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2008
27 November 2008: Announcement no. 3, 2008: Zealand Pharma and Helsinn Healthcare S...
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Product Pipeline
Zealand's Pipeline comprises 1 compound in phase III, 1 compound in phase II, 2 c...
GAP-134/ZP1609
GAP-134/ZP1609, a small modified dipeptide, has been identified as a potent and selective second generation gap junction modifier with oral bioavailability.
Gap-junctions are specialized pores that ensure the coordinated transmission of electrical impulses from cell to cell across the heart. This spreading is essential for synchronized contraction of the heart. During a heart attack (acute myocardial infarction) or during chronic heart disease gap-junction pores close, which inhibit spreading of electrical impulses. As a result, electrical impulses take atypical routes which may lead to irregular heart beats, or arrhythmias, and death. Using pre-clinical animal models, we demonstrated that our first generation gap junction modifier rotigaptide specifically inhibits the re-entry arrhythmia mechanism by normalizing the electrical conduction in the heart and preventing life-threatening arrhythmias during these conditions.
From a unique Zealand compound library for novel compounds with potential gap junction modifying properties Wyeth and Zealand have identified GAP-134/ZP1609, a small modified dipeptide, as a potent and selective second generation gap junction modifier with oral bioavailability. Following identification of this orally available gap junction modifier, further development of rotigaptide was stopped.
GAP-134/ZP1609 prevents postoperative AF and chronic AF in large animal models. In a canine model of acute sterile pericarditis, GAP-134/ZP1609 significantly reduced AF duration and overall AF burden. In a canine model of heart failure, induced by dual chamber simultaneous pacing of the right atria and right ventricle, GAP-134/ZP1609 significantly reduced mean AF duration, number of AF episodes and inducibility. This canine heart failure model is designed to mimic patients in the early stages of heart failure presenting with AF requiring cardioversion and chronic maintenance of sinus rhythm therapy.
GAP-134/ZP1609 may provide a safe and well-tolerated treatment option for atrial fibrillation patients with or without structural heart disease or heart failure, for whom the long-term maintenance of normal sinus rhythm is the strategy of choice thereby providing patients an improved quality of life.
In October, Wyeth advanced this first orally available gap junction modifier GAP-134/ZP1609 into phase I clinical trials in the US. With its oral formulation, this molecule represents a novel paradigm for the potential chronic prevention of both atrial and ventricular cardiac arrhythmias.
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