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BW 619C89

Known as: 619C89, BW-619C89, BW619C89 
National Institutes of Health

Related topics

Related topics

1 relation

Broader (1)

sipatrigine

Papers overview

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2004
2004
Sodium channel blocking activity of AM-36 and sipatrigine (BW619C89): in vitro and in vivo evidence
Highly Cited
2001
Highly Cited
2001
The neuroprotective agent sipatrigine (BW619C89) potently inhibits the human tandem pore-domain K+ channels TREK-1 and TRAAK
2000
2000
Inhibition of recombinant low-voltage-activated Ca2+ channels by the neuroprotective agent BW619C89 (Sipatrigine)
1999
1999
Nitric oxide stimulates cGMP formation in rat optic nerve axons, providing a specific marker of axon viability
A major transduction pathway for nitric oxide (NO) is stimulation of soluble guanylyl cyclase and the generation of cyclic GMP… 
1999
1999
Parallel dose-response studies of the voltage-dependent Na+ channel antagonist BW619C89, and the voltage-dependent Ca2+ channel antagonist nimodipine, in rat transient focal cerebral ischaemia.
1998
1998
On the inhibition of voltage activated calcium currents in rat cortical neurones by the neuroprotective agent 619C89
1 The lamotrigine analogue 619C89, utilised to reduce postischaemic and posttraumatic neuronal injury, has been shown to inhibit… 
Highly Cited
1997
Highly Cited
1997
Long-term beneficial effects of BW619C89 on neurological deficit, cognitive deficit and brain damage after middle cerebral artery occlusion in the rat
1997
1997
Neuroprotective effects of the glutamate release inhibitor 619C89 in temporary middle cerebral artery occlusion
1997
1997
Inhibition of human N-type voltage-gated Ca2+ channels by the neuroprotective agent BW619C89
1996
1996
A use-dependent sodium channel antagonist, 619C89, in reduction of ischemic brain damage and glutamate release after acute subdural hematoma in the rat.
Acute subdural hematoma kills or disables more severely head injured patients than any other complication of cranial trauma. The… 
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