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Alcobra Ltd.
(the "Company"), an emerging biopharmaceutical company primarily focused on
the development and commercialization of its proprietary drug, MG01CI
(Metadoxine extended-release), to treat cognitive dysfunctions, such as ADHD
and Fragile X Syndrome, announced today the results from a series of
preclinical studies that evaluated the mechanism of action of MG01CI. MG01CI
is composed of a dual-release formulation of Metadoxine that provides
immediate as well as extended-release formulations in a single oral dose.
"These studies shed important light on the novel mechanism of action and the
unique effects that MG01CI may have in treating cognitive dysfunctions,"
commented Dr. Yaron Daniely, President and CEO of Alcobra Ltd. "MG01CI appears
to enhance the ability of cells to correct abnormal signaling pathways that
may be involved with cognitive impairment, while not increasing levels of
neurotransmitters in the brain such as dopamine, norepinephrine and serotonin.
We believe these findings might account for the improved effect on attention
as well as the favorable tolerability profile that we have observed thus far
in clinical trials with MG01CI."
The studies showed that Metadoxine is a selective antagonist to the 5-HT2B
receptor, a member of the serotonin receptor family. Importantly, Metadoxine
did not show any binding to other serotonin receptors, and did not bind the
characterized targets of existing stimulant and non-stimulant medications
(dopamine and norepinephrine receptors and transporters). In accordance with
these findings, Metadoxine did not affect the concentration of these
neurotransmitters or their metabolites in the brain.
Metadoxine treatment affected several specific molecular targets residing
inside the cell in a dose-dependent manner, including critical signaling
modulators such as the proteins Akt and Extracellular signal-related Kinase
(ERK), but did not affect other targets such as cyclic AMP (cAMP) and Protein
Kinase A (PKA). In a preclinical Fragile X disease model, elevated levels of
Akt and ERK were normalized (reduced) by Metadoxine, while levels of the GST
protein were increased. Electrophysiological studies also showed that
Metadoxine caused a dose-dependent, reversible reduction in glutamatergic
excitatory transmission and enhancement of GABAergic inhibitory transmission,
changes that may be associated with cognitive regulation.
"Our findings to date suggest a distinct mechanism of action for Metadoxine in
treating cognitive disorders such as ADHD and Fragile X Syndrome," added Dr.
Jonathan Rubin, Chief Medical Officer of Alcobra Ltd. "We are eager to move
forward with additional clinical trials in these populations as we learn more
about the differentiated characteristics of our product."
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