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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


• 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

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


  • 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


  • 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

3:15 pm Closing Remarks