Amylyx

Amylyx is an IND-stage therapeutics company developing a proprietary therapeutic for Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s disease that targets the neuroinflammation and nerve cell death that characterize these disorders. The company’s therapeutic, AMX0035, is a proprietary, synergistic combination of existing compounds that blocks nerve cell death and neurotoxic inflammation. The approach has exhibited strong efficacy across nonspecific models of neurodegenerative disease as well as in transgenic models of ALS and Alzheimer’s. AMX0035 is expected to enter a pivotal, proof-of-concept clinical trial in ALS in 2016. Following a successful initial clinical trial, AMX0035 will be tested in a proof of concept trial of Alzheimer’s disease.

Funded Research

Project Description Researchers Funding
Evaluation of AMX0035, a Neuroprotecting and M1-Deactivating Therapeutic, in an Immunological Model of AD (Part 1)

In Alzheimer’s disease (AD) and other neurodegenerative diseases (ND) such as ALS, neurological inflammation and cell death form a vicious cycle that is one of the main causes of decline. Mitochondrial and endoplasmic reticulum stresses mediate these pathways, accelerating inflammation and triggering apoptosis. Therefore, we developed a combination therapeutic of repurposed compounds to simultaneously reduce endoplasmic reticulum stress and mitochondrial dysfunction to halt the cycle of inflammation and cell death.

2015
$150,000
Evaluation of AMX0035, a Neuroprotecting and M1-Deactivating Therapeutic, in an Immunological Model of AD (Part 2)

In Alzheimer’s disease (AD) and other neurodegenerative diseases (ND) such as ALS, neurological inflammation and cell death form a vicious cycle that is one of the main causes of decline. Mitochondrial and endoplasmic reticulum stresses mediate these pathways, accelerating inflammation and triggering apoptosis. Therefore, we developed a combination therapeutic of repurposed compounds to simultaneously reduce endoplasmic reticulum stress and mitochondrial dysfunction to halt the cycle of inflammation and cell death.

2015
$150,000