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EnVivo Pharmaceuticals Research Shows EVP-6124 Acts as Acetylcholine Co-Agonist

November 5, 2010 By Bio-Medicine.Org

WATERTOWN, Mass., Nov. 5, 2010 /PRNewswire/ — EnVivo
Pharmaceuticals today announced it has discovered that EVP-6124,
its alpha-7 nicotinic acetylcholine receptor agonist, possesses a
novel mechanism not previously seen in the scientific community: it
acts as a co-agonist with Acetylcholine (ACh) to enhance
cognition.

By acting as a co-agonist and sensitizing the alpha-7 receptor,
EVP-6124 makes it possible for smaller amounts of naturally
occurring ACh, typically found in individuals with memory disorders
such as Alzheimer’s, to be required to activate the receptor.
 In this scenario, EnVivo’s research demonstrated that memory
deficits can be minimized or entirely reversed by controlling the
neuronal channel with EVP-6124 alone or in combination with other
Alzheimer’s drugs.

“This is groundbreaking research in terms of understanding how
the alpha-7 receptor operates in conjunction with EVP-6124,” said
Kees Been, president and CEO of EnVivo.  “The potential, as
evidenced in our studies, is significant for how we look at and
approach the treatment of Alzheimer’s disease.”

EnVivo simulated physiologically relevant brain conditions in
vitro
and alpha-7 receptor action was measured in response to
ACh in the presence of low EVP-6124 concentrations.  At drug
concentrations resulting in pro-cognitive effects in in vivo
studies, EVP-6124 appeared to significantly increase the alpha-7
receptor response to ACh.  This suggests that at low
concentrations, EVP-6124 acts as a co-agonist and sensitizes the
alpha-7 receptor to its natural response to ACh, but does not
desensitize the receptor.  This co-agonist mechanism of action
was supported by testing the combined effect of sub-threshold doses
of both EVP-6124 and donepezil (Aricept) on the memory deficit in a
rat model.  While each drug alone at these very low doses had
no effect on reversing the deficit, dosing the two agents together
completely restored the

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SOURCE

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