9:00 am Panel Discussion: Reviewing the Past 12 Months of Progress in Understanding Myeloid Populations and their Role in Immunotherapy

  • Barbara Platzer Principal Scientist II , Novartis Institutes for BioMedical Research
  • Ryan Phennicie Senior Scientist - Immunology & Oncology Discovery , Generate Biomedicines
  • Daniel Getts Chief Executive Officer , Myeloid Therapeutics


  • With no validated clinical evidence of the effectiveness of a therapeutic targeting the TME, what evidence is available and most to those exploring the potential of a therapeutic in this area?
  • What discoveries have been most revealing over the last 12 months?
  • Based on our current understanding, which therapeutic modality is most likely to be the first medium for a myeloid therapeutic?

Activating Myeloid Cells to Drive Strong Responses

9:45 am Role of CD40 on Tumor Infiltrating Myeloid Cells in Immuno-Oncology

  • Peter Ellmark Principal Scientist & Vice President - Discovery , Alligator Bioscience AB


  • Mitazalimab is a CD40 agonistic antibody in clinical development that activates in myeloid cells and antigen presenting cells
  • Clinical biomarker data and preclinical data on Mitazalimab will be presented

10:15 am Virtual Speed Networking Break

11:15 am TTI-621 and TTI-622 Target the CD47 “Do Not Eat” Signal on Tumor Cells

  • Gloria Lin Associate Director of Translational Research, Trillium Therapeutics Inc.


  • TTI-621 and TTI-622 are soluble SIRPαFc decoy receptors that neutralize the suppressive effects of CD47 and deliver an activating signal to macrophages through Fc receptors
  • TTI-621 and TTI-622 are differentiated from other CD47 blocking agents by the lack of RBC binding and greater monotherapy activity
  • Emerging clinical data for both agents will be discussed

11:45 am Inducing Tumor Suppressive Microenvironments through Genome Edited CD47-/- Syngeneic Cell Vaccination

  • Kaiming Ye Chair of the biomedical engineering department , Binghamton University


  • Determined how the tumor microenvironment changes after vaccination with genome edited CD47-/- syngeneic tumor cells
  • Discovered that inactivated CD47-depleted mouse melanoma cells can protect mice from melanoma
  • Revealed a highly anti-tumorigenic and homogenous microenvironment after vaccination

12:15 pm Virtual Networking Break

1:15 pm AMV564 Depletes MDSC & Activates T Cells in Cancer Patients

  • Victoria Smith Chief Scientific Officer , Amphivena Therapeutics Inc.


  • AMV564 is a clinical-stage bivalent T cell engager that selectively targets myeloid derived suppressor cells (MDSC)
  • Subcutaneous injection of AMV564 is well tolerated with early evidence of clinical activity in cancer patients in a phase 1 study
  • Pharmacodynamic data from patients treated with AMV564 demonstrate significant decreases in MDSC in parallel with evidence of CD8 and CD4 T cell activation, polarization and repertoire expansion, with a favorable pro-inflammatory immune milieu

Reprogramming the Tumor Microenvironment to Overcome Resistance

1:45 pm Reprogramming of Tumor Microenvironment Via Macrophage Modulators

  • Tatiana Novobrantseva Chief Scientific Officer, Co-founder & Head of Research & Development , Verseau Therapeutics


  • Macrophages adopt functional roles in response to signals from their environment. Tumor-associated macrophages (TAMs) are regulators of interactions between immune system and cancer, fuel tumor progression, but impact responses to therapy.
  • We found novel targets that change macrophages into antitumor response enablers and validated targets modulating human macrophage biology.
  • Verseau lead program targeting PSGL-1 reprograms macrophages to a pro-inflammatory state, activates T cells, and attracts immune cells to generate anti-tumor responses.

2:15 pm Dynamic Interactions Between Myeloid and Lymphoid cells Regulate Response to Therapy in Solid Tumors

  •  Lisa M. Coussens, Professor and Chairwoman, Department of Cell, Developmental & Cancer Biology Associate Director for Basic Research, Knight Cancer Institute, Oregon Health & Science University

2:45 pm Virtual Networking Break

3:45 pm Identification of GPR65 As a Genetically-Validated, Innate Immune Checkpoint In Tumour Associated Macrophages And Discovery Of Potent And Selective GPR65 Antagonists


  • Tumor-associated macrophages (TAMs) are the major innate immune component in the microenvironment of solid tumors with large numbers associated with poor prognosis across numerous cancer types
  • One of the key determinants of the typically immunosuppressive characteristics of TAMs is the activation of the pH-sensing GPCR, GPR65, by the acidic tumor microenvironment which leads to a sequence of downstream signalling events that suppresses multiple pro-inflammatory cytokines such as TNFa, IL-6 and IL-12
  • Pathios has identified potent and selective small molecule inhibitors of GPR65 that are able to reverse this immunosuppressive signalling, thereby providing the basis for developing therapeutic agents that are able to unleash the power of the innate immune system against a range of cancers

4:15 pm Harnessing Myeloid Cells to Kill Cancer & Alter The TME


  • The functional potential of myeloid cells is unparalleled in the immune system
  • The ATAK myeloid cell platform arms myeloid cells with chimeric antigen receptors with specificity for proteins expressed on tumor cells.
  • Innate receptors allow for potent myeloid cell activation after engagement with tumor antigens.

4:45 pm Modulation of Tumor Microenvironment by Intra-Tumoral Delivery of ONCOS-102


  • ONCOS-102 is an oncolytic adenovirus which encodes human GM-CSF
  • Effects of intra-tumoral administration of ONCOS-102 have been investigated in several cancer indications
  • Profound reprogramming of tumor microenvironment induced by ONCOS-102 includes significant changes in the tumor associated myeloid compartment which is linked to observed clinical benefits

5:15 pm End of Day One