Leveraging disease-protective genes — starting with the APOE Christchurch variant — to develop therapies for early- and late-onset Alzheimer's disease.
A woman genetically destined for early-onset Alzheimer's stayed cognitively healthy for three decades longer than expected — protected by a rare variant called APOE Christchurch. Epoch Biotech is turning that natural protection into medicine.
Sits in the receptor-binding domain of ApoE. Homo- and heterozygous carriers show a gene-dose–dependent delay in Alzheimer's onset. Discovered in 2019 by Epoch co-founder Dr. Arboleda-Velasquez and collaborators.
Recreate that protection with 7C11, an antibody that binds ApoE at the same receptor-binding domain and disrupts its interaction with heparan sulfate proteoglycan (HSPG) receptors, mimicking the Christchurch variant and reducing pathological tau and amyloid.
A potential first-in-class, humanized IgG1 antibody to ApoE.
7C11 mimics the Christchurch variant therapeutically — competing for the biologically relevant receptor-binding domain on ApoE (aa 114–144) that overlaps the R136S variant. Because it acts on ApoE itself, the same mechanism has potential across both familial and late-onset Alzheimer's disease.
See the mechanism & dataApoE binds HSPGs and receptors like LRP1 — interactions central to amyloid and tau pathology in Alzheimer's disease.
The R136S variant sits in the receptor-binding domain and reduces ApoE's binding affinity for HSPGs — freeing HSPGs so pathological tau and amyloid can be taken up and cleared.
Epoch's antibody binds ApoE at the same receptor-binding domain, recreating the protective shift — less tau seeding and spread, and reduced pTau in vivo.
Epoch's approach is genetically validated in humans and confirmed independently by leading research labs across transgenic rodent models and human iPSC systems — including work published in Cell, Nature Neuroscience, and NEJM.
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