Our Approach

Alzheimer’s
Disease

Today, no disease-modifying therapy for AD is available. The hypothesis that amyloid-β peptide plays an early causative role in disease progression is supported by pathology, human genetics and biomarker studies. Ongoing clinical trials with technologies aimed directly at reducing amyloid-β levels in the human brain have largely failed.

Recent advances in our understanding of AD have pointed to amyloid-β oligomers as a distinctly toxic species, differentiated from soluble, fibril or plaque forms. As symptomatic patients already have saturating levels of amyloid-β in their brain, methods targeting removal of this toxic species are proving inadequate. There is an urgent need to develop new approaches to AD and strategies distinct from amyloid-lowering.

Lead Candidate
ALX-001

Allyx Therapeutics has obtained an exclusive license for use of ALX-001 from Bristol Meyers Squibb and Yale University. Preliminary studies demonstrate robust efficacy of this small molecule treatment in multiple preclinical mouse AD models.

Drug treatment recovers synapse density, restores hippocampal activity, and returns memory performance to normal levels. Pre-clinical development has characterized a highly drug-like profile allowing for the activation of the ALX-001 IND for the initiation of first time in human clinical studies.

The overall goal is to develop disease-modifying oral drug effective to slow, halt or partially reverse AD progression both in the MCI state and in mild dementia.

Clinical Trials

View all of the most recent status updates on our clinical trials:

Publications

Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein

September 2013

Metabotropic Glutamate Receptor 5 Couples Cellular Prion Protein to Intracellular Signalling in Alzheimer’s Disease

February 2016

Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer’s Mouse Phenotypes

July 2017