PLT012:

Reprogramming Metabolism to Combat Tumors

Modality

Discovery

IND-enabling Development

Phase I

Phase II

Immunotherapy
Pipelines

Indication

Discovery

IND-enabling
Development

First-in-Human
Study

Proof-of-Concept
Human Study

PLT012 anti-CD36
Monoclonal Antibody

Solid Tumors
(HCC, CRC)

Metabolic & Autoimmune Diseases

FY2025

FY2026

FY2027

FY2027

Our Target

CD36, also known as fatty acid translocase, is a transmembrane glycoprotein that plays a crucial role in various physiological processes, including lipid metabolism, inflammation, and immune response. Recent studies have shown that CD36 is overexpressed in various types of cancer, including liver, breast, ovarian, lung, and pancreatic cancer, as a poor prognosis marker. Emerging findings have shown that CD36 is selectively upregulated in various malignant cells and tumor-infiltrating immune cells, such as regulatory T cells, cytotoxic CD8 T cells, NK cells and macrophages, for their metabolic adaption in the tumor microenvironment to further dampen anti-tumor immunity and promote tumor progression.

PLT012 Mechanism of Action

PLT012 is a humanized anti-CD36 antibody with a dual mechanism of action. It simultaneously inhibits immunosuppressive cell populations and enhances effector T cell function. Preclinical studies as monotherapy have demonstrated its efficacy in both immune-hot and immune -cold tumor models, with a significant increase in GzmB-expressing CD8+ T cells and reductions in intratumoral Tregs and pro-tumorigenic macrophages. Additionally, PLT012 reshapes the exhaustion profile of cytotoxic CD8+ T cells by expanding both progenitor-exhausted (Texprog) and terminally-exhausted (Texterm) populations with rejuvenated effector functions, leading to enhanced tumoricidal immunity. These findings suggest that PLT012, functioning as a metabolic regulator, may provide therapeutic benefits in cancer treatment, either as a monotherapy or in combination with immune checkpoint inhibitors such as PD-1 or PD-L1 inhibitors. Other than oncology, the unique MOA as a metabolic regulator also shows the potential of reprogramming the metabolic environment with associated benefits, e.g. liver functional improvement, thus laying the groundwork for targeting a broader spectrum of metabolic and immunological diseases.

Key Features

FDA Orphan Drug Designation

Granted for liver and intrahepatic bile duct cancers, providing 7 years of market exclusivity upon approval

Preclinical Efficacy

Demonstrated single-agent anti-tumor activity in both immune-hot and immune-cold tumor models.

Combination Potential

Scientific findings suggest synergizing with ICIs like PD-1/PD-L1 inhibitors.

Excellent Drug Developability

PLT012 has favorable preclinical safety profile and robust manufacturing productivity.

Scientific Reference

CD36-mediated metabolic adaptation supports regulatory T cell survival and function in tumors.
Nature Immunology, Ping-Chih Ho et al., 2020

Uptake of oxidized lipids by the scavenger receptor CD36 promotes lipid peroxidation and dysfunction in CD8+ T cells in tumors.
Immunity, Ping-Chih Ho et al., 2021

Metabolic communication in the tumour–immune microenvironment.
Nature Cell Biology, Ping-Chih Ho et al., 2022

Metabolic programs tailor T cell immunity in viral infection, cancer, and aging.
Cell Metabolism, Yi-Ru Yu, Ping-Chih Ho, et al., 2022

PLT012, a monoclonal antibody targeting CD36, unleashes anti-tumor immunity via metabolic reprogramming in tumor microenvironment.
SITC, 2023 (Poster is available upon request).

Revitalizing Anti-Tumor Immunity Through PLT012 Monoclonal Antibody, Targeting CD36 for Metabolic Rewiring in the Tumor Microenvironment.
AACR Annual Meeting, 2024 (Poster is available upon request).

PLT012: A First-in-class Antibody Targeting CD36, Revolutionizing Immunotherapy by Unleashing Anti-Tumor Immunity through Metabolic Reprogramming in the Tumor Microenvironment.
SITC, 2024 (Poster is available upon request).

PLT012, a Humanized CD36-blocking Antibody, is Effective for Unleashing Anti-tumor Immunity in Fatty Acid-enriched Tumor Microenvironment.
AACR Annual Meeting, 2025 (Poster is available upon request).