The heart in hypertrophic cardiomyopathy A technical illustration of a heart whose muscular wall is abnormally thickened, traced over a fine measurement lattice with an electrocardiogram pulse. THICKENED SEPTAL WALL NARROWED CHAMBER FIG.01 — HCM ECG · SINUS

Clinical-stage biopharmaceutical · Hypertrophic cardiomyopathy

A selective therapy for the overactive heart.

Advancing a cardiac myosin inhibitor for hypertrophic cardiomyopathy — through global, late-stage clinical development.

EYEAM is a clinical-stage biopharmaceutical company built around a single conviction: that hypertrophic cardiomyopathy deserves a therapy aimed at its mechanism — not just its symptoms.

One disease. One mechanism-targeted compound. Pursued in depth, across both forms of the condition, toward potential availability to patients.

Start with the disease

01 — The Disease

Hypertrophic cardiomyopathy, explained.

A common rare disease in which the heart muscle grows too thick — and the heart is left to work harder to do less.

In hypertrophic cardiomyopathy (HCM), the muscular walls of the heart grow abnormally thickened. That thickening stiffens the chamber, crowds the space available for blood, and impairs the heart's ability to do the two things every heartbeat depends on — to pump blood out and to fill with it in return.

HCM is, in a sense, a paradox: it is counted among the most common of the rare diseases, estimated to affect roughly one in 500 people in the United States. That makes it widespread enough to touch families in every community, yet specific enough that it has long gone underserved by therapies designed for its underlying biology.

As the muscle thickens, it can also begin to contract too forcefully — an excess of the very force a heart is built to produce. The result, for many people living with the condition, is a cluster of symptoms that quietly narrows the boundaries of an ordinary day.

Normal heart wall compared with a thickened wall in HCM Two cross-sections of the heart's left ventricle. On the left, a normal wall surrounds an open chamber. On the right, the wall is thickened and the chamber is narrowed. wall NORMAL thickened HCM
Fig. 02 — Left-ventricular wall, schematic Healthy muscle  Thickened muscle
≈1 in 500
Estimated prevalence in the United States — among the most common rare diseases
2 forms
Obstructive & non-obstructive HCM — EYEAM's program addresses both
4 signs
Hallmark symptoms that can narrow the boundaries of an ordinary day

How it can feel.

Shortness of breath

Breathlessness on exertion — and sometimes at rest — as the stiffened heart struggles to keep pace with the body's demand.

Chest pain

Pressure or pain in the chest, often with activity, as the thickened muscle demands more oxygen than it readily receives.

Fatigue

A persistent, low-running tiredness — the cumulative cost of a heart that has to work harder for every beat.

Fainting

Light-headedness or sudden loss of consciousness, especially during exertion — a sign that can carry serious risk.

Two forms, one underlying mechanism.

Obstructive HCM

The path out is narrowed.

In obstructive HCM, the thickened muscle physically narrows the channel blood travels as it leaves the heart. Outflow is obstructed, and the heart must generate still more force to push blood past the blockage — compounding the burden the disease already places on it.

Non-obstructive HCM

The muscle is thick, but the path is clear.

In non-obstructive HCM, the muscle is thickened and stiff but does not block outflow in the same way. The obstruction may be absent — yet the abnormal mechanics of the muscle, and the symptoms they produce, remain very much present.

02 — Our Science

A cardiac myosin inhibitor, engineered for selectivity.

Our lead investigational candidate is designed to ease the excessive contraction that defines thickened heart muscle.

Cardiac myosin thick filament with force-generating heads A red technical render of a myosin thick filament, its motor heads reaching toward neighboring actin filaments — the machinery a selective inhibitor is designed to engage. motor head
Fig. 03 — Cardiac myosin (schematic)Target: force-generating cross-bridges

The fastest path to a better day for people with HCM runs through the muscle itself — by moderating contraction at its source, in a single secure mechanism, powered by selective cardiac myosin inhibition.

01

Targeting the motor of contraction.

Every heartbeat is powered by myosin — the motor protein that pulls the muscle's filaments past one another to generate force. In HCM, that machinery runs too hot. By selectively engaging cardiac myosin, the candidate is designed to moderate the number of active force-generating connections, dialing contraction back toward a healthier range.

02

Selective by design.

Selectivity is the point. Rather than broadly altering the heart's chemistry, the candidate is engineered to act on the specific protein at the center of HCM's mechanics — an approach intended to address the root of the problem while leaving the rest of the system as undisturbed as possible.

03

A small molecule for a defined disease.

As a small molecule directed at a single, well-characterized target, the candidate reflects EYEAM's whole posture: one mechanism, one disease, pursued in depth — with the aim of improving heart performance, clinical outcomes, and the everyday quality of life of the people who live with HCM.

The Thesis

The case for selective cardiac myosin inhibition.

For a long time, the thickened, overworking heart of HCM was managed largely around the edges — easing symptoms without reaching the mechanics underneath them. EYEAM is built on a different premise: that a therapy aimed directly at the force of contraction can change the equation for the disease itself.

We have made a deliberate choice to concentrate. Rather than spreading a broad portfolio thin across many therapeutic areas, EYEAM advances a single lead program, directed at a defined cardiac disease and grounded in clinical data — pursued through international, late-stage development and external collaboration.

Focus is not a limitation. It is the strategy.

Cardiac muscle as a repeating lattice of sarcomeres A large red technical render of heart muscle, drawn as rows of repeating contractile units — the structure EYEAM's mechanism is designed to act upon.
Fig. 04 — Heart muscle, as a repeating contractile lattice

03 — Pipeline

One compound, advancing across the disease.

EYEAM's pipeline is intentionally singular — a single lead cardiac myosin inhibitor, pursued with rigor across both major forms of hypertrophic cardiomyopathy and into global, late-stage clinical development. Mid-stage results have been positive in each form; the program now advances toward patients.

P-01

Lead cardiac myosin inhibitor

Indication · Non-obstructive HCM
Positive Phase 2

Positive Phase 2 results reported in non-obstructive HCM.

P-02

Lead cardiac myosin inhibitor

Indication · Obstructive HCM
Positive Phase 2

Positive Phase 2 results, reported with a pharmaceutical partner; includes international clinical data.

P-03

Lead cardiac myosin inhibitor

Program · Global, late-stage development
Advancing

Advancing through global, late-stage clinical development toward potential regulatory submission.

Phase 2 trials evaluate a candidate's effect and safety in people living with the condition; late-stage (Phase 3) development gathers the larger, confirmatory evidence regulators weigh for approval. Positive Phase 2 results across both the obstructive and non-obstructive forms underpin EYEAM's continued investment in advancing this single program. EYEAM's lead candidate is investigational and has not been approved by any regulatory authority.

04 — Careers

We're hiring as we advance toward patients.

Late-stage development is a team effort. As EYEAM moves its lead HCM candidate through global clinical development, we are growing — and we are looking for people who want their work to matter to a defined community of patients. If a focused, mechanism-driven cardiovascular mission resonates with you, we would like to meet you.

Enquire about roles General contact
MissionA single lead program, directed at a defined cardiac disease.
StageClinical-stage, advancing through global late-stage development.
Why it mattersWork that reaches a community living with one of medicine's most common rare diseases.

Get in touch

Let's talk.

Clinicians, investigators, investors, potential collaborators, prospective team members, and patients and caregivers are all welcome to reach out. Tell us a little about you, and we'll be in touch.

EYEAM LLC · Headquarters
5242 Veronica St, Los Angeles, CA 90008
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