- Poster presentation to showcase PLT012 targeting CD36 in metabolic dysfunction-associated steatohepatitis (MASH)
- Data demonstrate broad immune-metabolic reprogramming and reduction in key disease hallmarks across preclinical models
DOVER, Del. & EPALINGES, Switzerland--(BUSINESS WIRE)--#EASL26--Pilatus Biosciences, Inc., a clinical-stage biopharmaceutical company developing novel metabolic checkpoint therapies for cancer and immune-related diseases, today announced that it will present new preclinical data on its lead program, PLT012, at the European Association for the Study of the Liver (EASL) Congress 2026, held May 27-30, 2026, in Barcelona, Spain.
The presentation will highlight PLT012’s novel mechanism of action targeting CD36, a fatty acid transporter that plays a central role in lipid-driven immunometabolic dysfunction in metabolic dysfunction-associated steatohepatitis (MASH).
Presentation details are as follows:
- Poster Title: Reprogramming lipid-driven immunometabolic dysfunction in metabolic dysfunction-associated steatohepatitis through PLT012 targeting CD36
- Abstract Number: REG26-2250
- Poster Session: MASLD: Experimental and pathophysiology
- Presenter: Dr. Laura Fernandez-Rodriguez
- Date/Time: Saturday, May 30, 2026, 8:30 AM – 4:00 PM CET
MASH is driven by sustained hepatic lipid overload, leading to inflammation, fibrosis, and progressive liver damage. CD36 is upregulated across hepatocytes and liver-resident immune and stromal cells, promoting lipid accumulation and reinforcing a pro-inflammatory, pro-fibrotic microenvironment.
Preclinical findings to be presented demonstrate that PLT012, a humanized IgG4 antibody targeting CD36, modulates these processes by disrupting lipid uptake and reprogramming the hepatic microenvironment. Across multiple disease models, PLT012 reduced steatosis, inflammation, and fibrosis, while improving markers of liver injury and remodeling immune cell populations toward a more balanced, and less inflammatory state.
“These data underscore the potential of targeting metabolic checkpoints as a new therapeutic strategy in liver disease,” said Raven Lin, CEO & Founder, Pilatus Biosciences. “Pilatus is building a scalable metabolic checkpoint platform extending beyond oncology into additional high-burden diseases driven by immune and metabolic dysfunction, including MASH and fibrosis-related conditions.”
“Metabolic dysfunction and immune dysregulation are deeply intertwined in diseases like MASH, yet few approaches effectively target both,” said Ping-Chih Ho, Ph.D, Professor of Oncology at the University of Lausanne and Ludwig Institute for Cancer Research, and Co-Founder, Pilatus Biosciences. “By intervening at the level of lipid transport through CD36, PLT012 represents a promising strategy to reshape the disease microenvironment. The breadth of effects observed across steatosis, inflammation, and fibrosis in these models is encouraging for future clinical development.”
“By addressing the underlying MASH, PLT012 may also prevent the occurrence of MASH-associated hepatocellular carcinoma (HCC),” said George E. Peoples, M.D., Chief Medical Officer, Pilatus Biosciences. “Currently, we are studying PLT012 in a Phase 1a/1b study in advance solid tumors including HCC. With encouraging early results from selected gastrointestinal cancers, we believe that PLT012 has the capacity to bridge the gap between metabolic disease and oncology treatment paradigms addressing the full MASH-to-HCC continuum, which represents a major unmet medical opportunity, as no approved therapies directly target the biological progression from MASH to fibrosis, and ultimately to HCC.”
The data further show that PLT012 binds the lipid-binding domain of CD36, supporting a targeted mechanism on lipid transport, and demonstrated favorable tolerability in non-human primate studies.
About PLT012
PLT012 is a humanized monoclonal antibody designed to selectively block CD36-mediated lipid uptake, a key mechanism driving tissue injury, immune dysfunction, and disease progression across cancer, chronic and metabolic diseases. By inhibiting CD36, PLT012 interrupts upstream metabolic pathways that promote chronic inflammation, fibrosis, and loss of tissue function. In preclinical oncology studies, PLT012 has demonstrated potent monotherapy efficacy in models of liver malignancies, simultaneously depleting immunosuppressive cell populations while enhancing antitumor effector functions. These effects were achieved with a favorable safety profile across species. Leveraging its distinct mechanism of action, PLT012 further acts as a potent sensitizer in combination with anti–PD-L1 therapies, effectively overcoming drug resistance in immune “cold” tumors and liver metastases. Beyond oncology, PLT012 has demonstrated disease-modifying activity by reducing inflammation, modulating pathological tissue remodeling, and improving organ function, supporting its development as a first-in-class therapy with platform potential across multiple high-unmet-need indications.
About Pilatus Biosciences
Pilatus Biosciences is a clinical-stage biopharmaceutical company developing novel metabolic checkpoint immunotherapies to address unmet medical needs in cancer and immune-related diseases. Founded in 2022 from the Ludwig Institute for Cancer Research, and supported by the Cancer Research Institute, Pilatus operates internationally with R&D teams in Switzerland and Taiwan. The company’s lead program, PLT012, targets CD36 to reprogram the lipid-driven dysfunction across diseases and restore effective cellular function in solid tumors, and chronic and metabolic diseases. For more information, visit www.pilatusbio.com.
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