Pilatus Targets CD36 to Reverse PD-1 Resistance
Pilatus Biosciences presented preclinical data on its anti-CD36 antibody PLT012 at the SITC 2026 annual meeting in Phoenix.
Updated on Nov. 5, 2026 in Cancer
Pilatus Biosciences presented new preclinical data on PLT012, an investigational anti-CD36 monoclonal antibody, at the SITC 41st Annual Meeting. In preclinical liver cancer models with acquired PD-1 resistance, PLT012 significantly inhibited tumor growth.
Why it matters
Acquired resistance to PD-1 therapy limits benefit for many patients with cancer, and the research links that resistance to lipid metabolism and immunosuppression within tumors. The findings point to CD36 as a potential target for patients whose disease no longer responds to anti-PD-1 treatment.
The findings come from preclinical models rather than human trials, and the resistance model was built through three generations of consecutive anti-PD-1 treatment and selection. Whether these effects will hold in patients has not yet been established.
The players
Pilatus Biosciences
A company based in Epalinges, Switzerland, developing PLT012 and planning its Phase 1/2 clinical development in hepatocellular carcinoma.
Zhongshan Hospital, Fudan University
A major teaching hospital in Shanghai, China, that collaborated on the preclinical research behind PLT012.
The details
The study combined a preclinical model of acquired PD-1 resistance with multi-omic analyses of tumor metabolism and immune activity. Researchers found that increased CD36 expression on tumor-infiltrating immune cells was associated with reduced effector T-cell and natural killer cell activity, and that targeting CD36 with PLT012 mitigated this lipid-associated immunosuppression. The research was conducted with investigators at Zhongshan Hospital, Fudan University.
Timeline
November 4-8, 2026: SITC 41st Annual Meeting held in Phoenix, Arizona.
November 5, 2026: Pilatus announced the new preclinical PLT012 data.
November 7, 2026: Poster 380 on PLT012 presented at the Phoenix Convention Center.
Health Landscape
The work extends efforts to understand why checkpoint inhibitors such as anti-PD-1 therapies lose effect over time, a challenge that has limited their benefit in liver cancer. By pointing to CD36-driven lipid metabolism as a driver of resistance, the research adds a metabolic dimension to a field that has largely focused on immune checkpoints.
For patients whose liver cancer stops responding to PD-1 therapy, a future CD36-targeting treatment could become an option if clinical trials confirm the preclinical results. Until then, current treatment decisions remain unchanged and should be discussed with an oncologist.
The takeaway
Acquired resistance to immunotherapy may stem partly from tumor metabolism, not only immune checkpoints alone. Whether CD36 targeting can reverse that resistance in patients is the question the planned clinical trials will need to answer.
What happens next
Pilatus plans to begin Phase 1/2 development of PLT012 in hepatocellular carcinoma, prioritizing monotherapy dose optimization and rational combination studies.
Further reading
Learn more about cancer research and treatment in our Cancer section.
Source note: This article includes information reported by Firstwordpharma.
