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Neurochem Res. 2017 Sep;42(9):2639-2645. doi: 10.1007/s11064-017-2223-y. Epub 2017 Mar 31.

Senicapoc: Repurposing a Drug to Target Microglia KCa3.1 in Stroke.

Author information

1
Alentis Pharma LLC, 72 Hillside Avenue, Metuchen, NJ, 08840, USA.
2
Department of Neurology, School of Medicine, University of Washington, Seattle, WA, 98195, USA.
3
Neuroinflammation Disease Biology Unit, Lundbeck Research USA Inc., 215 College Rd, Paramus, NJ, 07652, USA.
4
Abbvie, Foundational Neuroscience Center, Cambridge, MA, 02139, USA. thomas.moeller@abbvie.com.

Abstract

Stroke is the leading cause of serious long-term disability and the fifth leading cause of death in the United States. Treatment options for stroke are few in number and limited in efficacy. Neuroinflammation mediated by microglia and infiltrating peripheral immune cells is a major component of stroke pathophysiology. Interfering with the inflammation cascade after stroke holds the promise to modulate stroke outcome. The calcium activated potassium channel KCa3.1 is expressed selectively in the injured CNS by microglia. KCa3.1 function has been implicated in pro-inflammatory activation of microglia and there is recent literature suggesting that this channel is important in the pathophysiology of ischemia/reperfusion (stroke) related brain injury. Here we describe the potential of repurposing Senicapoc, a KCa3.1 inhibitor, to intervene in the inflammation cascade that follows ischemia/reperfusion.

KEYWORDS:

Drug repurposing; Ischemia; Microglia; Neuroinflammation; Stroke

PMID:
28364331
DOI:
10.1007/s11064-017-2223-y
[Indexed for MEDLINE]

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