Preclinical · Cardiovascular Therapeutics

A first-in-class therapy targeting the molecular biology of heart failure.

Cormir Therapeutics is developing anti-miR-210 LNA, an investigational antisense therapeutic designed to address convergent metabolic and inflammatory pathways that drive heart failure with reduced ejection fraction (HFrEF).

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Lead program

Anti‑miR‑210 LNA — an antisense oligonucleotide therapeutic silencing miR‑210 to relieve suppression of PPARα/PDHE2 (cardiomyocyte fuel use) and TET2 (inflammatory signaling) — the convergent metabolic and inflammatory pathways driving HFrEF.

Target indication: HFrEF

60‑70M

people living with heart failure worldwide

~29M

people estimated to be living with HFrEF worldwide

~50%

five-year mortality after an HFrEF diagnosis

Approximate global heart failure and HFrEF prevalence estimates; five-year mortality figure from U.S. AHA / CDC heart failure surveillance data.

The gap

Guideline-directed therapy manages the heart. Nothing yet refuels it.

Where current care stops

Beta-blockers, RAAS inhibitors, ARNI, and SGLT2i therapy improve hemodynamics and slow remodeling, but none directly correct the shift away from fatty-acid oxidation that leaves the pressure-overloaded heart short on fuel at the cellular level.

Where Cormir is aimed

Our approach targets the regulatory node — miR‑210 — that drives that metabolic shift, with the goal of a disease-modifying therapy that complements, rather than replaces, guideline-directed medical therapy.

The science

Why the pressure-overloaded heart runs out of fuel

Chronic pressure overload stabilizes HIF‑1α in cardiomyocytes, driving up microRNA‑210. Elevated miR‑210 drives two converging failure paths: suppressing PPARα and PDHE2 to block mitochondrial fatty-acid oxidation and force a shift to glycolysis, while suppressing TET2 to drive macrophage-mediated inflammation. Both paths converge on cardiac fibrosis, remodeling, and declining contractility.

Diagram: pressure overload raises HIF-1 alpha, which raises microRNA-210. miR-210 suppresses PPAR alpha and PDHE2, blocking mitochondrial fatty-acid oxidation and forcing a shift to glycolysis, leading to bioenergetic failure. miR-210 also suppresses TET2, driving inflammation and macrophage/IL-1 beta activity. Both paths converge on heart fibrosis and remodeling, reducing contractility. Cormir's miR-210 LNA is shown blocking microRNA-210 upstream of both paths. — Pressure overload raises HIF-1α and microRNA-210. miR-210 suppresses PPARα and PDHE2, blocking mitochondrial fatty-acid oxidation and forcing a shift to glycolysis — bioenergetic failure — while separately suppressing TET2 to drive macrophage-mediated inflammation (IL-1β). Both paths converge on heart fibrosis and remodeling, reducing contractility. Cormir's anti-miR-210 LNA (red) is designed to block miR-210 upstream of both paths.

Evidence base: the hypothesis is supported by proof-of-concept data in a murine transverse aortic constriction (TAC) model and by translational findings from neonatal lamb pulmonary hypertension studies. The program is now advancing into a large-animal ovine model of pressure-overload HFrEF — the translational step that most closely predicts human physiology ahead of IND-enabling work.

Pipeline

One mechanism, one program, one clear next step

Program

Anti-miR-210 LNA

Modality

Locked nucleic acid (LNA) antisense oligonucleotide

Indication

Heart failure with reduced ejection fraction

U.S. patent pending

Discovery

PreclinicalActive

IND-enabling

Clinical

Currently advancing dose-response and reversal studies in a large-animal ovine model of pressure-overload HFrEF, generating the data package intended to support IND-enabling development.

Leadership

Built by the scientists who found the mechanism

Lubo Zhang, PhD

Co-Founder, Chairman & Chief Scientific Officer

Originated the miR-210 → HFrEF hypothesis underlying Cormir's platform, drawing on decades of NIH-funded research in cardiovascular and perinatal physiology.

Arlin B. Blood, PhD

Co-Founder & Chief Executive Officer

Associate Professor, Department of Basic Sciences, Loma Linda University School of Medicine. Vascular and cardiopulmonary physiologist leading translation of the program's large-animal ovine model work toward IND-enabling development.

Rui Song, PhD

Scientific Lead, Molecular Mechanisms

Co-inventor of Cormir's core intellectual property; leads biochemical and molecular characterization of the miR-210 regulatory axis.

Origin & backing

Lab-originated science, built for translation

Cormir Therapeutics spun out of cardiovascular physiology research in Dr. Zhang's laboratory in the Lawrence D. Longo, MD Center for Perinatal Biology, a long-standing home for world-class large-animal translational research. Cormir was founded by Drs. Zhang and Blood, and Loma Linda University's business incubator, N3Eight.

Foundational research. The miR-210/HFrEF hypothesis builds on NIH NHLBI-funded discovery work (R01 HL149608, R01 HL169157) led by the company's founding scientists.

Intellectual property. The core anti-miR-210 LNA technology is covered by a pending U.S. patent application.

Grant support. Research to date has been funded by NIH. Cormir has applied to the NIH NHLBI CATALYZE program to fund a large-animal proof-of-concept study, and is looking for investment partners for IND-enabling development.

Interested in the science, the program, or partnering with us?

We welcome conversations with investors, prospective collaborators, scientific or business advisors, or experienced biotech entrepreneurs interested in helping us bring this solution to patients.

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