This is the second Zealand-developed gap junction modifier, known as ZP1609 (GAP-134), that Wyeth has advanced into clinical trials. ZP1609 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, according to the companies.
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.