Boehringer Ingelheim has discontinued BI 770371 (anti-SIRPα) in metabolic dysfunction-associated steatohepatitis (MASH) after it “did not demonstrate efficacy” in an exploratory Phase II study, OSE Immunotherapeutics said. OSE added that BI 770371’s oncology development is unaffected, with multiple Phase I studies ongoing.

Why It Matters To Oncology

• SIRPα is a myeloid checkpoint target; a MASH efficacy miss underscores how indication expansion can de-risk (or derail) programs without necessarily reading through to tumor biology.

• OSE is also narrowing its own early oncology work: it will discontinue exploratory research on its CLEC‑1 program despite calling the target “scientifically promising,” citing lack of near-term clinical/partnership priority.

• Strategic focus is shifting to later-stage value inflection points, including Tedopi (Phase III in non–small-cell lung cancer) while partnered oncology work on BI 770371 continues in Phase I.

The Financials

• AbbVie paid $48M upfront in 2024 for an exclusive global license to OSE-230 and could owe up to $665M in milestones.

• Under a December amendment, OSE is responsible for preclinical and Phase I development of OSE-230, contingent on “securing adequate funding”; AbbVie would resume full development/commercialization after successful Phase I.

• Boehringer paid a one-time “partial royalty buy-out” of €25.3M ($27.4M) in 2024 when it expanded BI 770371 beyond oncology into cardiovascular-renal-metabolic diseases.

What They're Saying

• OSE said Boehringer stopped BI 770371 in MASH because it “did not demonstrate efficacy” in an exploratory Phase II study.

• OSE stressed the oncology program is “unaffected,” with multiple Phase I studies underway.

• CEO Marc Le Bozec: “By stepping away from selected early‑stage programmes… we are concentrating our resources where OSE can create the greatest value in the near term.”

What's Next

• Watch for any details on the exploratory Phase II MASH dataset (endpoints, magnitude of effect, and whether there were biomarker signals despite no efficacy).

• In oncology, the key readouts will be Phase I safety/tolerability and pharmacodynamic evidence of myeloid checkpoint engagement for BI 770371, plus early response signals in selected tumor types.

• OSE’s near-term catalysts shift to Tedopi Phase III progress in NSCLC and continued development of lusvertikimab (OSE-127) in inflammatory indications, while OSE-230 remains paused pending funding.