Human genetics · first-in-class antibody

One protective variant.
A new path to treating
Alzheimer's.

Leveraging disease-protective genes — starting with the APOE Christchurch variant — to develop therapies for early- and late-onset Alzheimer's disease.

1,200+
Carriers in the world's largest familial Alzheimer's kindred studied.
~62.5%
Reduction in pathological tau (pTau) in ApoE4 mice treated with 7C11.
90–95%
Of Alzheimer's cases are late-onset — addressable by the same pathway.
2019
Christchurch variant discovered by Epoch's scientific co-founder.
The insight

We're not chasing symptoms. We're mimicking nature's own defense.

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.

The Christchurch variant (APOE R136S)

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.


Epoch's approach

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.

Lead asset
7C11

A potential first-in-class, humanized IgG1 antibody to ApoE.

  • Binds all three human ApoE isoforms with high affinity
  • Blocks the ApoE/HSPG interaction that drives pathology
  • Reduces tau phosphorylation in ApoE4 and retina-tau models
  • Favorable profile; potential modular BBB shuttle
The pipeline

A first-in-class antibody, ready for IND-enabling work.

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 & data
How it works

The Christchurch pathway, in three steps

1

ApoE drives pathology

ApoE binds HSPGs and receptors like LRP1 — interactions central to amyloid and tau pathology in Alzheimer's disease.

2

Christchurch frees the HSPGs

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.

3

7C11 mimics the effect

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.

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Advancing the next epoch of Alzheimer's therapy

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