PLT012:

Reprogramming Metabolism to Combat Tumors

Target

Discovery

IND-enabling Development

Phase 1/2

Phase 3/4

CD36
Gastrointestinal (GI) Cancers

Discovery

IND-enabling Development

Phase 1/2

Phase 2/3

Target:  
CD36
Gastrointestinal (GI) Cancers

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

Phase 1 Clinical Trial

PLT012 is currently being evaluated in a first-in-human study in patients with advanced solid tumors

A First-in-Class IgG4 anti-CD36 Humanized Antibody

CD36 as Central Immunometabolic Checkpoint

CD36 drives fatty-acid uptake–mediated immune suppression and tumor progression.

Tumor Microenvironment Reprogramming

PLT012 restores Effector Cell functions and disarms Immunosuppressive Cell populations to combat tumors.

Excellent Drug Developability

PLT012 has favorable preclinical safety profile and robust manufacturing productivity.

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.

PLT012: FDA Designations

Fast Track Designation

Granted by the FDA to facilitate development and expedite review of PLT012 for hepatocellular carcinoma, a serious condition with high unmet medical need.

Orphan Drug Designation

Granted by the FDA to support the development of PLT012 for hepatocellular carcinoma and intrahepatic bile duct cancer, including regulatory incentives and potential market exclusivity.

Expanded Access Policy

Pilatus Biosciences is committed to developing investigational therapies through carefully controlled clinical trials designed to evaluate safety and effectiveness.
At this time, Pilatus Biosciences does not offer expanded access (also known as compassionate use) to its investigational products outside of ongoing clinical trials.
We believe that participation in clinical trials is the most appropriate way to access investigational therapies when ensuring patient safety and generating the data necessary for regulatory review.
Information about our active trials is available at www.clinicaltrials.gov. (NCT07337525)
This policy may be updated as our development programs progress.

Publications

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).

PLT012, a Humanized CD36-blocking antibody, induces durable anti-tumor immunity via immunometabolic reprogramming.

SITC, 2025 (Poster is available upon request).