AlzeCure announced that data from its TrkA and TrkB positive allosteric modulator program for Alzheimer’s disease will be presented at the 17th International Conference on Alzheimer’s Drug Discovery in Jersey City, NJ, USA. The oral presentation will include preclinical in vivo Proof-of-Principle data of AC-1122, an approved drug that is undergoing repurposing for the treatment of Alzheimer’s disease.
The data to be presented support the use of positive allosteric modulators (PAMs) of Trk A and Trk B, enhancing the effects of the endogenous neuronal growth factors NGF and BDNF, for the treatment of Alzheimer’s disease:
• AC-1122 and PAMs from two back-up series reversed memory impairment caused by both cholinergic and glutamatergic deficits in an in vivo animal model at clinically relevant exposure.
• Based upon existing literature and previous clinical trials, we anticipate that the final drug will be a disease modifier with potent cognition enhancing effects.
”We are very excited about these promising data. The program comprises a high degree of innovation in combination with well-validated pathways for neuroprotection and neurorestoration genetically linked to Alzheimer’s disease. We have identified an approved medicine (AC-1122), which show potent cognitive enhancing effects in vivo. Our plan is to repurpose this drug for the treatment of Alzheimer’s disease and to pursue two promising lead optimization-series into preclinical development. By using pre-existing toxicology and safety pharmacology data for AC-1122, both costs and risks are kept at a low level”, said Jonas Ekstrand, PhD, CEO of AlzeCure Foundation.
AlzeCure’s positive allosteric modulators (PAMs):
The drug discovery program is composed of one lead candidate drug and two back-up series of drug-like molecules. Their primary mechanism of action is to enhance the effect of two important neuronal growth factors, NGF and BDNF, by acting as positive allosteric modulators of the receptors TrkA and TrkB. NGF and BDNF both play pivotal and complimentary roles in neurorestoration as well as in synaptic plasticity and cognitive function. Interestingly, BDNF is today the only genetic factor known to moderate downstream effects of amyloid-beta induced neurotoxicity, suggesting that methods to increase BDNF signaling are a unique and viable therapeutic alternative for the treatment of Alzheimer’s disease. It is also envisioned that such a treatment would be an excellent complement to the many different anti-amyloid and tau strategies that are currently in clinical development.