Our Science
The Problem
Metastasis causes the majority of cancer deaths, yet there are no FDA-approved therapies designed specifically to target metastatic spread. Patients with metastatic disease are managed, not cured — and resistance to standard-of-care therapies is nearly universal.
The Insight
Metastatic tumors face overwhelming oxidative stress during dissemination, circulation, and colonization of distant organs. Only cancer cells that activate antioxidant defense programs survive to seed metastases. These same defenses also drive resistance to chemotherapy, radiation, and targeted therapies — making redox stress adaptation a shared vulnerability across metastatic disease and treatment failure.
This insight was first established in Piskounova et al., Nature, 2015, and has since been replicated across multiple tumor types.
Our Target: FTSJ1
In 2024, our founder's laboratory identified FTSJ1, an RNA 2'-O-methyltransferase, as the enzyme responsible for the tRNA modifications that enable metastatic cells to produce the selenoproteins (GPX, TXNRD, SEPP1) they require to neutralize oxidative stress.
In Nease et al., Nature Cancer, 2024, we demonstrated that genetic loss of FTSJ1:
Sensitizes melanoma cells to oxidative stress
Prevents metastatic colonization in vivo
Drives regression of established metastases (proprietary unpublished data)
FTSJ1 represents a first-in-class druggable target for metastatic disease. Human genetics support tolerability: congenital loss-of-function in FTSJ1 is associated with neurodevelopmental phenotypes during development but no major adult organ pathology — supporting the feasibility of chronic dosing in adult oncology patients.
Our Strategy
O₂nix Bio is developing small-molecule FTSJ1 inhibitors in partnership with Synfini Inc., an AI-driven drug discovery platform. Our combination-first clinical strategy positions our therapies to deepen and prolong response when layered onto standard-of-care regimens — turning the tumor's adaptive redox buffering into an Achilles' heel.
We are advancing our lead program through hit-to-lead optimization, with the goal of nominating a clinical candidate within 24 months.
Publications
Nease LA, Church KP, Delclaux I, et al. Selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis. Nature Cancer, 2024.
Piskounova E, Agathocleous M, Murphy MM, et al. Oxidative stress inhibits distant metastasis by human melanoma cells. Nature, 2015.