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Budiodarone
Budiodarone (ATI-2042) is an antiarrhythmic agent and chemical analog of amiodarone that is currently being studied in clinical trials. Amiodarone is considered the most effective antiarrhythmic drug available,〔Roy, D. et al. Amiodarone to prevent recurrence of atrial fibrillation. N Engl J Med. 2000;342:913-920〕〔Singh, B.N., et al. Amiodarone versus sotalol for atrial fibrillation. N Engl J Med. 2005;352:1861-1872〕〔Kochiadakis, G.E., et al. Low dose amiodarone and sotalol in the treatment of recurrent, symptomatic atrial fibrillation: a comparative, placebo controlled study. Heart. 2000;84:251-257〕 but its adverse side effects, including hepatic, pulmonary and thyroid toxicity as well as multiple drug interactions,〔Morey, T.E. et al. Structure-activity relationships and electrophysiological effects of short-acting amiodarone homologs in guinea pig isolated heart. J Pharmacol Exp Ther. 2001;297:260-266〕 are discouraging its use. Budiodarone only differs in structure from amiodarone through the presence of a ''sec''-butyl acetate side chain at position 2 of the benzofuran moiety.〔Mason, P.K., DiMarco, P. Advances in Arrhythmia and Electrophysiology. Circulation. 2009;2:588-597〕 This side chain allows for budiodarone to have a shorter half-life in the body than amiodarone (7 hours versus 35–68 days) which allows it to have a faster onset of action and metabolism while still maintaining similar electrophysiological activity.〔 The faster metabolism of budiodarone allows for fewer adverse side effects than amiodarone principally due to decreased levels of toxicity in the body.
==Creation of arrythmias==
Arrhythmias may be caused by changes in ion channel mRNA and protein expression which modify action potential generation through dysfunctional channels and increase the likelihood of inappropriate electrical re-entry (electrical stimulus entering back into the cell to prematurely start the next action potential).〔Bosch, R.F., Nattel, S. Cellular electrophysiology of atrial fibrillation. Cardiovasc Res. 2002;54:259-269〕 The increase in electrical re-entry causes the fibrillation or uncontrolled action potential discord of atrial myocytes. Arrhythmias have historically been treated using atrial ablation or antiarrhythmic drugs to decrease electrical re-entry and therefore fibrillation.
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