Paul, my knowledge is very limited on this meter and I will tried my best.
NMDA receptors cause the permeability of the neurons membrane for the ions, calcium and sodium. Also this receptors are activated by glutamate. This is normal neuron activity. In stroke glutamate level increase exponentially, and NMDA is overstimulated, causing increase of ions concentration in the neurons-death.
Drug which can deactivate glutamate NMDA receptors-antagonist can prevent and reduce the neuron damage in stroke. AMPA is another receptor which, according to article, is permeable for ions when is not deactivated by GluR2 protein (glutamate containing active protein). Gene which express this protein is deactivated by influx of calcium ions in neurons membrane-NMDA receptors. It means that NMDA receptor and AMPA receptor permeability is controlled by NMDA glutamate receptor.
Crerestat is non-competitive NMDA antagonist-it did not compete with glutamate for receptor site on neurons membrane. Instead it deactivate neurons membrane permeability by interacting on other membrane site. Also, by nature, Cerestat can be AMPA deactivator, but take this with big grain of salt. In article is stated that natural acidity in the brain turns NMDA receptors of within minutes. Personally, I think that this acidity control is competing with glutamate, reversible reaction, and in elevated glutamate concentration acidity does not work. But, I will strongly suggest that you and others discuss this with professionals.
Because the potent AMPA receptor antagonist is far away from clinic, Cerestat, if show positive clinical results, will be successful drug for stroke, and big PLUS for CNSI. As the PIII trials are ongoing, interim check is probably OK, otherwise the trials will be stopped, the stock price will volute. We can expect some up-movement in near future as pressure rise.
mz |
