Key result
Oral gap-junction modifier GAP-134 shows potent activity in a mouse cardiac conduction block model.
Why the study?
Small molecule gap-junction modifiers with improved physical properties compared to rotigaptide were needed for the treatment of atrial fibrillation.
GAP-134 was identified as a potent, orally active gap-junction modifier with potential for clinical development in treating atrial fibrillation.
Answers are grounded in this paper and cite their sources.
Supports preclinical development of oral gap-junction modifiers; leaves open translation to human AF trials.
Rotigaptide (3) is an antiarrhythmic peptide that improves cardiac conduction by modifying gap-junction communication. Small molecule gap-junction modifiers with improved physical properties were identified from a Zealand Pharma peptide library using pharmaceutical profiling, established SAR around 3, and a putative pharmacophore model for rotigaptide. Activity of the compounds was confirmed in a mouse cardiac conduction block model of arrhythmia. Dipeptide 9f (GAP-134) was identified as a potent, orally active gap-junction modifier for clinical development.
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Butera et al. (2009) studied Atrial Fibrillation. Dipeptide 9f (GAP-134) was evaluated on Activity in a mouse cardiac conduction block model of arrhythmia. Dipeptide 9f (GAP-134) was identified as a potent, orally active gap-junction modifier with confirmed activity in a mouse cardiac conduction block model of arrhythmia.
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