CorPhylaxisFirst, the heart loses muscle.
Interrupted blood flow injures the myocardium. The damaged wall needs structural repair to withstand every beat.
A new precision for the healing heart
Preserve repair.
Prevent failure.
Heart injury is only the beginning. The cells that respond determine what comes next.
A scar holds the heart together.
Scar replaces lost muscle and preserves the integrity of the ventricular wall. This repair is essential to survival.
Fibrosis reaches surviving muscle.
Excessive fibrosis can spread beyond the injury, stiffening the heart and contributing to adverse remodeling and heart failure.
Suppress repair. Risk rupture.
Broadly suppressing the cellular response can also weaken the essential scar. In experimental models, compromised repair can lead to catastrophic cardiac rupture.
The post-infarction heart01 / 04
Injury site
Our scientific thesis
The same cell type.
A different role in disease.
Broad targeting cannot reliably distinguish injury-driving biology from the repair the heart needs.
Our award-winning discovery identifies distinct cell subpopulations with opposing roles after cardiac injury. Some exacerbate damage. Others protect the healing heart.
This distinction underpins our approach: develop therapies directed at the disease-driving populations while preserving protective repair.
Our award-winning scienceOur precision approach
Target the disease-driving cells.
Spare protective repair.
Two complementary selectivity filters are designed to direct therapeutic activity to disease-causing cell subpopulations while preserving other reparative cells.
Reach the relevant cardiac cells.
A cardiac-homing lipid nanoparticle enriches delivery to the relevant cardiac cell compartment.
Control where the payload is expressed.
A state-selective promoter is designed to activate therapeutic expression in disease-driving cells while remaining silent in protective cell populations.
CorSilico
From human biology
to causal evidence.
The human heart data engine that enabled our founding discovery—and our path toward a Virtual Heart.
2.5M+human cardiac cells and nuclei
The world’s largest harmonized human heart-failure cell data engine, by our assessment.
CorSilico
Explore the system, stage by stage.
CorSilico: the complete system
Human cardiac data, evidence-ranked hypotheses and staged experimental validation form one learning loop.
The Virtual Heart
An integrated view of human cardiac cells connects single-cell, spatial, regulatory and genetic evidence to the biology of heart failure.
500–700candidate hypotheses
DiscoveryOS
Specialist agents assemble evidence, challenge mechanisms and rank the hypotheses most likely to merit experimental testing.
30–60prioritized candidates
In Vivo Perturbation & Spatial Readout
Pooled perturbation tests mechanisms in vivo. Spatial readouts then identify which candidates move the intended state in the relevant tissue context.
10–20 → 3–5from perturbation to spatial validation
Human & Animal Disease Modeling
Beating human cardiac tissue and mouse myocardial-infarction models connect a cellular mechanism with tissue function, remodeling and structural safety.
1–2candidates in focused functional studies
Virtual Heart500–700candidate hypotheses
DiscoveryOS30–60prioritized candidates
Perturbation + spatial10–20 → 3–5from perturbation to spatial validation
Human + animal models1–2candidates in focused functional studies
Read the CorSilico workflow description
The Virtual Heart
An integrated view of human cardiac cells connects single-cell, spatial, regulatory and genetic evidence to the biology of heart failure.
500–700 · candidate hypotheses
DiscoveryOS
Specialist agents assemble evidence, challenge mechanisms and rank the hypotheses most likely to merit experimental testing.
30–60 · prioritized candidates
In Vivo Perturbation & Spatial Readout
Pooled perturbation tests mechanisms in vivo. Spatial readouts then identify which candidates move the intended state in the relevant tissue context.
10–20 → 3–5 · from perturbation to spatial validation
Human & Animal Disease Modeling
Beating human cardiac tissue and mouse myocardial-infarction models connect a cellular mechanism with tissue function, remodeling and structural safety.
1–2 · candidates in focused functional studies
HeartDecoder
The right intervention.
The right patient.
Connect circulating molecular signals with the cardiac cell states resolved by the Virtual Heart.
HeartDecoder
Explore the system, stage by stage.
HeartDecoder: the complete system
From injury-linked signals in plasma to tissue-informed decoding, biological stratification and mechanism-matched development.
Heart Injury
Injured cardiac cells can release molecular signals into plasma, providing a potential window into the biology active within the heart.
Cardiac originsignals released into circulation
Liquid Biopsy
Cell-free RNA, extracellular-vesicle RNA and cell-free DNA provide complementary molecular signals from a blood sample.
Plasmacell-free RNA, EV RNA and cell-free DNA
Decode with the Virtual Heart
Circulating signals are anchored to replication-scored cell-state signatures in the Virtual Heart, rather than interpreted without cardiac context.
Tissue-informedcell-of-origin inference
Circulating Cell-State Signature
A circulating signature is designed to indicate which target-relevant cardiac cell states are active in an individual patient.
Mechanism-linkedactivity relevant to a therapeutic target
Patient Stratification
Mechanism-based stratification aims to distinguish patients who share a diagnosis but have different underlying disease biology.
Target-relevantenrichment beyond clinical phenotype
Mechanism-Matched Studies
The development goal is better alignment between a therapeutic mechanism, the patients enrolled and the biological response being measured.
Right biologya more informed development strategy
Read the HeartDecoder workflow description
Heart Injury
Injured cardiac cells can release molecular signals into plasma, providing a potential window into the biology active within the heart.
Cardiac origin · signals released into circulation
Liquid Biopsy
Cell-free RNA, extracellular-vesicle RNA and cell-free DNA provide complementary molecular signals from a blood sample.
Plasma · cell-free RNA, EV RNA and cell-free DNA
Decode with the Virtual Heart
Circulating signals are anchored to replication-scored cell-state signatures in the Virtual Heart, rather than interpreted without cardiac context.
Tissue-informed · cell-of-origin inference
Circulating Cell-State Signature
A circulating signature is designed to indicate which target-relevant cardiac cell states are active in an individual patient.
Mechanism-linked · activity relevant to a therapeutic target
Patient Stratification
Mechanism-based stratification aims to distinguish patients who share a diagnosis but have different underlying disease biology.
Target-relevant · enrichment beyond clinical phenotype
Mechanism-Matched Studies
The development goal is better alignment between a therapeutic mechanism, the patients enrolled and the biological response being measured.
Right biology · a more informed development strategy
Scientific recognition
Discovery with a
distinguished foundation.
American Heart Association
Innovative Project Award
Research support for the founding science.
American Heart Association
Katz Award, Top 5
Recognized among the Top 5 at Scientific Sessions 2025.
AHA Innovation Forum
Top 5 Ventures
Selected to present among five ventures.
Deerfield & Cure
Top 15 ventures
Selected for the MEHA II venture program.
Our founders
Deep biology.
Complementary expertise.
Founder & Chief Executive Officer
Cardiovascular physician-scientist and computational biologist. AHA-recognized research. More than 30 indexed publications.
Founder & Chief Operating Officer
Genomics operations leader with more than five years of R&D building single-cell and spatial biology workflows.
A shared ambition for the human heart.
We welcome conversations with scientific collaborators, biotech and pharma partners, and investors who share our commitment to precision.