How Nyrada’s Xolatryp Shields Cells to Combat Brain and Heart Injury

Preclinical Breakthrough in Brain Injury Model

Nyrada Inc., a clinical-stage biotech company, has unveiled further analysis from its collaborative study with the Walter Reed Army Institute of Research and UNSW Sydney, reinforcing the protective effects of its lead drug candidate, Xolatryp. The study focused on a penetrating traumatic brain injury (TBI) rodent model, where Xolatryp demonstrated a significant reduction in mitochondrial calcium ion overload, a key driver of cellular damage.

This mitochondrial protection is crucial because excessive calcium ion accumulation in mitochondria leads to the generation of reactive oxygen species (ROS), which can cause irreversible damage to cells. By improving calcium handling, Xolatryp helps preserve the brain’s energy centers, potentially mitigating the secondary injury cascade that follows trauma.

Implications for Cardiac Injury Treatment

Beyond neuroprotection, these findings have important implications for cardiac health. Myocardial ischemia reperfusion injury (MIRI), a common complication following heart attacks and interventions like percutaneous coronary intervention (PCI), shares a similar pathological mechanism involving calcium overload and ROS damage in heart cells.

Nyrada’s data suggest that Xolatryp’s inhibition of TRPC3/6/7 ion channels can limit pathological calcium entry into cardiomyocytes, reducing mitochondrial damage and cell death. This aligns with previous in vivo studies showing infarct-sparing and functional benefits, positioning Xolatryp as a promising first-in-class therapy to reduce heart tissue damage after reperfusion.

Robust Evidence of Mitochondrial Function Enhancement

The study’s mitochondrial assay revealed an 11 percent improvement in calcium buffering capacity in mitochondria isolated from Xolatryp-treated animals compared to controls. This enhancement is not only statistically significant but also biologically meaningful, as even a 10 percent reduction in mitochondrial calcium load can determine cell survival versus death.

Importantly, this is the first time mitochondrial function has been evaluated following systemic drug administration in this TBI model, demonstrating that Xolatryp effectively crosses the blood-brain barrier and engages its molecular targets in a living system.

Next Steps – Phase IIa Clinical Trial on the Horizon

With a successful Phase I trial behind it, Nyrada is preparing to initiate a Phase IIa clinical trial in early 2026. This trial will assess the safety and efficacy of Xolatryp in patients experiencing acute myocardial infarction, specifically those undergoing PCI for ST-Elevation Myocardial Infarction (STEMI).

CEO James Bonnar emphasized the significance of the mitochondrial data, stating it provides a coherent rationale for Xolatryp as an adjunct therapy at reperfusion, potentially reducing infarct size, shortening hospital stays, and lowering the risk of subsequent heart failure.

Broader Impact and Market Potential

Currently, no approved therapies directly protect heart cells from reperfusion injury, marking Xolatryp’s mechanism as a potentially transformative advance. If clinical trials confirm these preclinical benefits, Nyrada could position itself at the forefront of a new class of cardioprotective and neuroprotective treatments.