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Cambridge Healthtech Institute’s 2nd Annual

Oncolytic Virus Immunotherapy

Commercializing the Exciting Potential of Oncolytic Virotherapy
August 28-29, 2017 | Sheraton Boston | Boston, MA


Oncolytic virotherapy represents an exciting new area of cancer treatment which exploits a virus’s ability to selectively replicate and kill tumor tissue while stimulating a patient-specific immune response against cancer. Interest in the field is at an all-time high following significant deals by Pfizer, Celgene, Amgen, BMS and Boehringer Ingelheim, however, questions still remain around delivery, product and clinical development, pre-clinical modelling, scale-up, manufacturing and suitable commercial models. CHI’s Second Annual Oncolytic Virus Immunotherapy conference brings together the leading industry and academic leaders to discuss the critical steps driving oncolytic virotherapy forward.



Final Agenda


MONDAY, AUGUST 28

7:30 am Registration & Morning Coffee

 

LATEST UPDATES AND FUTURE DIRECTIONS IN ONCOLYTIC VIRUS IMMUNOTHERAPY

8:25 Chairperson’s Opening Remarks

Brian R. Champion, Ph.D., CSO, Psioxus Therapeutics Ltd.


8:30 KEYNOTE PRESENTATION: Engineering and Bio-Selection to Optimize an Oncolytic Virus Platform

John_BellJohn Bell, Ph.D., Senior Scientist, Center for Innovative Cancer Research, Ottawa Hospital Research Institute

Oncolytic viruses are therapeutics that are designed or selected to specifically infect and destroy cancer cells. There are multiple strategies that can be employed to create viruses that replicate in and kill tumors; however, one common feature of malignant cells is that they lack a potent anti-viral response. I will discuss the molecular basis for these defects, how best to exploit them to create tumor killing therapeutics and strategies to improve manufacturing output of oncolytic viruses from manufacturing cell lines based upon these principles.

IMPROVING THE TARGETING AND EFFICACY OF ONCOLYTIC VIRUSES

9:00 Tumor Selective HSV-Based Oncolytic Vectors for Treatment of GBM

Paola_GrandiPaola Grandi, Ph.D., Senior Research Director, Immunology/Virology, Oncorus, Inc.

Oncorus oHSV is controlled by certain microRNAs (miRNAs) that are present in healthy cells, but absent in cancer cells. Typically, miRNAs regulate the ability of classical messenger RNA (mRNAs) to be translated into protein or promote the degradation of mRNAs. By engineering miRNA binding sites into essential viral genes, oHSV replication and cellular destruction is prevented in healthy cells. Since cancer cells lack these specific miRNAs, Oncorus oHSV is free to replicate in and destroy them.

9:30 Coffee Break

10:00 WO-12, a Multi-Mechanistic Immuno-Oncolytic Therapy

Steve_ThorneSteve H. Thorne, CSO, Western Oncolytics Ltd.

The next generation of oncolytic viruses will likely combine multiple genetic modifications (transgenes and viral genetic alteration) that act to synergistically target tumors through multiple mechanisms. In particular, approaches that (i) enhance systemic delivery and viral spread within and between tumors, (ii) activate a potent anti-tumor T-cell response, and (iii) modify the tumor microenvironment to enhance the activity of both the viral therapy and other therapies would produce additional benefits. The Western Oncolytics platform and its lead product WO-12 aim to achieve these goals. WO-12 has demonstrated enhanced activity in preclinical models and will soon enter clinical testing.

10:30 Pepticrad, a Novel Oncolytic Virus-Based Therapeutic Cancer Vaccine

Sari_PeseonenSari Pesonen, Vice President, Clinical Development, Valo Therapeutics

PeptiCRAd (Peptide-coated Conditionally Replicating Adenovirus) is an innovative and unique way of combining two clinically proven cancer immunotherapy approaches: an oncolytic adenovirus and a cancer-specific peptide vaccine, to take advantage of the best features of both technologies. The idea is straightforward: to use immunogenic virus as active carrier of tumor-specific peptides to direct the immune system to specifically target and kill cancer cells.

11:00 Synthetic Virology: Modular Assembly of Designer Viruses for Cancer Therapy

Clodagh_OSheaClodagh O’Shea, Ph.D., Howard Hughes Medical Institute Faculty Scholar; Associate Professor, William Scandling Developmental Chair, Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies

Design is the ultimate test of understanding. For oncolytic therapies to achieve their potential, we need a deep mechanistic understanding of virus and tumor biology together with the ability to confer new properties. To achieve this, we have developed combinatorial modular genome assembly (ADsembly) platforms, orthogonal capsid functionalization technologies (RapAd) and replication assays that have enabled the rational design, directed evolution, systematic assembly and screening of powerful new vectors and oncolytic viruses.

11:30 Sponsored Presentation (Opportunity Available)

12:00 pm Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own

12:30 Session Break

 

ONCOLYTICS IN DEVELOPMENT: UPDATE ON MAJOR CLINICAL AND PRECLINICAL THERAPIES

1:25 Chairperson’s Remarks

Fares Nigim, M.D., Massachusetts General Hospital and Harvard Medical School

1:30 Development of OV Immunotherapy Using a Novel Preclinical GBM Model

Hiroshi_NakashimaHiroshi Nakashima, Ph.D., Instructor, Neuroscience, Brigham and Women’s Hospital

Mechanism of action of the Oncolytic virus includes direct tumor killing and vaccine adjuvant. Since OV immunotherapy is emerge to apply in incurable glioblastoma multiforme (GBM) for the durable therapeutic effects, our new glioma mouse model will provide new opportunity to evaluate the combined OV therapies that work under the patient-mimicked immunological condition.

2:00 FEATURED PRESENTATION: Long-Term Follow-Up in Recurrent High Grade Glioma Patients with Durable Responses Treated with Toca 511 and Toca FC

Asha_DasAsha Das, M.D., Vice President, Clinical Development and Medical Affairs, Tocagen Inc.

Toca 511 is an investigational cancer-selective retroviral replicating vector that delivers cytosine deaminase, which converts the investigational prodrug Toca FC into 5-fluorouracil. Results from three Phase I studies include good safety, gene transduction within tumors, support of immunologic MOA, durable responses, and increased median OS compared to historical studies. Ongoing objective responses start 6-19 months after Toca 511 administration, with 26.7 months’ median duration, and are associated with prolonged survival.

2:30 Pexa-Vec: A Multi-Mechanistic Immunotherapeutic Modulator of the Tumor Microenvironment

Naomi De Silva, Associate Director, Preclinical Science, Sillajen Biotherapeutics, Inc.

Pexa-Vec (pexastimogene devacirepvec, JX-594) is an oncolytic and immunotherapeutic vaccinia virus, engineered to preferentially infect tumor cells, disrupt vasculature, and stimulate anti-tumor immune responses. A Phase III trial evaluating Pexa-Vec in the treatment of advanced primary liver cancer is underway.

3:00 Refreshment Break

3:30 Designing Clinical Trials to Elucidate Oncolytic Virus Mechanisms-of-Action

Caroline_BreitbachCaroline Breitbach, Ph.D., Vice President, Translational Development, Turnstone Biologics

Oncolytic viruses have been shown to target tumors by multiple complementary mechanisms-of-action, including direct oncolysis, tumor vascular targeting and induction of anti-tumor immunity. Phase I/II clinical trials can be designed to validate these mechanisms. Development experience of an oncolytic vaccinia virus and a novel rhabdovirus oncolytic vaccine will be summarized.

CMC, SCALE-UP AND COMMERCIAL MANUFACTURING

4:00 Development of an Attenuated Oncolytic Influenza a Virus Expressing Mycobacterial ESAT-6 Protein

Michael Bergmann, M.D., Ph.D., CMO, Vacthera

We have expressed ESAT-6 in a partial NS1-deletion influenza virus. ESAT-6 expressing viruses were associated with lower levels of NF-kB activating as compared to empty viral vectors. ESAT-6 expressing viruses led to higher titers in eggs up to 1010 TCID50. ESAT-6 expressing deletion viruses were still attenuated when applied to the upper respiratory tract of mice. Intra-tumoral application of virus into B16 melanoma significantly delayed tumor growth.

4:30 Testing and Characterization of Oncolytic Viruses

Jerrod_DenhomJerrod Denham, Ph.D., Principal & Senior Consultant, Dark Horse Consulting

Testing and characterization of oncolytic viruses typically follow the current principles for the majority of gene therapy product critical quality attributes. There are specific challenges with respect to adventitious agent safety testing and viral clearance studies. This presentation will walk through examples of how these challenges were resolved.


5:00 End of Day


TUESDAY, AUGUST 29

7:00 am Registration

7:25 Breakout Discussion Groups with Continental Breakfast

 

ONCOLYTICS IN AN ERA OF COMBINATION THERAPIES

8:25 Chairperson’s Opening Remarks

Matthew Mulvey, Ph.D., CEO, BeneVir Biopharm, Inc.

8:30 Rationale for Oncolytic Viruses as the Backbone of Combination Immunotherapy Regimens

Howard_KaufmanHoward L. Kaufman, M.D., FACS, Surgical Oncologist, Rutgers Cancer Institute of New Jersey

Oncolytic viruses (OVs) mediate anti-tumor activity through direct cell lysis and induction of host anti-tumor immunity. The ability to attract and activate T cells within the tumor microenvironment and induce interferon release suggests that OVs could be used as the backbone in combination immunotherapy strategies designed to promote anti-tumor immunity. Emerging clinical data is demonstrating significant improvement in studies of melanoma, and further clinical development for other cancers is anticipated.

9:00 FEATURED PRESENTATION: Developing Tumor-Specific Immunogene (T-Sign) Combination Immunotherapies by Arming the Oncolytic Group B Adenovirus Enadenotucirev

Brian_ChampionBrian R. Champion, Ph.D., CSO, Psioxus Therapeutics Ltd.

We have developed a broadly applicable platform system, based on the potent chimeric oncolytic adenovirus enadenotucirev (EnAd), for directing the selective localized production of a combination of immunotherapeutic agents within tumors following systemic dosing, while minimizing the potential for systemic off-target effects of such combination approaches. The presentation will highlight recent data supporting both the platform and specific T-SIGn virus candidates.

9:30 T-Stealth Technology Promotes Synergy between Oncolytic Viruses and Immuno-Stimulatory Agents

Matt_MulveyMatthew Mulvey, Ph.D., CEO, BeneVir Biopharm, Inc.

BeneVir is developing an OV platform based on T-Stealth Technology, which hides infected cells from anti-viral T-cells. This allows an OV to complete its replication program, produce progeny viruses, and spread in the tumor microenvironment despite a robust anti-viral T-cell response. In immune-competent murine tumor models, regimens that simultaneously combine immuno-stimulatory agents with T-Stealth armed OV show efficacy. However, there is no effect on tumor burden in these models when simultaneous combination regimens utilize a “Visible” OV that does not encode T-Stealth Technology. BeneVir’s lead OV will enter a Phase I trial in solid tumors in Q2 2018.

10:00 Sponsored Presentation (Opportunity Available)

10:30 Grand Opening Coffee Break in the Exhibit Hall with Poster Viewing

11:15 What Does It Take to Cure Glioblastoma; Combinations Plus?

Samuel_RabkinSamuel D. Rabkin, Ph.D., Professor, Neurosurgery, Massachusetts General Hospital and Harvard Medical School

We will discuss combination therapies for glioblastoma in representative preclinical models, involving oncolytic herpes simplex viruses (oHSV), cytokine expression, and immune checkpoint inhibitors. OHSV induce anti-tumor immunity and can be armed with therapeutic transgenes. The complex multicomponent strategy illustrates both the difficulty in treating non-immunogenic tumors and the opportunities in coupling immunovirotherapy with other immunotherapeutic approaches.

11:45 Oncolytic Virus-Induced Rad51 Degradation: Synergy with Poly(Adp-Ribose) Polymerase Inhibitors in Treating Glioblastoma

Jianfang_NingJianfang Ning, Ph.D., Instructor, Neurosurgery, Massachusetts General Hospital, Harvard Medical School

Oncolytic herpes simplex virus (oHSV) sensitized glioblastoma stem cells (GSCs) to poly(ADP-ribose) polymerase inhibitors (PARPis), irrespective of their PARPi sensitivity through selective proteasomal degradation of key DNA damage response protein, Rad51, mediating the combination effects. This synthetic lethal-like interaction increased DNA damage, apoptosis, and cell death in vitro and in vivo. Combined treatment of mice bearing PARPi-sensitive or -resistant GSC-derived brain tumors greatly extended survival compared to either agent alone.

12:15 pm Close of Oncolytic Virus Immunotherapy

 

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