RNS60 is an investigational therapeutic designed to provide safe and effective treatments for neurological conditions by targeting the root cause of cellular decline: mitochondrial dysfunction. By activating the Type 1A PI3K-Akt pathway, RNS60 uniquely triggers intracellular signaling that promotes:
The global impact of stroke is staggering. It’s the #1 cause of disability and the #2 cause of death worldwide, with an estimated global cost of $890 billion.1 Over 160 million years of healthy lives are lost each year to ischemic stroke-related death and disability.1 Caregivers are also affected, and often experience physical challenges in caring for their loved ones, as well as depression, anxiety, social isolation, and financial burden.2,3
Ischemic stroke represents an injury where oxygen and glucose deprivation leads to acute mitochondrial failure and thereby to rapid cell death leading to long-term disability. The majority of people (87%) who have a stroke have an acute ischemic stroke, in which blood supply to a part of the brain is interrupted. Without oxygen, brain cells begin to die within minutes. Only ~20% of people having a stroke are eligible to receive endovascular thrombectomy (clot removal) or thrombolytics (clot-busting drugs), leaving ~80% of people at risk for greater brain damage and long-term disability.4
While standard of care focuses on restoring blood flow in ischemic stroke patients (reperfusion), RNS60 acts as a cytoprotective agent to preserve brain after a stroke. In the Phase 2 RESCUE clinical trial, RNS60 as an adjunctive therapy demonstrated:5,*
Our research continues to explore how protecting mitochondria can also help reduce brain loss and improve outcome in non-ischemic neuronal injury, as well as combat the progressive decline in neurodegenerative diseases and aging.
We have several discovery programs including:
