Addex Therapeutics announced publication of new preclinical research demonstrating that ADX71743, a selective negative allosteric modulator (NAM) of metabotropic glutamate receptor 7 (mGlu7), significantly modulates sleep-wake regulation and stress-related neurochemistry in animal models. The data, published in the International Journal of Neuropsychopharmacology, expands the growing body of evidence supporting mGlu7 as an important mechanism regulating key brain functions and a promising therapeutic target across a range of central nervous system disorders, including mood disorders, anxiety disorders, post-traumatic stress disorder (PTSD), and other conditions associated with dysregulated stress responses.
“This publication demonstrating the role of mGlu7 modulation in sleep and wakefulness adds another important piece of evidence supporting the therapeutic potential of targeting these receptors with allosteric modulation,” said Tim Dyer, CEO at Addex. “ADX71743 has consistently helped establish the biological role of mGlu7 across multiple disease-relevant models, and we are pleased to see this body of work continue to strengthen the scientific rationale for Neurosterix’s ongoing development of this exciting target.”
In the study, ADX71743 increased wakefulness while reducing both REM and non-REM sleep in rats. The compound also altered stress-induced changes in key neurotransmitters, including glutamate, GABA and monoamines, across multiple brain regions in awake animals, producing neurochemical effects consistent with modulation of stress-responsive neural circuits. Together, these findings further validate the pharmacological profile of selective mGlu7 inhibition in vivo and provide additional support for the therapeutic potential of this novel mechanism.
Previous studies have demonstrated that selective mGlu7 inhibition can modulate anxiety-related behaviours, disrupt maladaptive fear memory reconsolidation and influence glutamatergic signalling in both rodent and human brain tissue.
Source: Addex Therapeutics
