Immuno Oncology Europe
Immuno Oncology Europe

Immunomodulatory Approaches track banner


Immunomodulatory Approaches track banner



Final Agenda


13:00 Conference Registration

14:00 Chairperson's Opening Remarks

Catherine Sabatos-Peyton, Ph.D., Senior Investigator II, Exploratory Immuno-Oncology, Novartis Institutes for BioMedical Research (NIBR)


14:05 Multiple Checkpoint Blockade with Bispecific Antibodies

John_DesjarlaisJohn Desjarlais, Ph.D., CSO, Xencor, Inc.

We have optimised an Fc-containing bispecific antibody platform with high stability, efficient production, and antibody-like pharmacokinetics. We will present application of the platform to dual checkpoint blockade bispecifics for T-cell activation. We show that a PD1 x CTLA4 bispecific antibody enhances T-cell activation relative to anti-PD1 alone and comparably to a combination of anti-CTLA4 and anti-PD1 antibodies. Additional checkpoint combinations also display promising preclinical activity.

14:35 Application of the DART Platform to Enhance Checkpoint Blockade

Paul_MoorePaul Moore, Ph.D., Vice President, Cell Biology and Immunity, Macrogenics, Inc.

The flexibility afforded by the DART platform for creation of bispecific antibodies incorporating desired targeting specificities or binding valencies, lends itself to a range of therapeutic applications. As example, the functional characterisation of MGD013, a DART molecule designed to simultaneously block PD-1 and LAG-3, non-redundant checkpoint pathways leveraged by tumours to evade immune surveillance, will be presented. Additional strategies to enhance anti-tumour immune responses using the DART platform will also be shared.

15:05 Understanding the Immune Landscape and Fc Receptors in the Tumour Microenvironment for Engineering of Immune Modulatory Antibodies

Fred_Arce_VargasFrederick Arce Vargas, Ph.D., Haematology, University College London Cancer Institute

It has been demonstrated in the pre-clinical setting that the activity of certain immune modulatory antibodies extends beyond simple receptor stimulation or blockade, relying on an additional capacity to deplete Treg by antibody dependent cell-mediated cytotoxicity (ADCC). Translation of this into the clinic depends on understanding the immune landscape of immune modulatory antibody targets and of the Fc receptors in the tumour microenvironment. We have evaluated this in in vivo models and tested the effects of antibody engineering in the anti-tumour immune response. 

15:35 Sponsored Presentation (Opportunity Available)  


15:50 Refreshment Break in the Exhibit Hall with Poster Viewing


16:30 Tumour and Host Cell PD-L1 Expression Is Required to Mediate Suppression of Anti-Tumour Immunity

Maike_SchmidtMaike Schmidt, Ph.D., Scientist and Group Leader, Cancer Immunology, Genentech, Inc.

Immune oncology therapeutics such as PD-1/PDL-1 blockade have shown unprecedented responses in various indications. PDL-1 expression on tumour or immune cells are independent predictors of response to PDL-1 blockade. Unique mechanistic contribution of tumour and immune cell PDL-1 to tumour immunity was revealed by cell type specific genetic deletion in preclinical models.

17:00 Immunomodulatory Approaches Beyond PD-1

Andrea_van_ElsasAndrea van Elsas, Ph.D., CSO, Aduro Biotech Europe

T cell checkpoint inhibitors set a clinical paradigm providing significant benefit to patients diagnosed with advanced cancer. Despite success, the majority of patients do not respond to PD-1, PD-L1 or CTLA-4 blockade. Raising the number of patients benefiting from cancer immunotherapy requires novel therapeutic approaches aimed at these non-responders, for instance using novel immunomodulatory antibodies and combination with active immunization.

17:30 Adapting a 3D Microfluidic Culture System to Study Immune Checkpoint Blockade for Personalised Immunotherapy

Amir_ArefAmir R. Aref, Ph.D., Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School

Immunotherapy with PD-1 blockade can provide prolonged and durable responses for patients with metastatic melanoma, but only in a limited number of patients. We have successfully adapted a novel microfluidic cell culture technology that recapitulates the tumour microenvironment (TME) by incorporating a model extracellular matrix (ECM), and allowing controlled analysis of growth factor and cytokine-mediated effects. Improved understanding of the response to immune checkpoint inhibitors within the tumour microenvironment will facilitate future efforts to screen for compounds that enhance the response to immune checkpoint blockade, and may ultimately provide a platform for the 'personalization' of immunotherapy.

18:00 End of Day One of Novel Approaches for Cancer

18:00 Dinner Short Course Registration

18:30 - 21:30 SC1: New Directions in Cancer Immunotherapy or SC2: CAR T and TCR Manufacturing Challenges to Anticipate and Overcome

Separate registration required.


08:30 Chairperson's Remarks

Nicolai Wagtmann, Ph.D., Executive Vice President and CSO, Innate Pharma



08:35 Investigations into Mechanisms of Immune Tumour Rejection

Dario_NeriDario Neri, Ph.D., Professor, Chemistry and Applied Biosciences, Swiss Federal Institute of Technology (ETH), Zurich

Certain immunotherapy approaches (e.g., immunological check-point inhibitors, bispecific antibodies, antibody-cytokine fusion proteins) have the potential to eradicate cancer and to confer protective anticancer immunity. Recently, advances in MHC class-I peptidome analysis and multiplex tetramer technology have enabled characterisation of the process of tumour cell recognition by T cells at the molecular level. In this lecture, I will present preclinical and clinical data, outlining how certain tumours are rejected as a consequence of immunotherapeutic interventions.

09:05 Immuno-Oncology: Current and Future Advances

Robert_WilkinsonRobert W. Wilkinson, Ph.D., Director, Oncology Research, MedImmune Ltd.

Immuno-oncology (IO) therapies, such as checkpoint inhibitors (e.g. anti-CTLA-4 and anti-PD-1/PD-L1 antibodies) are demonstrating significant promise in the treatment of haematological and solid cancers. However some patients fail to respond, it is believed that the lack of activity in these patients is limited by insufficient immune priming and or by immunosuppression, within the tumour microenvironment. Further advances to the IO field are taking the form of novel immunotherapies aimed at targeting: T-cell effector responses (such as, TNFRSF agonists); antigen presenting cell function (such as, TLR agonists and virotherapy); and the elimination of immune suppression pathways.

09:35 Problem Solving Roundtable Discussions

Table 1: Challenges with Targeting Immune Checkpoint Inhibitors

John Desjarlais, Ph.D., CSO, Xencor, Inc.

Table 2: Pros and Cons of Immunocytokine-Based Immunotherapeutics

Dario Neri, Ph.D., Professor, Chemistry and Applied Biosciences, Swiss Federal Institute of Technology (ETH), Zurich

Table 3: Stimulation of Agonistic Pathways for Antibody-Based Cancer Immunotherapy

Moderator to be Announced

Table 4: Targeting the Innate Immune Response

Catherine Sabatos-Peyton, Ph.D., Senior Investigator II, Exploratory Immuno-Oncology, Novartis Institutes for BioMedical Research (NIBR)

Table 5: Enhancing Fc Receptor Effector Function in Cancer

Stephen Beers, Ph.D., Associate Professor, Cancer Sciences Unit, Faculty of Medicine, University of Southampton

10:35 Coffee Break in the Exhibit Hall with Poster Viewing


11:20 Tumour-Localised Costimulatory T-Cell Engagement by Bispecific CD137 (41BB) Agonists

Christine_RotheChristine Rothe, Ph.D., Vice President, Discovery & Alliance Management, Pieris Pharmaceuticals, Inc.

 We used the Anticalin platform to generate the CD137 bispecifics PRS-343 (CD137/HER2) and PRS-342 (CD137/GPC3). In ex vivo assays we could show that T cells are efficiently activated when incubated with bispecifics and tumour-target-positive cells. T-cell activation is tumour target-dependent and heavily influenced by geometry of the bispecific. We will present in vivo proof of concept data utilizing a humanised mouse model as well as data on drug-like properties of the bispecifics.

11:50 Multivalent Nanobodies for Development of Differentiated Immuno-Oncology Therapeutics

Catelijne_StortelersCatelijne Stortelers, Ph.D., Senior Project Leader, Technology, Discovery, Ablynx NV

An overview of Ablynx's Nanobody platform technology and advantages in the development of bi-and multi-specific Nanobody drugs for immune checkpoint modulation will be presented, including the selection of Nanobodies to either the same target or to different targets for generating formats with additional or synergistic activity. This presentation will cover a multivalent approach for an agonistic Nanobody against the co-stimulatory immune checkpoint receptor GITR. 

12:20 Sponsored Presentation (Opportunity Available)

12:50 Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own

13:20 Session Break

14:00 Chairperson's Remarks

Stephen Beers, Ph.D., Associate Professor, Cancer Sciences Unit, Faculty of Medicine, University of Southampton



14:05 Novel Combination Immunotherapy Engaging with Myeloid Cells

Wei_Xu Wei Xu, M.D., Ph.D., Senior Scientist, Cancer Immunotherapy Discovery, Roche Pharmaceutical Research and Early Development, Roche Innovation Center Zurich

I will discuss the rationale and data supporting the selected use of immunotherapeutic combinations that are modulating the innate myeloid cells in preclinical models of cancer. Further I will discuss the novel discovery of biomarkers in clinical trials with immune checkpoint inhibition.

14:35 TTI-621 (SIRPaFc): An Innate Immune System Checkpoint Inhibitor Targeting the CD47 "Do Not Eat" Signal

Bob_UgerBob Uger, Ph.D., CSO, Trillium Therapeutics, Inc.

TTI-621 is a soluble SIRPa-Fc fusion protein designed to block CD47, a "do not eat" signal that suppresses macrophage phagocytosis. There is strong evidence that many tumours express high levels of CD47 to escape macrophage-mediated immune surveillance and thus CD47 has recently emerged as a promising target in immune-oncology. The preclinical rationale and emerging clinical data for this novel innate immune system checkpoint inhibitor will be discussed.

15:05 TIM-3: Beyond T-Cell Checkpoints

Catherine_Sabatos-PeytonCatherine Sabatos-Peyton, Ph.D., Senior Investigator II, Exploratory Immuno-Oncology, Novartis Institutes for BioMedical Research (NIBR)

TIM-3 was initially described as a co-inhibitory receptor expressed on IFN-gamma-secreting T cells, now broadly understood to be part of the class of "checkpoint proteins." However, in addition to its role on dysfunctional T cells, TIM-3 is broadly expressed on cells of the innate immune system, including myeloid cells and NK cells. Emerging evidence supports a critical inhibitory role for TIM-3 on myeloid populations, and that blockade of TIM-3 on myeloid cells can support an anti-tumour immune response.

15:35 Refreshment Break in the Exhibit Hall with Poster Viewing

16:00 Development of Antibodies to KIR Checkpoint Receptors on NK Cells

Nicolai_WagtmannNicolai Wagtmann, Ph.D., Executive Vice President and CSO, Innate Pharma

NK cells play important roles in control of cancer by directly killing target cells and by secreting cytokines and chemokines that stimulate T cells. These NK cell activities are controlled by activating and inhibitory NK cell surface receptors, which recognise ligands on target cells. The talk will describe the rationale and early development of lirilumab, a first-in-class therapeutic antibody designed to block KIR checkpoint receptors on NK cells.

16:30 Innate Immune Agonists Can Overcome a Suppressive Tumour Microenvironment to Repolarise Tumour-Associated Macrophages and Augment Antibody Therapy

Stephen_BeersStephen Beers, Ph.D., Associate Professor, Cancer Sciences Unit, Faculty of Medicine, University of Southampton

Tumour-associated macrophages (TAM) typically are poorly cytotoxic and contribute to immune suppression making treatments less effective. We assessed a panel of innate immune agonists for their ability to re-polarise macrophages into a state optimal for mAb-mediated immunotherapy. Reagents which were able to overcome immunosuppression in the tumour microenvironment effectively reversed the TAM inhibitory FcrR profile and provided strong adjuvant effects to anti-CD20 mAb in murine models of normal and malignant B cell depletion.

17:00 Close of Immunomodulatory Approaches

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