Nyrada Confirms Xolatryp Offers Mitochondrial Stabilisation after Traumatic Brain Injury

Nyrada (ASX: NYR) has confirmed its small molecule therapy Xolatryp can reduce mitochondrial calcium ion loading in the brain following traumatic injury.

A collaborative study with the University of New South Wales and the Walter Reed Army Institute of Research sought to evaluate the efficacy of Xolatryp in a penetrating traumatic brain injury (TBI) rodent model.

Further analysis of that study has now concluded that Xolatryp could significantly preserve brain tissue integrity.

Additional Animal Cohort

An additional cohort of animals underwent TBI followed by a 72-hour continuous intravenous infusion administration of either Xolatryp (dosed at 5 milligrams per kilogram per hour) or a vehicle (inactive) substance.

At the 72-hour mark, mitochondria were seen to have isolated from the TBI core and the surrounding peri-injured area and assessed for cytosolic calcium ion buffering capacity using a fluorescence-based assay.

Mitochondria from Xolatryp-treated animals demonstrated a significant improvement in cytosolic calcium ion buffering ability compared to vehicle-treated controls, with an overall 11% enhancement in mitochondrial function.

Improved Calcium Handling

The results confirmed that Xolatryp helps preserve mitochondrial health by improving calcium handling, thus protecting the brain’s energy centres from reactive oxygen species (ROS)-related damage.

The additional analysis has increased Nyrada’s confidence that it can replicate Xolatryp’s protective effects on mitochondria to reduce myocardial ischemia reperfusion injury (MIRI, or heart damage), as ROS and calcium-driven mitochondrial damage occur in both TBI and MIRI.

Importantly, the study results also support Nyrada’s previous stroke and TBI study findings, where treatment with Xolatryp significantly preserved brain tissue integrity compared to vehicle control and provided evidence of Xolatryp’s protective effect at the cellular level.

‘Strong Cardioprotective Efficacy’

Nyrada chief executive officer James Bonnar said the company was focusing on translating the study results into patient benefits.

“The mitochondrial data demonstrates a significant reduction in cytosolic calcium ion loading, providing a coherent rationale for Xolatryp as a first-in-class adjunct at the point of reperfusion,” he said.

Xolatryp (formerly known as NYR-BI03) is a small-molecule inhibitor that limits the pathological entry of calcium ions, stabilises mitochondrial function, and mitigates reperfusion injury in acute heart damage and related settings.

Calcium ions act as a cellular messenger, playing a critical role in diverse physiological processes including muscle contraction, nerve signalling, blood clotting, and cell division.