Arresting heart failure progression through the world’s first cell-subpopulation-targeted genetic medicines.

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Recognized science.
Exceptional pedigree.
American Heart AssociationKatz AwardAmerican Heart Association
American Heart AssociationInnovative Project AwardAmerican Heart Association
UC San Diego
Albert Einstein College of Medicine
Deerfield at CureTop 15 ventureCure MEHA II
01 / Rethinking cardiac fibrosis

The scar is part of the solution.
Its spread is the problem.

To change the course of heart failure, we must understand the boundary between essential repair and progressive damage.

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A heart worth protecting.

Damage to the heart is irreversible because heart muscles cannot regenerate.

01 / Healthy

A heart worth protecting.

Damage to the heart is irreversible because heart muscles cannot regenerate.

02 / Injury & repair

The patch that saves a life.

After a heart attack, injured muscle is replaced by a fibrous scar: an essential structural patch that keeps the heart intact.

03 / Scar expansion

When repair goes too far.

Fibrosis can extend beyond the original injury into surviving myocardium, disrupting healthy tissue as the ventricle dilates and its contraction weakens.

04 / The paradox

The fatal paradox of fibrosis after heart attack.

Suppressing fibrosis indiscriminately compromises the protective scar as well as harmful expansion, creating a risk of heart rupture.

05 / Our discovery

Our award-winning discovery enables spatial precision.

We discovered spatially distinct fibroblast subpopulations: reparative cells forming the scar and invasive cells invading the healthy heart beyond the scar.

06 / Precision

Stop the invasion. Preserve the repair.

Our therapeutic strategy is to arrest harmful fibroblast invasion into the healthy heart areas, while leaving reparative cells to maintain an intact structural scar.

Conceptual illustration · not to scale · therapeutic effects shown are the intended mechanism, not established clinical outcomes.
02 / Human & preclinical evidence

Distinct biology.
Converging evidence.

Human genetic evidence and experimental models inform our selection of targets at the scar border.

Human genetic validation

A risk signal that extends across cardiovascular disease.

Human genetics confirm that higher genetically predicted expression of our lead target increases the risk of heart failure.

Odds ratio per 1-SD higher genetically predicted expression; 1.00 indicates no association.

Preclinical proof of concept

Halting invasion.
Protecting heart structure.

Target X inhibition reduced fibroblast invasiveness

ControlTarget inhibited
80%reduction in invasion
in the company’s 3D model

Target Z: Ejection fraction is preserved by the protective regulator

In a mouse model of myocardial infarction, loss of Target Z worsens cardiac function.

ControlTarget Z loss

Ejection fraction (%) at 28 days post-infarction.

Explore the publications
03 / AI-developed ultra-specific targeting platform

Delivery with direction.
Expression with precision.

Our ambition: the world’s first precision therapy for heart failure that acts only in harmful invasive fibroblasts.

Lipid nanoparticle + precision targeting + genetic payload
01

The delivery key

Cardiac-homing lipid chemistry and a fibroblast-targeting antibody are designed to bring the lipid nanoparticle to the heart’s fibroblast compartment.

02

The expression key

A synthetic promoter is designed to recognize the transcriptional program of invasive fibroblasts and activate the payload within those cells.

03

Computational Cis-Regulatory Discovery

We developed a machine-learning pipeline integrating single-cell RNA-seq and single-nucleus ATAC-seq to identify cell-state-associated accessible chromatin regions, transcription-factor regulons, and candidate cis-regulatory elements. Combinations of enriched motifs are assembled upstream of minimal promoters and experimentally screened for selective transcriptional activity. This machine-learning pipeline is the basis for both our SynPro and LNP design.

Reparative fibroblasts

Payload designed to remain dormant.
Protective scar preserved.

Invasive fibroblasts

Payload designed to activate.
Harmful invasion arrested.

Platform design and intended selectivity are under development and require further preclinical validation.

04 / A multi-pronged precision pipeline

Two payloads.
One protective purpose.

Two genetic payloads designed to completely arrest fibrosis expansion into healthy heart regions — without disrupting the protective scar.

ProgramModalityIntended therapeutic effectStage
CPX-001LNP–SynPro genetic expression

Degradation-resistant protective regulator

Reprogram invasive fibroblasts to repress fibrosis in viable myocardium surrounding the scar.Preclinical validation
CPX-002LNP–SynPro RNA interference

Targeted inhibition of a motility driver

Suppress fibroblast motility and halt invasion into viable tissue beyond the injury border.3D culture proof of concept
CPX-003Platform expansion

Adapted synthetic promoter

Extend the dual-key approach to disease-driving fibroblast subsets in pulmonary fibrosis.Target discovery

Program stages reflect the company development plan. Specific payload identities remain undisclosed; none of these candidates is approved for clinical use.

05 / A different therapeutic position

Precision and protection.
By design.

Built on our proprietary discovery, we are the only platform that combines cell-subpopulation precision with preservation of the protective scar — zero direct competition.

Proprietary discovery. Zero direct competition.

Addressing the destructive process at its source.

Therapeutic objectiveStem cell
therapies		Cardiomyocyte
proliferation		AngiogenesisCorPhylaxis
Arrest fibrotic tissue damage✕✕✕✓
Prevent border-zone fibrosis expansion✕✕✕✓
Preserve the protective core scar✕✕✕✓
Support lasting structural protection○○○✓

Conceptual company positioning; not a head-to-head clinical comparison or evidence of proven superiority. Standard-of-care therapies have established clinical benefits; this investigational approach is not a replacement.

06 / Business model

Build value in the heart.
Extend it beyond.

A dual-key precision platform: arrest the invasive fibroblast population while preserving reparative cells — first in post-infarction heart failure, then across fibrotic disease.

Explore a partnership
Core programs · Retained global rights

Internal clinical development

Advance CPX-001 and CPX-002 through IND-enabling studies and into early clinical trials for post-infarction heart failure, with the aim of retaining global commercial rights.

Platform partnerships · Non-dilutive potential

Selective out-licensing

Pursue strategic partnerships for non-core indications — including pulmonary and hepatic fibrosis — to extend the platform beyond the heart.

Current raise · Post-money SAFE

$2M to the next milestone

We are raising a $2M post-money SAFE to advance the dual-key genetic medicine platform toward IND-enabling studies and early development.

07 / Intellectual property & strategic moat

Built on a deeper
understanding of cells.

01Synthetic promoter library

Cell-state-specific gene sequences, motif arrangements, and logic-gated architectures.

02LNP formulations

Cardiac-homing lipid chemistry and fibroblast-targeting surface modifications.

03Broad target protection

A planned strategy covering delivery approaches and drivers of invasive myofibroblasts.

04Methods of treatment

Preventing border-zone fibrosis expansion through selective targeting.

Company IP strategy; issued patent coverage and freedom to operate are not represented as established.

08 / The US market opportunity

A meaningful intervention.
A multi-billion-dollar opportunity.

A focused entry population: heart attack survivors at high risk of progressing to heart failure.

$58.6B

Theoretical total US market

781,600 annual surviving myocardial infarction patients × $75,000 per prophylactic course.

$14.65B

Target addressable market

195,400 high-risk survivors, representing the estimated 25% subgroup.

$2.63B

Modeled peak US opportunity

18% penetration of the target market, or approximately 35,170 treated patients.

Company scenario estimates; not independently validated forecasts. Pricing, eligibility, reimbursement, adoption, and regulatory approval are assumptions; actual outcomes may differ materially.
09 / The development roadmap

20 months.
A path to the next inflection point.

An estimated development plan from formulation selection to large-animal proof of concept and Series A readiness.

Months 1–6

Select the formulation

Screen LNP formulations, establish assays, verify in vitro selectivity, and define the IP and filing plan.

Months 7–10

Validate delivery

Assess biodistribution, target engagement, dose range, tolerability, and manufacturing stability.

Months 11–15

Establish murine proof of concept

Evaluate efficacy, heart function, and scar integrity; align the regulatory strategy.

Months 16–20

Advance to porcine proof of concept

Complete delivery and efficacy studies, prepare the data package, and pursue Series A financing.

Milestones are targets, measured from funding and subject to experimental results. Post-Series A priorities: IND-enabling toxicology, GMP clinical supply, IND submission, and Phase 1 entry.

10 / Financing & use of funds

Raising $2M.

A post-money SAFE to translate our preclinically validated targets into genetic medicines — for a premier Series A.

Discuss the opportunity
50%In vivo preclinical validation$1.0M
25%Dual-key LNP formulation$500K
15%Key hires, CROs & operations$300K
10%Intellectual property & FTO$200K

Planned allocation; subject to development needs and financing terms.

11 / Leadership & scientific pedigree

Deep science.
The experience to move it forward.

Cardiovascular discovery meets expertise in spatial biology and the operations that turn research into progress.

CorPhylaxis founder and chief executive officer
Founder & CEO
Anis Hanna, MD

Cardiovascular medicine, computational biology, and award-winning research in post-infarction heart failure.

CorPhylaxis founder and chief operating officer
Founder & COO
Polina Alieva

Single-cell and spatial biology target discovery, with deep experience managing and scaling genomics laboratories.

Building a cardiovascular industry advisory board to support the next stage.

Meet our founders
A new future for the healing heart

Invest in the future of
heart failure gene therapy.

We are happy to discuss. Let’s move the science forward, together.

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