Wyeth and Zealand Pharma Advance the First Orally Available Gap Junction Modifier into Phase I Clinical Trials
This is the second gap junction modifier developed by Zealand that Wyeth advanced into clinical trials. ZP1609 (GAP-134) has shown pharmacological effects in animal models of both ventricular and atrial arrhythmias, and with its oral formulation, the molecule represents a novel paradigm for the potential chronic prevention of cardiac arrhythmias.
In the heart, gap junctions are responsible for conducting electrical impulses between cells to maintain the heart's normal rhythm. Gap junction modulation is considered a promising and novel mechanism of action for the treatment of cardiovascular disorders.
Zealand Pharma entered into a development and license agreement with Wyeth in 2003 to co-develop gap junction modifiers for the treatment of cardiovascular diseases. In 2004, the collaboration was expanded by an R&D agreement, and in 2005, a third agreement between the two companies was signed. Under the 2005 agreement, Zealand granted Wyeth rights to the unique Zealand compound library for novel compounds with potential gap junction modifying properties. From this library the two companies have identified ZP1609 (GAP-134), a small modified dipeptide, as a potent and selective gap junction modifier with oral bioavailability.
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