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


• 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

  • George Fromm Vice President of Research & Development, Shattuck Labs


• 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


• 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


• 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


• 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

  • Sandhya Girish Vice President Clinical Pharmacology, Gilead Sciences


• 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


• 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

  • Suba Krishnan Senior Vice President, Clinical Development, Mereo BioPharma


• 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

  • Eran Ophir Senior Vice President Research & Drug Discovery, Compugen


• 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?


• 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?

3:30 pm Chair’s Closing Remarks & End of Summit