Pilatus Biosciences to Present Preclinical Data Highlighting PLT012’s Disease-Modifying Potential in COPD at ERS International Congress 2026
Pilatus Biosciences, a clinical-stage biopharmaceutical company focused on developing innovative metabolic checkpoint immunotherapies for cancer and immune-mediated diseases, has announced that new preclinical findings for its lead investigational therapy, PLT012, will be presented at the European Respiratory Society (ERS) International Congress 2026, taking place from September 5–9, 2026, in Barcelona, Spain. The presentation represents an important milestone for the company as it expands the potential applications of its CD36-targeting platform beyond oncology and metabolic disorders into chronic respiratory diseases.
The upcoming presentation will showcase encouraging preclinical evidence demonstrating that PLT012, a first-in-class monoclonal antibody targeting the CD36 receptor, may offer disease-modifying benefits in chronic obstructive pulmonary disease (COPD). The results build upon earlier research in cancer immunotherapy and metabolic dysfunction, suggesting that inhibition of CD36 may have broad therapeutic value across multiple diseases driven by chronic inflammation, lipid dysregulation, and impaired tissue repair.
Expanding the Potential of the CD36 Metabolic Checkpoint Platform
Pilatus Biosciences has positioned CD36 as a novel metabolic checkpoint with the potential to influence numerous biological pathways involved in disease progression. Unlike traditional therapeutic strategies that focus on individual inflammatory mediators, PLT012 is designed to selectively block CD36, a receptor that plays a central role in lipid metabolism, immune regulation, chronic inflammation, and tissue remodeling.
According to the company, targeting CD36 offers an opportunity to simultaneously address several pathological mechanisms that contribute to disease development rather than treating symptoms alone. This broader biological impact supports Pilatus’ long-term strategy of creating a versatile therapeutic platform capable of addressing diverse conditions through a common molecular mechanism.
The new COPD findings further strengthen this strategy by demonstrating that modulation of CD36 activity may improve outcomes in chronic lung diseases characterized by progressive tissue destruction and persistent inflammation.
COPD Remains a Significant Global Health Challenge
Chronic obstructive pulmonary disease is among the leading causes of illness and mortality worldwide. The disease is characterized by persistent airflow limitation, chronic inflammation of the lungs, destruction of alveolar structures, and gradual loss of respiratory function.
Current treatments for COPD—including bronchodilators, inhaled corticosteroids, and combination therapies—primarily focus on relieving symptoms, reducing exacerbations, and improving quality of life. However, none of the currently available therapies are capable of reversing lung tissue damage or significantly altering the underlying progression of the disease.
As a result, there remains an urgent need for therapies capable of slowing or halting structural lung damage while promoting tissue repair and regeneration.
Researchers have increasingly recognized that disturbances in lipid metabolism contribute significantly to COPD progression. Elevated expression of CD36 has been associated with abnormal lipid accumulation, excessive inflammatory signaling, oxidative stress, and impaired repair of damaged lung tissue. These discoveries have made CD36 an attractive therapeutic target for disease-modifying intervention.
PLT012 Demonstrated Promising Activity in Preclinical COPD Models
The data to be presented at ERS 2026 indicate that PLT012 successfully modulated several biological processes involved in COPD progression.
According to Pilatus Biosciences, treatment with PLT012 produced multiple beneficial effects in preclinical models, including:
- Significant reduction of chronic inflammatory responses within lung tissue.
- Preservation of alveolar architecture that is typically damaged during COPD progression.
- Improvement in overall lung function.
- Modulation of immune activity through selective inhibition of CD36.
- Evidence supporting enhanced tissue repair and regeneration.
Collectively, these findings suggest that PLT012 may go beyond symptom management by targeting the biological drivers responsible for progressive lung damage.
Rather than simply suppressing inflammation, the therapy appears to interrupt the cycle of chronic injury, immune activation, and failed tissue repair that characterizes COPD.
A Differentiated Therapeutic Strategy
Unlike many currently available COPD treatments that primarily reduce inflammation or relax airway muscles, PLT012 is designed to influence metabolic pathways that regulate immune cell behavior and tissue remodeling.
CD36 functions as an important receptor involved in fatty acid uptake, immune-cell activation, and cellular metabolism. Excessive activation of this pathway has been implicated in multiple chronic inflammatory diseases.
By selectively blocking CD36, PLT012 seeks to restore healthier metabolic balance while reducing pathological immune activation.
This dual activity may distinguish the therapy from existing anti-inflammatory medications by simultaneously promoting structural repair alongside immune regulation.
If future clinical studies confirm these findings, PLT012 could represent a completely new therapeutic class for COPD treatment.
Supporting a Pipeline-in-a-Product Strategy
Pilatus Biosciences continues to emphasize what it describes as a “Pipeline-in-a-Product” approach.
Instead of developing unrelated medicines for separate diseases, the company is leveraging a single biological target—CD36—to potentially treat multiple conditions that share overlapping mechanisms involving chronic inflammation, metabolic dysfunction, and impaired regeneration.
The company’s research efforts currently extend across several therapeutic areas, including:
- Oncology
- Metabolic dysfunction-associated steatohepatitis (MASH)
- Chronic inflammatory disorders
- Respiratory diseases such as COPD
The latest COPD data expand the potential reach of this platform while reinforcing earlier findings generated in cancer and liver disease research.
Leadership Highlights Platform Expansion
Raven Lin, Chief Executive Officer and Co-Founder of Pilatus Biosciences, described the upcoming ERS presentation as further validation of the company’s scientific platform.
According to Lin, the new results demonstrate the versatility of CD36 inhibition across multiple disease areas. Following encouraging oncology data and recently published findings in metabolic-associated steatohepatitis, COPD represents another important indication where targeting CD36 may provide meaningful therapeutic benefit.
He noted that the company’s expanding research portfolio supports its strategy of advancing a single differentiated mechanism capable of addressing diseases characterized by persistent inflammation, metabolic imbalance, and inadequate tissue repair.
Understanding the Biology Behind COPD
Growing scientific evidence suggests that COPD progression involves much more than chronic inflammation alone.
Repeated exposure to harmful particles—most commonly cigarette smoke but also environmental pollutants and occupational hazards—leads to ongoing injury within lung tissue.
Over time, immune cells become chronically activated, inflammatory mediators accumulate, and structural components of the lungs gradually deteriorate.
Recent research indicates that abnormal lipid metabolism contributes significantly to these pathological processes.
Elevated CD36 activity appears to encourage excessive lipid uptake by immune cells, fueling inflammation while interfering with normal tissue regeneration.
Consequently, therapies capable of modulating CD36 may interrupt several interconnected disease pathways simultaneously.
Scientific Perspective on PLT012
Yi-Ru Yu, Ph.D., Head of Biology at Pilatus Biosciences, emphasized that PLT012 was specifically designed to interfere with these underlying biological mechanisms.
According to Yu, selectively blocking CD36 offers a fundamentally different therapeutic approach compared with conventional anti-inflammatory therapies.
Rather than acting on isolated inflammatory signals, PLT012 seeks to reduce inflammation while simultaneously promoting regeneration of damaged tissue.
She stated that the latest findings strengthen the company’s belief that CD36 functions as a central disease driver across multiple therapeutic areas.
If validated clinically, this mechanism may enable disease-modifying benefits extending well beyond oncology into numerous immune-mediated disorders.
Building Upon Existing Oncology and MASH Research
The COPD research complements Pilatus Biosciences’ broader development efforts involving PLT012.
Previous studies have investigated CD36 inhibition within oncology, where metabolic checkpoints influence tumor growth, immune suppression, and resistance to therapy.
The company has also generated encouraging findings in MASH, demonstrating the potential impact of CD36 modulation on liver inflammation and fibrosis.
Adding COPD to the development portfolio broadens the possible applications of PLT012 while reinforcing the versatility of the company’s platform.
ERS 2026 Presentation
The new findings will be formally presented during the European Respiratory Society International Congress 2026, one of the world’s largest scientific meetings dedicated to respiratory medicine.
Presentation details include:
- Presentation Title: Targeting CD36 with PLT012 for Tissue Regeneration and Immune Modulation in COPD
- Presentation Date: Tuesday, September 8, 2026
- Presentation Time: 8:00–9:30 AM
- Presenter: Dr. Laura Fernandez-Rodriguez
- Venue: Fira Gran Via, Barcelona, Spain
The presentation will provide researchers and clinicians with a detailed overview of the preclinical evidence supporting PLT012 as a potential disease-modifying therapy for COPD.
While PLT012 remains in clinical development, the expanding body of preclinical evidence underscores the growing interest in targeting metabolic checkpoints as a novel therapeutic strategy.
The upcoming ERS presentation represents another important step for Pilatus Biosciences as it seeks to demonstrate that CD36 inhibition can provide benefits across oncology, metabolic disease, and chronic inflammatory disorders. By focusing on mechanisms that regulate immune function, lipid metabolism, and tissue repair simultaneously, the company hopes to establish PLT012 as a versatile therapeutic candidate capable of addressing significant unmet medical needs in multiple disease areas.
As research continues, future clinical studies will determine whether these promising preclinical findings can translate into meaningful improvements for patients living with COPD and other chronic inflammatory diseases.
About PLT012
PLT012 is the lead investigational therapy from Pilatus Biosciences’ first-in-class CD36 metabolic checkpoint platform. The humanized IgG4 monoclonal antibody selectively blocks CD36, a key regulator of lipid metabolism, inflammation and tissue repair. PLT012 is currently being evaluated in an ongoing Phase 1 oncology clinical trial, where it has demonstrated early evidence of disease control together with a favorable safety profile. In preclinical studies, PLT012 has demonstrated disease-modifying activity across oncology, MASH and COPD, supporting Pilatus’ Pipeline-in-a-Product strategy to develop a single differentiated mechanism across multiple high-unmet-need indications.
About Pilatus Biosciences
Pilatus Biosciences is a clinical-stage biopharmaceutical company pioneering metabolic checkpoint therapeutics for 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, U.S, and Taiwan. The company’s lead program, PLT012, targets CD36 to reprogram the tumor microenvironment and restore anti-tumor immunity in solid tumors.