Day Two Agenda
Please Note: Times Listed as EST | PST
8:00 am Registration & Virtual Networking
8:50 am Chair’s Opening Remarks
Showcasing the Breadth of Next Era TIGIT Axis Targeted Approaches in Preclinical Development
9:00 am Exploring TIGIT in Heme Malignancies
Synopsis
• Details to be Announced
9:30 am Understanding How & Why LIGHT (TNFSF14) Co-Simulation Enhances Myeloid Cell Activation & Anti-Tumor Immunity in the Setting of PD-(L)1 & TIGIT Checkpoint Blockade
Synopsis
• Outlining how TIGIT-Fc-LIGHT was designed to block all TIGIT-ligand interactions, provide immune co-stimulation to CD8+ T and NK cells via HVEM and myeloid cells by LTBR
• In combination with CPI, TIGIT-Fc-LIGHT may broaden anti-tumor responses into PDL1-low and CPI acquired resistance tumors
• Addressing why TIGIT-Fc-LIGHT differs from antibody blockade of TIGIT, since its co-stimulatory activity (HVEM and LTBR versus DNAM-1) are not directly inhibited by PD1 nor down-regulated on TIL in advanced tumors
10:00 am Sharing a Summary of Preclinical Development of NTX2R13 – A Best-in-Class CD112R Asset
Synopsis
• Details to be announced
10:30 am Morning Break
11:00 am Discussing an Oral Immune Checkpoint Antagonist Dually Targeting TIGIT & PD-1 Pathways for Cancer Therapy
Synopsis
• Identifying an orally bioavailable dual TIGIT and PD-L1 inhibitor
• The compound shows potent rescue of PVR-mediated inhibition of IL-2 and IFN-γ production from T-cells and PD-L1 mediated PBMC proliferation
• Discovering that in syngeneic tumor models, upon oral administration the compound shows excellent tumor distribution and exhibits profound anti-tumor activity coupled with immune PD on both T and NK cells
Disease Selection & Maximizing the Role of TIGIT Outside of Oncology Indications
11:30 am Delving into the Role of TIGIT in Infectious Diseases & Autoimmunity
Synopsis
• Demonstrating evidence for TIGIT dampening immune responses and ameliorating autoimmunity
• Revealing that TIGIT is highly expressed upon infection
• Discovering that TIGIT dampens immune pathology in infectious settings
Assessing the Immunotherapy Armamentarium to Optimize Combinations & Dosing Strategies
12:00 pm Discussing Dosing Considerations in the Development of CPIs: PD1/L1 & TIGIT Therapies
Synopsis
• Clinical pharmacology of checkpoint inhibitors is well understood given the wealth of data
• Outlining quantitative approaches that can help with optimizing dose for monotherapy and combination treatments
• Addressing the confounding factors at play in assessing the impact of therapies on outcomes
Showcasing Clinical Data of Drugs in Development Against the TIGIT Axis Network of Targets
12:30 pm Targeting PVR as a Superior Strategy for DNAM1 Restoration
Synopsis
• PVR blockade prevents both TIGIT and CD96 inhibitory signaling
• PVR blockade restores DNAM1 to the surface of key immune cells
• Demonstrating that the restoration of DNAM1 results in unprecedented anti-tumor activity by CD8 T and NK cells
1:00 pm Lunch
2:00 pm Sharing Preliminary Safety & Efficacy Data of Etigilimab Combined with Nivolumab: Going Beyond NSCLC
Synopsis
• Demonstrating durable clinical benefit in tumor types that are not typically responsive to PD-1/PD-L1 inhibitors
• Highlighting robust target engagement
• The combination is safe and well tolerated; there are no new safety signals
2:30 pm Unlocking the Potential of PVRIG & TIGIT Pathways to Deliver the Next Transformational Cancer Immunotherapy Drugs
Synopsis
• CPIs have been successful in treatment of some cancer patients; however, majority of patients do not respond. Using its pioneering computational discovery platform, Compugen discovered the checkpoints TIGIT and PVRIG
• Data to date suggests triple blockade of PVRIG/TIGIT/PD-1 may be required for optimizing clinical responses in both inflamed and less inflamed tumors where other CPIs have been unsuccessful. Blocking PVRIG has the potential to reinvigorate exhausted T-cells and generate a new wave of T-cells to infiltrate the tumor microenvironment
• Phase 1 clinical data with potentially first in class anti-PVRIG, COM701 alone and in combination demonstrated durable disease control rates, consistent immune activation and good tolerability. Phase 1 clinical data with potentially best in class anti-TIGIT COM902 showed a disease control rate of 50%, good tolerability and crucially unlike some other anti-TIGITs avoided depletion of CD9+T cells. Translational data supports synergistic immune activation with the triple combination
Optimizing TIGIT Axis Targeted Drug Design to Improve Pharmacology Profiles
3:00 pm Engagement of FcγR by a-TIGIT mAbs: Does It Matter & Why?
Synopsis
• Comparing differentiated mechanisms of action of Fc-live and Fc-dead a-TIGIT drugs
• How do Fc-live and Fc-dead a-TIGIT compare in preclinical setting?
• How do Fc-live and Fc-dead a-TIGIT compare in patients?