Restoring the failing heart's energy supply
CoArdia is developing first-in-class PANK1 activators — a new medicine for heart failure built on the newly discovered mechanism behind one of cardiology's most important drug classes.
A clinical paradox
SGLT2 inhibitors deliver remarkable benefit in heart failure — yet SGLT2 itself is not expressed in the heart. For years, no one knew why the drugs worked.
The discovery
Research from the Arany Lab at Penn Medicine, published in Science, identified the answer: these drugs directly activate PANK1, the gatekeeper enzyme of the heart's energy metabolism.
A new medicine
CoArdia is designing selective PANK1 activators to deliver the cardiac benefit directly – without the liabilities that come from acting on SGLT2.
The foundational science was published in Science in August 2026 by our scientific founders at the University of Pennsylvania. Read the paper
About CoArdia
A cardiac metabolism company founded to translate a landmark discovery into a first-in-class therapy for heart failure.
The science
SGLT2 inhibitors, originally developed for type 2 diabetes, have become foundational therapy in heart failure — reducing death and hospitalization in patients with both preserved and reduced ejection fraction, with or without diabetes. But the mechanism was a mystery: SGLT2 is not expressed in heart tissue.
In 2026, researchers in the Arany Lab at the Perelman School of Medicine at the University of Pennsylvania solved the puzzle. Working in human heart tissue, they showed that SGLT2 inhibitors directly bind and activate pantothenate kinase 1 (PANK1), the rate-limiting enzyme in coenzyme A synthesis. Activating PANK1 restores the failing heart's ability to convert fuel into energy — and this activation is both necessary and sufficient for the improved contractility these drugs produce in human heart cells. The work was published in Science in August 2026.
Our approach
CoArdia was founded by the scientists behind the discovery, together with experienced biotech leadership, to develop selective PANK1 activators. By engaging PANK1 directly — rather than through the incidental activity of a diabetes drug — we aim to deliver greater cardiac benefit while avoiding the known side effects tied to SGLT2 inhibition.
The company is in-licensing foundational intellectual property from the University of Pennsylvania and is advancing a discovery-stage program of novel PANK1 activator chemistry as a first mover in this new field of cardiac metabolic medicine.
Team
The scientists who made the discovery, and leadership with a track record of building biotech companies.
Mark Kaufmann
Co-founder & Chief Executive Officer
Mark Kaufmann, MBA, brings more than 35 years of biotech leadership across CEO, CFO, CBO, and COO roles. He led Ardelyx's 2014 IPO, which was 3.5x oversubscribed and upsized to $70M, and has raised over $700M in public and private equity across his career. He has structured more than $1B in business development transactions. He has served three times as a full-time CEO for therapeutic biotech companies. Across these roles he has built and led teams spanning scientific, clinical, regulatory, and finance functions. He holds a degree in biochemical sciences from Harvard University and an MBA from the University of Michigan's Ross School of Business. He is based in the San Francisco Bay Area.
Zoltan Arany, MD, PhD
Co-founder & Scientific Advisor
Zoltan Arany, MD, PhD, is the Samuel Bellet Professor of Cardiology and Chair of Physiology at the Perelman School of Medicine at the University of Pennsylvania, the Co-Director of the Cardiovascular Institute at the University of Pennsylvania, and a member of the National Academy of Medicine. Over 35 years as an academic researcher, he has built one of the field's leading programs in cardiovascular metabolism, publishing more than 200 articles in journals including Nature, Cell, Science, NEJM, and JACC. His seminal work established the role of PGC-1α in cardiac metabolism and identified ANT's function in mitophagy, and his 2020 Science paper provided the first comprehensive map of fuel consumption in the human heart.
Nicholas Forelli, MD
Co-founder & Scientific Advisor
Nick Forelli, MD, is a Cardiovascular Disease Fellow at the Hospital of the University of Pennsylvania, where he also completed his Internal Medicine residency. He is lead author of Forelli 2026, the Science paper describing PANK1 activation in heart failure that forms the scientific foundation of CoArdia. He earned his MD from Albert Einstein College of Medicine and was a Sarnoff Cardiovascular Research Fellow from 2022 to 2024. His research background spans synthetic chemistry and natural product discovery at The Rockefeller University in the Brady Lab, where he worked on genetically encoded small molecules, and he previously served as a medicinal chemist at GlaxoSmithKline.
Diseases
Heart failure is one of the largest unmet needs in medicine — and half of its patients have almost no effective options.
Heart failure with preserved ejection fraction
In HFpEF, the heart contracts normally but cannot relax and fill properly. It represents more than half of all heart failure worldwide, is growing with the aging population, and has historically resisted nearly every therapy that works in reduced ejection fraction. SGLT2 inhibitors are the only drug class with demonstrated efficacy in this population — which makes the mechanism behind that efficacy, PANK1 activation, an extraordinary starting point for new medicine.
The energy hypothesis
A failing heart is an energy-starved heart. Coenzyme A sits at the center of every major fuel pathway the heart uses — sugars, fats, amino acids, and ketones — and CoA levels are depleted in failing human hearts. PANK1 controls the first and rate-limiting step of CoA synthesis. By activating PANK1 selectively, CoArdia aims to restore the heart's capacity to produce energy and improve its ability to contract and relax.
Beyond the limits of SGLT2 inhibition
The side effects of SGLT2 inhibitors — including urinary tract infections and euglycemic diabetic ketoacidosis — arise from their action on SGLT2 in the kidney, not from PANK1. A selective PANK1 activator is designed to capture the cardiac benefit while leaving those liabilities behind and may allow dosing beyond the ceiling that SGLT2-related effects impose.
Contact Us
We welcome inquiries from investors, potential partners, and scientists interested in cardiac metabolism.
General inquiries
Partnering & investors
Location
PO Box 370462
Montara, CA 94037