All times shown in EST. Please refer to the brochure for other time zones.
8:50 am Chair’s Opening Remarks
The Potential of LAG-3 in Haemotological Cancers
9:00 am LAG-3 Blockade with Relatlimab Restores Anti Leukemic Immune Response in Chronic Lymphocytic Leukemia
- Segundo Gonzalez Leader , Universidad de Oviedo
• Chronic lymphocytic leukemia (CLL) is one of the cancers in which LAG-3 has
more clinical influence
• Relatlimab restored NK cell and T-cell mediated responses in CLL ex vivo
• The immunomodulatory drug lenalidomide boost relatlimab activity
Investigating the Mechanism of Action of LAG-3 in Cancer
9:30 am Panel Discussion: Tug of War: Understanding How LAG-3 & PD-1 Interplay with One Another
- Jessica Chacon Assistant Professor , Texas Tech University Health Sciences Center
- Andrew Pierce Vice President - Translational Biology, Crescendo Biologics
- Paul Moore Vice President - Immunology & Cell Biology, MacroGenics
- What are the key learnings and questions that have come out of the RELATIVITY-047 Trial?
- How do we rationally test PD-1/LAG-3 combinations in a way that further elucidates their interplay with one another?
- Will our understanding grow more in vivo with mice, or in the clinic?
Biomarkers, Clinical Endpoints & Patient Stratification
10:15 am Bridging Preclinical & Clinical Worlds
- Giuseppe Gullo Clinical Lead, Regeneron Pharmaceuticals
11:15 am | Speed Networking Break
11:30 am Screen Break
LAG-3 Cell Signalling & Ligand Analysis
12:15 pm How does LAG-3 mediate its inhibitory function?
- Creg Workman Research Assistant , University of Pittsburgh
- LAG-3 functions in the absence of MHC class II ligation
- LAG-3 interacts with the TCR/CD3 complex
- LAG-3 mediates its inhibitory function by inducing co-receptor:p56lck dissociation
Non-PD-1 Based LAG-3 Combinations
12:45 pm Sequential Targeting of PI3Kd & LAG-3 as an Effective Anti- Cancer Approach
- Sarah Lauder Research Associate, Cardiff University
- Immunomodulation by PI3Kδ-blockade led to tumor regressor and nonregressor mice, with complete control of tumor burden reliant on: (1) the dampening of a Treg response and (2) the generation of an improved antigen-specific CD8 response
- Differences in Treg phenotype delineated which mice displayed tumor regression, with non-regressor tumors significantly enriched with cells expressing the coinhibitory receptor LAG-3, compared with Treg in regressor and untreated tumors
- This striking difference prompted us to sequentially block PI3Kδ and LAG-3. This combination enabled successful therapy of all mice, demonstrating the functional importance of LAG-3 in non-regression of tumors with PI3Kδ inhibition therapy
1:15 pm | Lunch Break
Comparing Different Drug Modalities
2:15 pm Panel Discussion: Compare Bispecific & Combination Therapeutic Approaches
- Yvonne Saenger Director of Melanoma Immunotherapy, Columbia University
- Richard Wu Professor , Ohio State University
- Ella Ioffe Director , Regeneron Pharmaceuticals
- Highlighting strengths and weaknesses of the different approaches
- Discussing the variety of unique drug development challenges that come with these different modalities at the clinical stages
Beyond Oncology: What are we Learning in other Therapeutic Areas?
2:45 pm The role of LAG-3 in Mediating Alpha-Synuclein Pathology in Parkinson’s Disease
- Xiaobo Mao Associate Professor, Johns Hopkins School of Medicine
- LAG-3 is the receptor of pathogenic alpha-synuclein fibrils
- Neuronal LAG-3 facilitates the uptake of pathogenic alpha-synuclein fibrils and pathology spreading
- The efficacy of anti-LAG-3 against alpha-synuclein-related pathogenesis