• Sanofi-Aventis, 2005-2033, EFC5555: A Placebo-Controlled, Double-Blind, Parallel Arm Trial to Assess the Efficacy of Dronedarone 400 Mg BID for the Prevention of Cardiovascular Hospitalization or Death From any Cause in Patients with AF/AFL (Athena)
• Research Pharmaceutical Services, Inc., 2001-2028, 20000038-A Six-Month, Multicenter, Double-Blind, Placebo-Controlled, Parallel-Group Design Clinical Study to Assess the Efficacy and Safety of a 125 Mg Daily Oral Dose of Azimilide Dihydrochloride for the Treatment
• Kendle International, Inc., 2007-2034, A Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Trial to Assess the Efficacy and Safety of Omacor for the Prevention of Recurrent, Symptomatic Atrial Fibrillation

• 7,012,082 - Method of correcting HERG channel dysfunction, granted Mar 2006.

• "Coexistence of hERG current block and disruption of protein trafficking in ketoconazole-induced long QT syndrome"

Takemasa H, Nagatomo T, Abe H, et al., Brit J Pharmacol 153 (3): 439-447 Feb 2008. These data show that ketoconazole, a drug implicated in drug-induced long QT syndrome, also disrupts the trafficking of the HERG potassium channel.

• "Human embryonic stem cell-derived cardiomyocytes: drug discovery and safety pharmacology"

He J-Q, January CT, Thomson JA, et al., Expert Opin Drug Discov  2: 1-16 2007. This is a review of the application of human embryonic stem cell-derived cardiomyocytes to drug discovery and safety pharmacology.

• "Kv11.1 (ERG1) K+ channels localize in cholesterol and sphingolipid enriched membranes and are modulated by membrane cholesterol"

Balijepalli RC, Delisle BP, Balijepalli SY, et al., Channels 1 (4): 263-272 Jul-Aug 2007. This manuscript report that HERG channels localize to a specific membrane microdomain and that its function can be modulated by membrane cholesterol.  This work has implications for targetting drugs to membrane microdomains than might alter cellular electrophysiology.

• "Drug-induced long QT syndrome: hERG K+ channel block and disruption of protein trafficking by fluoxetine and norfluoxetine"

Rajamani S, Eckhardt LL, Valdivia CR, et al., Brit J Pharmacol 149: 481-489 2006. These findings show that both fluoxetine and norfluoxetine at similar concentrations selectively reduce IhERG by two mechanisms, (1) direct channel block, and (2) indirectly by disrupting channel protein trafficking. These two effects are not mediated by a single drug binding site. The findings add complexity to understanding the mechanisms that cause drug-induced long QT syndrome.

• Intra-University Collaboration: Physiology, Bioengineering
• University of Occupational and Environmental Health, Internal Medicine, Japan

• Cellular and Molecular Arrhythmia Research Program (CMARP)