The molecular architecture of Anavex 2-73, however, very closely (perhaps exactly) matches the binding sites of the sigma-1 receptor proteins in the neuron. It makes a strong molecular connection, a binding fit, to the cellular structures and chemistries that control, chaperone, (among other things) calcium signaling between the endoplasmic reticulum and the mitochondrion.
Is there evidence to support those assertions relative to other known agonists? Why would you make this statement? There is certainly evidence AGAINST a relatively "strong molecular connection".
The molecular architecture of Anavex 2-73, however, very closely (perhaps exactly) matches the binding sites of the sigma-1 receptor proteins in the neuron. It makes a strong molecular connection, a binding fit, to the cellular structures and chemistries that control, chaperone, (among other things) calcium signaling between the endoplasmic reticulum and the mitochondrion.
In short, the sigma-1 receptor effects of Aricept are minor and incidental. For Anavex 2-73, they are direct and firm; because of its favorable (dare I say, unique) molecular architecture. A shriveled apple/sweet orange comparison.
It seems there is interest in exactly what you mean by "strong molecular connection". Most chemists would consider that the binding affinity but some are taking it as agonist effect. Either way we'd certainly like to hear the evidence you have for such an action.
We'd also like to hear about the evidence for relative cellular structures and finally and most importantly evidence that allows you to declare DZP's receptor effects as "minor and incidental" while 2-73's are "direct and firm". These are spectacular assertions and MANY on this board would like to be able to evaluate the evidence you must have to make such statements.