On October 30, 2025 Pilatus Biosciences, a biopharmaceutical company developing novel metabolic checkpoint immunotherapies for liver and gastrointestinal cancers, reported the Company will present new preclinical data on its lead product candidate, PLT012, in a poster presentation at the upcoming Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 2025 Annual Meeting, being held November 5-9, 2025 in National Harbor, Maryland.
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"Immunometabolism is a key lever for overcoming resistance in solid tumors," said Dr. Yi-Ru Yu, Lead Scientist at Pilatus Biosciences and presenting author. "Our preclinical results demonstrate that PLT012, a first-in-class anti-CD36 monoclonal antibody, exerts a dual mechanism of action by reprogramming immune-metabolic pathways—suppressing immunosuppressive Tregs while enhancing CD8⁺ T-cell responses in lipid-rich tumors. These combined effects have been shown to drive durable and superior anti-tumor efficacy across multiple cancer models, outperforming anti–PD-1/PD-L1 blockade and inducing long-lasting immune memory that sustains tumor control and protects against rechallenge." Dr. Raven Lin, CEO of Pilatus Biosciences, added "Alongside a favorable GLP toxicology profile, these data support our planned Phase I study, with first patient in (FPI) targeted for Q1 2026."
Details of the SITC (Free SITC Whitepaper) poster presentation are as follows:
Abstract Title: PLT012, a Humanized CD36-Blocking Antibody, Induces Durable Anti-Tumor Immunity via Immunometabolic Reprogrammig
Presenting Author: Yi-Ru Yu, Ph.D., Lead Scientist, Pilatus Biosciences
Date: Friday, November 7, 2025
Time: 12:15 p.m. – 1:45 p.m. EST
Poster Number: 1205
The abstract for this presentation will be available on SITC (Free SITC Whitepaper)’s website on November 4, 2025, and the poster presentation will be available on Pilatus’ website following the meeting.
About PLT012
PLT012 is a humanized monoclonal antibody designed to selectively block CD36-mediated lipid uptake, a key mechanism driving immunosuppression and immune exclusion within the tumor microenvironment. By targeting lipid metabolism, PLT012 exerts a unique mechanism of action: it depletes immunosuppressive cell populations, including Tregs and pro-tumor macrophages, while simultaneously enhancing anti-tumor activities of intratumoral NK cell and cytotoxic CD8+ T cell that are otherwise susceptible to lipid-induced exhaustion. In preclinical studies, PLT012 has demonstrated potent monotherapy efficacy in models of liver malignancies, 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.
(Press release, Pilatus Biosciences, OCT 30, 2025, View Source [SID1234657175])