Get to know Drive’s Othelium Therapeutics

May 12, 2026

We recently sat down with the five biotech companies accepted into the Spring 2026 Drive cohort to learn more about their science, their “ah-ha” moments, and how Drive is changing the trajectory of their business. Today it’s Othelium Therapeutics, a company developing first-in-class biologics to restore endothelial function and treat microvascular disease and heart failure. We spoke with Othelium’s Chief Executive Officer Emily Ricq, PhD.

Othelium Therapeutics CEO Emily Ricq, PhD.

What problem are you obsessed with solving—and why does it matter right now?

Exercise intolerance is the defining symptom for patients with heart failure with preserved ejection fraction (HFpEF), and a major driver of reduced quality of life. Despite decades of work, there are still very few therapies that meaningfully improve functional capacity outside of incretin mimetics in obese patients. That leaves a large segment of the HFpEF population, particularly older, non-obese women, with limited options. I’ve become obsessed with how we can build a clear translational bridge between the mechanism of our compound, restoring endothelial signaling and microvascular responsiveness, and objective measures of exercise tolerance. If we can link mechanism to function in a rigorous way, we have a much better chance of developing therapies that truly move the needle for patients.

What’s a recent moment that made you think, ‘this could really work’?

We’ve spent a lot of time dissecting prior failures in HFpEF, particularly therapies aimed at increasing myocardial blood flow through vasodilation. What stands out is that many of these approaches improve resting hemodynamics, but fail to impact symptoms like exercise intolerance. The key insight for me was recognizing that the problem isn’t simply insufficient blood flow, it’s that blood flow is not appropriately coupled to demand. Increasing baseline vasodilation doesn’t fix that mismatch. Our approach is fundamentally different. By restoring endothelial signaling through S1PR1, we aim to re-establish the ability of the vasculature to sense changes in demand and respond appropriately. The distinction between increasing flow at rest versus restoring flow reserve under stress has been a turning point in how I think about the opportunity. It gives me real conviction that this could translate into meaningful improvements in patient function.

Since joining Drive, what’s one shift in your thinking, strategy, or network that’s had a real impact on your company?

As a scientist, I naturally gravitate toward mechanism, data, and experimental design. One of the most valuable shifts since joining Drive has been several prompts to step back and ask: who is the patient we’re trying to help, and what would success actually look like for her? We’ve spent time building out a detailed patient vignette, including what her day-to-day life looks like today, and how it might change with an effective therapy. That exercise has been surprisingly powerful. Not only has it made our story much more concrete and relatable, it also meaningfully increased our sense of urgency. Once you can clearly picture the patient, the unmet need becomes much harder to ignore.

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