Cambridge Healthtech Institute’s 3rd Annual

Emerging Immuno-Oncology Targets

Novel Targets and Pathways for Cancer Immunotherapy and Combinations

August 8-9, 2019



While cancer immunotherapy has made a giant leap in the past five years, the majority of therapies at advanced stages of development are clustered in a similar target space. The increased investment in immuno-oncology has created an urgent opportunity to discover and populate new target spaces that either present new classes of immunotherapies or can be used in combination with existing products. Cambridge Healthtech Institute’s Third Annual Emerging Immuno-Oncology Targets conference will cover the emerging target space, including immunomodulatory inhibitor and agonist targets, stromal and immune cell targets, and strategies for rational combination immunotherapy. Case studies of preclinical and translational approaches to the discovery and validation of new immuno-oncology targets and combinations will be presented.

Final Agenda

THURSDAY, AUGUST 8

7:45 am Registration Open and Morning Coffee


8:30 PLENARY KEYNOTE SESSION

PANEL DISCUSSION: Partnering and Licensing in Immuno-Oncology

Big pharma and biotech are under pressure to compete in the booming Immuno-Oncology market and to capitalize on new technologies and innovations to bring next-generation immunotherapies to the patients. This insider panel will share what they look for in a partner or investment, and discuss opportunities for collaboration or in-licensing of novel immunotherapies, IO targets or biomarkers, and potential combination therapies.

Moderator

Jeroen H. Blokhuis, PhD

Director, Business Development, Partnerships, Parker Institute for Cancer Immunotherapy

 

 

 

 

Panelists

Michael Woo, MBA

Head, Search & Evaluation, Immuno-Oncology, Business Development & Licensing, Novartis Institutes for BioMedical Research, Inc.

 

 

 

 

Kathryn McCabe, PhD

Senior Director, Business Development, Emerging Technology and Innovation, Eli Lilly and Company

 

 

 

 

Scott M. DeWire, PhD

Global Head, Business Development and Licensing, Cancer Immunology, Boehringer Ingelheim Pharmaceuticals, Inc.

 

 

 

 

Philip Arlen, MD

President & CEO, Precision Biologics

 

 

 

 

Stephen Doberstein, PhD

Senior Vice President, R&D and Chief Research and Development Officer, Nektar Therapeutics

 

 

 

 

9:30 Coffee Break in the Exhibit Hall. Last chance for poster viewing.

NEOANTIGEN TARGETED THERAPIES

10:10 Chairperson’s Opening Remarks

Andrew Allen, MD, PhD, President and CEO, Gritstone Oncology

10:15 Preliminary First-in-Human Data with a Novel MAB, NEO 201, Targeting a Novel Neoantigen in Solid Tumors

Arlen_PhilipPhilip Arlen, MD, President & CEO, Precision Biologics

NEO-201 was developed from a cancer vaccine derived from an immunogenic component of a cell membrane preparation derived from pooled surgical tumor specimens. NEO-201 demonstrated the ability to bind to wide variety of human epithelial carcinomas but did not react with the normal epithelial tissue. In addition, it has demonstrated tumor destruction through antibody dependent cell mediated cytotoxicity (ADCC). A companion diagnostic IHC based assay has been developed to identify patients expressing the target. An ongoing phase I study in patients with refractory solid tumors commenced in early 2019.

10:45 KEYNOTE PRESENTATION: Driving T Cell Responses to Neoantigens - The Importance of Priming and Accurate Target Selection

Andrew Allen, MD, PhD, President and CEO, Gritstone Oncology

Tumor neoantigens (NeoAg) are a key class of tumor-specific T cell antigens which can drive a therapeutic immune response. To harness them therapeutically, we must first accurately identify true NeoAg from a typically large pool of DNA mutations, the large majority of which are not processed and presented on the tumor cell surface. Then we must prime and boost a potent and polyfunctional naïve T cell response against these antigens.

11:15 Synthetic DNA-Based Neoantigen Targeted Delivery to Address a Wide-Range of Neoantigenic Payloads

Sardesai_NiranjanNiranjan Y. Sardesai, PhD, Co-Founder, CEO & President, Geneos Therapeutics

Tumor neoantigen targeting has emerged as a viable approach for treating cancer and a considerable attention has focused on improved prediction, prioritization, and/or down-selection, and validation of the neoantigenic targets. Beyond prediction and selection algorithms, neoantigen delivery platforms and platform capacity, manufacturability, and potency are important considerations to drive immune responses in vivo. This presentation will discuss the plasmid DNA platform for development of neoantigen targeted personalized cancer immunotherapy.

11:45 Sponsored Presentation (Opportunity Available)

12:15 pm Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own

12:45 Session Break

TARGETING INNATE IMMUNITY

1:40 Chairperson’s Remarks

Michael A. Curran, PhD, Associate Professor, Immunology, Scientific Director, ORBIT Platform, The University of Texas MD Anderson Cancer Center

1:45 Novel, High-Potency STING Agonists Regress Immunotherapy-Resistant Cancers

Curran_MichaelMichael A. Curran, PhD, Associate Professor, Immunology, Scientific Director, ORBIT Platform, The University of Texas MD Anderson Cancer Center

Working with MD Anderson’s Institute for Applied Cancer Science (IACS), we have developed novel, highly potent agonists of the Stimulator of Interferon Genes (STING) pathway. Not only do these STING agonists outperform existing agents in murine syngeneic melanoma models, but they also synergize with T cell immune checkpoint blockade to treat multi-focal pancreatic cancer which responds poorly, if at all, to weaker agonists.

2:15 Targeting the Innate Immune Checkpoint CD47 with TTI-621

Uger_BobBob Uger, PhD, CSO, Trillium Therapeutics, Inc.

CD47 binds to SIRPα on the surface of macrophages and delivers a “do not eat” signal that suppresses phagocytosis. There is strong evidence that many tumors upregulate cell surface expression of CD47 to escape macrophage-mediated immune surveillance. Trillium Therapeutics is developing TTI-621, a soluble SIRPα IgG1 Fc fusion protein to neutralize the suppressive effects of CD47 and promote the eradication of tumor cells by host macrophages.

2:45 Sponsored Presentation (Opportunity Available)

3:15 Refreshment Break


3:45 KEYNOTE PRESENTATION: TNFR2 Antagonism for Cancer: The Value of Treg and Tumor Elimination and Teffector Proliferation

Denise Faustman, MD, PhD, Associate Professor & Director, Immunobiology Lab, Massachusetts General Hospital, Harvard Medical School

The TNFR2 receptor has an important role in the tumor microenvironment, both as a receptor for Treg expansion, as a frequent oncogene for direct tumor expansion and as a frequent escape mechanism for check point inhibitor failures. Over the past 10 years we have worked to create tumor site-specific TNFR2 antagonism and create antibodies that are dominant over the agonistic properties of TNF itself. Extensive modeling and functional studies now confirm this novel class of TNFR superfamily antagonists and regardless of the human mutations in the signaling pathway and regardless of the concentration of the natural ligand, they continue to have in vitro functional activity in end-stage human tumor specimens.

4:15 Targeting “Protector” Cells of the Innate Immune System

Tesi_RaymondRaymond Tesi, MD, CEO/CMO, INmune Bio

In the complex immunobiology of the TME, the cancer subverts the patient’s immune cells as protection from immunotherapy. An alphabet soup of “protector cells”, MDSC, TAM, CAF, TAN, are part of the innate immune system. Today’s therapeutic strategies target effector cells, cytotoxic T and NK cells, that are ineffective in the face of the protector cells of the TME. Eliminating protector cells will alter the immunologic balance in favor of tumor eradication.

4:45 JTX-8064, an Anti-LILRB2 Antagonist Antibody, for Reprogramming Tumor-Associated Macrophages

Shaffer_DonaldDonald R. Shaffer, PhD, Director, Head of Discovery, Jounce Therapeutics

Ligation of LILRB2 on myeloid cells, via its endogenous ligands, classical MHC I molecules and non-classical MHC I molecules (e.g. HLA-G), provides a negative signal that inhibits stimulation of an immune response. We have generated a panel of monoclonal antibodies that bind specifically to LILRB2, but not other LILR family members, and can block binding of LILRB2 to MHC I molecules reprogramming macrophages to promote anti-tumor immunity.

5:15 Close of Day

FRIDAY, AUGUST 9

8:30 am Breakout Discussion Groups with Continental Breakfast

SMALL MOLECULES AND ADCs FOR EMERGING IMMUNOTHERAPY TARGETS

9:30 Chairperson’s Remarks

Roger R. Beerli, PhD, CSO, NBE-Therapeutics AG

9:35 Novel Immune-Stimulatory ADCs (iADCs) for Effective Targeting of Solid Tumors

Beerli_RogerRoger R. Beerli, PhD, CSO, NBE-Therapeutics AG

This presentation will cover: 1) exploring site-specific conjugates with ultra-potent anthracycline toxins; 2) discovering immune-oncology function of NBE’s iADCs; and 3) reviewing preclinical validation of a ROR1 targeting iADC.

10:05 TPST-1120 Antagonism of PPARα Metabolic Checkpoint Suppresses Tumor Growth and Stimulates Anti-Tumor Immunity

Chan Whiting, PhD, Senior Vice President, R&D, Tempest Therapeutics

Tumors evolve fatty acid oxidation (FAO) metabolism to promote their own survival and to suppress tumor-specific immunity. Peroxisome proliferator-activated receptor alpha (PPARα) is the principal transcription factor that regulates the expression of FAO genes. TPST 1120 is a first-in-class selective competitive antagonist of the human PPARα. TPST-1120 induces direct tumor cytotoxicity and generates potent anti-tumor immunity. Preclinical studies indicate TPST-1120 confers anti-tumor efficacy as a monotherapy and augments response when combined with anti-cancer agents including anti-PD1 therapy. A Phase 1/1b open-label, dose-escalation and dose-expansion study of TPST-1120 as a single agent or in combination with systemic anti-cancer therapies is initiated.

10:35 Tomivosertib (eFT508), a Potent and Highly Selective Inhibitor of MNK1 and MNK2, Enhances Checkpoint Inhibitor and CAR T Cell Activity through Modulating T Cell Differentiation

Webster_KevinKevin R. Webster, PhD, Senior Vice President, eFFECTOR Therapeutics

Tomivosertib is a potent, highly selective inhibitor of MNK1/2 that biases T cell differentiation towards TSCM and TCM populations through regulating mTOR signaling. Tomivosertib treatment of T cells yields increased memory populations in vitro and in vivo while maintaining or increasing T cell proliferation, interferon-ɣ production and cytotoxic function. Combination of tomivosertib with checkpoint inhibitors or CAR T cell therapy delivers improved efficacy consistent with increased memory T cell function.

11:05 Small Molecule Approaches to Enhancing Immunity in the Tumor Microenvironment

Wustrow_DavidDavid Wustrow, PhD, Senior Vice President, Drug Discovery and Preclinical Development; FLX Bio, Inc.

Tumors negatively modulate the immune system through a variety of mechanisms. Studies have revealed that regulatory T cells (Treg), myeloid derived suppressor cells (MDSCs) and T cell anergy can play important roles in suppressing the immune response to cancer cells in the tumor microenvironment. This talk will highlight FLX’s platform to identify and develop small molecules which target mechanisms of tumor immune suppression.

11:35 am Close of Conference

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Cambridge Healthtech Institute
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