthy volunteers. Methods: In this Phase 1, randomized, doubleblind, placebo- and active-controlled, 3-arm, parallel, single-center study, healthy subjects received placebo; moxifloxacin 400 mg; or vilazodone (sequentially escalated every 3 days) 10, 20, 40, 60, and 80 mg/day. The primary endpoint was the time-matched change from baseline in the QT interval corrected for heart rate (QTc) using an individual correction method (QTcI). Results: Placebo-corrected time-matched analysis of the QTcI duration for the vilazodone treatment effect indicated that no vilazodone dose had an upper bound that approached or exceeded 10 ms, demonstrating no signal for a significant vilazodone effect on cardiac repolarization. Vilazodone had no significant effect on heart rate, PR, or QRS interval duration. The pharmacokinetic/ pharmacodynamic model showed that the QTcI slope for vilazodone was not different from 0.0 and that the predicted increase from baseline in the QTc at Cmax for the highest therapeutic dose (156 ng/ml after 40 mg/day) was < 1 ms. The incidence of adverse events (AEs) was higher in the vilazodone group (57.6%) than in the moxifloxacin (37.0%) and placebo (35.6%) groups, though AEs were generally mild to moderate in severity and resulted in few discontinuations. Conclusions: Vilazodone had no significant effect on cardiac repolarization, heart rate, PR or QRS interval duration, or ECG morphology in healthy adult participants. ©2013 Dustri-Verlag Dr. K. Feistle.

Elitech Group, VITAL DIAGNOSTICS HOLDING Corporation, Vital Inc and Clinical Data Inc. | Date: 2007-07-17

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