Governments and agencies in the US and EU have declared nuclear defense and radiation protection a critical priority. Rising geopolitical tensions, renewed nuclear strategies, and expanding civilian energy programs underscore the urgent need for effective countermeasures. USIL Therapeutics addresses this recognized global emergency with patented solutions designed to protect populations and strengthen resilience.
We are advancing two breakthrough formulations, UT-241 and UT-242, currently in development to deliver next-generation protection against ionizing radiation.


USIL Therapeutics has been selected by the European Space Agency (ESA) for an in-orbit validation mission on the International Space Station (ISS), conducted in partnership with Yuri GmbH. The study will test our full-body radioprotection and mitigation compound under microgravity and intense cosmic radiation, replicating some of the harshest conditions known to science to validate its stability and efficacy in space.
Funded by ESA, this project represents a breakthrough in dual-use biotechnology: bridging defense, healthcare, and space exploration. Insights from orbit will accelerate our path toward field-ready biological protection for soldiers, first responders, astronauts, and future space travelers, reinforcing resilience for both terrestrial crises and future space missions.

This review highlights the role of hydrogensulfide (H₂S) as a key regulator of vascular remodeling, inflammation, andoxidative stress in pulmonary hypertension (PH). It shows how disrupted H₂Smetabolism affects KATP channel activity and hypoxia responses, identifying H₂S supplementation as a promising antioxidative and vasoprotective therapy. Click here to access this publication.
This study demonstrates thatanetholdithiolthione (ADT), a pro-glutathione antioxidant, inhibits NF-κBactivation in human T-cells under oxidative and inflammatory stress. ADT reduced lipid peroxidation, boosted glutathione levels, and showed a protective redox-modulating effect, highlighting its potential in HIV and oxidative stress–related disorders. Click here to access this publication.
This preclinical study shows that AOL, amitochondrial ROS suppressor (S1QEL), reduces tumor growth in human lung adenocarcinoma by lowering ROS without affecting complex I activity. AOL reprograms cancer metabolism, suppresses the Warburg effect, and modulates NDUFV1, its identified binding site - demonstrating a dual role in REDOX controland cancer signaling. Click here to access this publication.
This study highlights the cardioprotective effects of OP2113, a mitochondrial ROS–modulating compound, in a ratischemia/reperfusion model. OP2113 reduced mtROS generation, preserved ATPlevels, and significantly lowered infarct size and no-reflow area withoutaffecting hemodynamics, supporting its potential as a mitochondrial-targetedtherapy for myocardial injury. Click here to access this publication.
This study identifies OP2113 as the first approved drug to selectively inhibit mitochondrial ROS production at the IQ site of complex I without affecting oxidative phosphorylation. In ex vivo ratheart models, it protected cardiac tissue and preserved contractile function, highlighting its potential as a mitochondrial ROS blocker (S1QEL) for neurodegenerative and ischemia-reperfusion disorders. Click here to access this publication.