Remodeless CV

Stopping the Second Injury.

When blood flow is restored after a heart attack or stroke, the treatment that saves a patient's life can also cause further tissue damage. Remodeless CV is developing a novel therapy to protect vital organs from this reperfusion injury.

Heart Attack & Stroke Repetitive Head Trauma

01The Problem

Restoring blood flow is life-saving — and damaging.

Acute myocardial infarction and ischemic stroke both require urgent restoration of blood flow (reperfusion) to keep tissue alive. But reperfusion itself triggers a second wave of injury — driven by locally produced leptin, which fuels inflammation and microvascular thrombosis. Despite decades of research, no FDA-approved therapy exists to prevent it.

700,000+ US patients treated with PCI for acute coronary occlusion annually
70,000+ US stroke patients undergoing invasive thrombectomy annually
$200B annual US healthcare cost linked to post-MI heart failure

02Market Opportunity

A massive, growing burden — and a therapy aimed at its root cause.

Heart failure is one of the costliest chronic conditions in U.S. healthcare, and it is frequently a downstream consequence of the acute cardiac events LepA is designed to protect against. Reducing reperfusion injury at the moment of revascularization has the potential to reduce the population that goes on to develop it.

6.7M+ US adults living with heart failure today, rising toward 8.7M by 2030
$22.0B 2025 US heart failure therapeutics market, growing at a 7.3% CAGR
$227B Annual direct US economic burden of heart failure — projected to reach $858B by 2050

Figures reflect 2025 U.S. market estimates for heart failure and myocardial infarction compiled from third-party healthcare-economics research, provided for illustrative context.

03The Science

LepA: a targeted leptin antagonist.

Ischemia induces local leptin production. That leptin binds local receptors to form an active complex that drives reactive oxygen species, inflammation, and microvascular thrombosis — compounding tissue damage. LepA is a super-active leptin-antagonist mutant, administered selectively intra-arterially to the affected organ, that competes with native leptin and blocks this cascade.

01

Ischemic event

Arterial occlusion cuts off oxygen supply, and local leptin production rises.

02

Reperfusion injury

Leptin binds local receptors, driving oxidative stress, inflammation, and clotting.

03

LepA intervention

LepA competes with native leptin, forming an inactive complex and blocking the damage cascade.

Anti-apoptotic

Supports cell survival in tissue under acute stress.

Anti-inflammatory

Reduces the inflammatory response that compounds tissue injury.

Anti-thrombotic

Limits microvascular thrombosis at the site of injury.

Immunomodulatory

Modulates the local immune response during reperfusion.

04Applications

One mechanism, two windows of vulnerability.

The same leptin-driven cascade that damages heart and brain tissue after an acute ischemic event may also underlie the chronic neuroinflammation seen after repeated head impacts — a pathway increasingly implicated in CTE and accelerated cognitive decline among contact-sport athletes.

Acute Cardiac & Cerebrovascular Events

RCV's primary clinical focus. After a heart attack or stroke, restoring blood flow triggers a single, intense reperfusion injury — the target of RCV's lead clinical program.

Repetitive Head Trauma

An emerging area of exploration. Repeated subconcussive impacts — common in football, soccer, and other contact sports — may drive cumulative, leptin-mediated neuroinflammation linked to CTE and Alzheimer's-like cognitive decline. RCV is evaluating LepA's relevance to this chronic injury pattern.

The repetitive head trauma application is exploratory, is supported only by RCV's preclinical brain ischemia-reperfusion data, and has not been evaluated in human clinical studies.

05Evidence

Validated across organ systems.

RCV has demonstrated the efficacy of its therapeutic approach in preclinical ischemia-reperfusion models of the brain, kidney, and heart — preserving tissue viability and organ function.

Brain

Preclinical IR models show preserved tissue viability following LepA administration.

Kidney

Demonstrated protection of organ function in renal ischemia-reperfusion models.

Heart

In a porcine IR model, LepA diminished infarct size and helped prevent left ventricular functional damage — reducing the likelihood of downstream heart failure.

Our primary clinical focus is LepA therapy for patients with acute myocardial infarction undergoing emergent coronary revascularization. Results described are from preclinical animal studies; LepA is an investigational therapy and has not been approved for clinical use.

06IP & Regulatory Path

Protected science, advancing toward the clinic.

RCV holds granted patents in the US and Europe covering LepA and its methods of therapy for ischemia-reperfusion injury. The FDA has reviewed RCV's experimental data and granted approval to proceed with toxicology and safety studies — the next step on the path to clinical development.

Granted patents

US and European patents granted on LepA and its therapeutic methods.

FDA-reviewed data

Experimental data reviewed by the FDA, with approval to proceed to toxicology and safety studies.

Clear clinical path

Toxicology and safety studies precede FDA IND submission and Phase I clinical development.

07Leadership

Led by clinical and scientific authority.

Jacob Schneiderman, MD, FAHA

Chief Executive Officer

Professor of Surgery at Tel Aviv University and a cardiovascular surgeon-scientist. Past Director of the Department of Vascular Surgery at Sheba Medical Center, Israel. Visiting Professor at Harvard Medical School and the University of Pennsylvania.

Interested in the science, the IP, or a partnership?

Get In Touch

Get In Touch

Let's talk about what comes next.

Whether you're an investor, a strategic partner, or a researcher in the field — we'd like to hear from you.

n@impactechgroup.com