Potassium channel blockers and openers as CNS neurologic therapeutic agents
Potassium (K+) channels are the most heterogeneous and widely distributed class of ion channels. K+ channels are dynamic pore-forming transmembrane proteins known to play important roles in all cell types underlying both normal and pathophysiological functions. Essential for such diverse physiological processes as nerve impulse propagation, muscle contraction, cellular activation and the secretion of biologically active molecules, various K+ channels are recognized as potential therapeutic targets in the treatment of multiple sclerosis, Alzheimer's disease, Parkinson's disease, epilepsy, stroke, brain tumors, brain/spinal cord ischemia, pain and schizophrenia, migraine, as well as cardiac arrhythmias, pulmonary hypertension, diabetes, cervical cancer, urological diseases and sepsis. In addition to their importance as therapeutic targets, certain K+ channels are gaining attention for their beneficial roles in anesthesia, neuroprotection and cardioprotection. The K+ channel gene families (subdividing into multiple subfamilies) include voltage-gated (Kv: Kv1-Kv12 or KCNA-KCND, KCNF-KCNH, KCNQ, KCNS), calcium-activated (KCa: KCa1-KCa5 or KCNM-KCNN), inwardly rectifying (Kir: Kir1-Kir7 or KCNJ) and background/leak or tandem 2-pore (K2P: K2P1-K2P7, K2P9-K2P10, K2P12-K2P13, K2P15-K2P18 or KCNK) K+ channels. Worldwide, the pharmaceutical industry is actively developing better strategies for targeting ion channels, in general, and K+ channels, in particular, already generating over $6 billion in sales per annum from drugs designed to block or modulate ion channel function. This review provides an overview of recent patents on emerging K+ channel blockers and activators (openers) with potential for development as new and improved nervous system therapeutic agents. Â© 2007 Bentham Science Publishers Ltd.
Recent Patents on CNS Drug Discovery
Judge, S. I. V.; Smith, P. J.; Stewart, Peggy E.; and Bever Jr., C. T., "Potassium channel blockers and openers as CNS neurologic therapeutic agents" (2007). PCOM Scholarly Papers. 1236.
This document is currently not available here.