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March 19-21, 2019 | Boston, MA



Day One
March 20, 2019

Day Two
March 21, 2019

Chair’s Opening Remarks

Re-Training Innate Immunity: Combining the Novel Beta Glucan, Imprime PGG, with Checkpoint Inhibitors to Drive a Robust, Coordinated Anti-Cancer Immune Response

  • Jeremy Graff Chief Scientific Officer and Senior Vice President, Research, Biothera


  • Imprime PGG binds directly to cells of the innate immune system driving innate immune cell-mediated tumor killing, re-orienting macrophage polarization and enhancing antigen presentation capacity
  • Imprime PGG thereby stimulates T cell-mediated immunity
  • Imprime PGG mechanistically complements immune checkpoint inhibitor therapy to trigger a robust anti-cancer immune response

T Cell Engagers, Checkpoints and Cytokines to Broaden Immune Responses to Cancer


  • IO therapy is limited by poor immune recognition, multiple checkpoints and insufficient T cell infiltration
  • Xencor’s pipeline is focused on overcoming these obstacles to broaden the reach of IO therapy
  • CD3 bispecifics overcomes limited immune recognition by directly activating T cells by targeting common hematologic and solid tumor specific targets (CD20, CD123, SSTR2). Clinical trials and next gen approaches will be discussed
  • Bispecific checkpoints clinical trials have been initiated at Xencor (DUET studies) targeting PD1, CTLA4, ICOS and LAG3. Rationale, preclinical antitumor activity and clinical plans/updates will be discussed
  • Rationally designed T cell cytokines (IL-15 and others) with T cell targeting and long acting pharmacodynamic preclinical activity will be discussed that potently enhance intratumoral T cell infiltration

Panel Discussion: Mind the Gap – Considering New Targets from Biological Rationale to Therapeutic Protein Delivery


  • Hear the perspectives from both biological and protein chemistry sides of the discussion, with the goal of honing in on the key areas that each can support one another in tir shared goal of bringing about the new opportunities for developers to pursue
  • Look at the future targets for ICIs and IO combination therapies and assess their true value

Morning Refreshments

Preclinical Testing and Tumor Modelling

11.00 Pre-Clinical Modeling of Immune Responses to Cancer: From Bench-Side to Clinical Outcomes


  • Translatability of pre-clinical murine models in immunooncology.
  • Pre-clinical models for investigating combination therapies.
  • Fundamental differences in the immune system and tumor microenvironments of mice and humans

Mithun Khattar, Scientist & Immuno-Oncology Lead, Takeda

11.30 Stromal-Imposed Immunosuppresion in the Era of Checkpoint Blockade

  • Mesenchymal stromal cells impinge on anti-tumor immunity
  • We still lack a full understanding of the cellular and molecular mechanisms by which stromal-imposed immunosuppression is exerted
  • We have identified a discrete population of FAP+ stromal cells in immune-excluded breast cancers with potent immunomodulatory potentia

Viviana Cremasco, Investigator, Novartis

12.00 Panel Discussion: Reviewing the Future Challenges in Tumor Modeling for IO Combinations

  • Hear the perspectives from both biological and protein chemistry sides of the discussion
  • Look at the future targets for ICI and IO combination therapies

Mithun Khattar, Scientist & Immuno-Oncology Lead, Takeda
Viviana Cremasco, Investigator, Novartis

Clinical Biomarkers, Immunogenicity and Toxicity

11.00 Understanding Immune-Related Toxicities in the Era of Combination Immunotherapies

  • Patterns of immune-related toxicities
  • Factors that determine toxicities
  • Comprehensive program to manage and prevent immune-toxicities

Osama Rahma, Assistant Professor, Dana Faber

11.30 Immunogenicity of I-O Therapeutics: The Good and The Bad

  • I-O therapeutic depended on manipulating immune checkpoints, one consequence of this is an a decreased tolerance including the therapeutic
  • Is it possible that the MOA of I-O therapeutics contribute to immunogenicity to these therapeutics
  • Are I-O combination therapies increasing immunogenicity and are there strategies to screen for this preclinical
  • Strategies to mitigate immunogenicity to I-O therapeutics

Jochem Gokemeijer, Associate Director, Bristol-Myers Squibb

12.00 Panel Discussion: What Are the Solutions to The These Immunogenicity Challenges

  • Consider a framework by which the effects of specific IO combos can be predicted, based on what was learnt in the talks prior
  • Discuss trends that were seen between the previous presentations to solve their respective challenges
  • Look at combining the capabilities of pharma and academia to srolve these problems

Osama Rahma, Assistant Professor, Dana Faber
Jochem Gokelmeier, Associate Director, Bristol-Myers Squibb


Stages 4 – 7: Trafficking and Infiltration of Immune Cells, Improving the Effectiveness Cell Destruction Mechanisms

Innate Myeloid-Cell Inhibition: Explore the Capability of CD-27 Novel Checkpoint-Modulation as an Inhibitor


  • Understand the mechanism behind the blocking of immuno-modulatory capabilities can have anti-tumor effects
  • Gain an understanding of the scientific rationale behind their approach to Myeloid- Based Therapy

PD-1-Based Bispecific Antibody Therapies

  • Paul Moore Vice President - Cell Biology & Immunology, Macrogenics


  • Bispecific antibody strategies simultaneously targeting the PD-1 axis and an additional non-redundant immune pathway provides opportunity for synergistic biological responses and potentially enhanced therapeutic/safety window above that achieved by simple mAb combinations
  • Three case study programs ranging from concept to clinic will be presented: PD1xLAG3; PD1xCTLA4 and PD-L1xCD137
  • Topics covered will span selection of antibody binding specificities and optimization of molecular structure to match desired biology; preclinical pharmacology including comparison to corresponding mAb combinations; IND enabling studies and clinical study design


Panel Discussion – How Can We Sort Through the Huge Number of Trials that are Currently Active?


  • Should we pay more attention to the successes, or the failures?
  • Have we made progress on developing preclinical rationales for immuneoncological combinations which will be more predictive in the clinic and allow earlier prioritization?
  • What clinical data and results in early clinical development allow at the earliest point to decide to discontinue a combination?

Chair’s Closing Remarks