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7:30 am Check-In & Light Breakfast
8:20 am Chair’s Opening Remarks
Making Strides in the Development of PAN-RAS Inhibitors to Overcome Mutational Heterogeneity & Drug Phenotypically Diverse Cancers
8:30 am Learning from Sotorasib: From Mutant-Selective Covalent Inhibitors to Reversible Pan-KRAS Inhibitors
Synopsis
• How structural insights from KRAS G12C inhibitors guided the design of inhibitors of other oncogenic KRAS mutants
• Pharmacological profiling of pan-KRAS inhibitors and demonstrations of pre-clinical efficacy
• Insights on the tolerability of wild-type KRAS inhibition and the role of on- and off-state targeting
9:00 am Panel Discussion: Does Pan-RAS Hold the Future of Precision Medicine? Exploring Combination Potential & Targeting Novel Isoforms
Synopsis
- What is the current scope and strides in developing pan-RAS inhibitors?
- What combination therapies should be deployed with pan-RAS and how can we inform this?
- What is the future of pan-RAS? Will it replace mutant-specific therapies?
9:45 am Advancing PAN-RAS Inhibitors: Tackling Mutational Heterogeneity in Diverse Cancers Using Cutting-Edge Modalities
Synopsis
- Alternatives to small-molecule drugs for mutant KRAS targeting
- Rationale for bacteria-mediated intracellular delivery of single-domain antibodies (VHH) as a next-generation therapy
- Introducing SVC-KRAb: a first-in-class pan-KRAS-targeting therapeutic
10:15 am Beyond G12: Comprehensive RAS Biomarker Strategy and Clinical Development
Synopsis
- KRAS, HRAS, and NRAS amplifications, over-expression, and mutations, in addition to tumor immune microenvironment factors that may influence response to RAS neoantigen vaccines, reveal critical insights for targeted therapy development
- Tempus’ multimodal, de-identified data and certain assays can help identify a broad set of biomarkers in responsive patients
- Gain perspective on the significance of RAS alteration patterns to outcomes to standard of care and their potential to guide precision oncology, enhancing treatment efficacy and patient outcomes
10:45 am Morning Break & Speed Networking
Synopsis
Our speed networking is the ideal opportunity to get face-to-face time with many of the brightest minds working in the field and introduce yourself to the attendees that you would like to have more in-depth conversations with. Benchmark against industry leaders & establish meaningful business relationships to pursue for therest of the conference and beyond
TRACK A: Drug Discovery & Pre-Clinical Development
Pioneering the Development of Non-Small Molecules as the Next Phenomenon in Precision Oncology with Improved Depth & Durabilityt
11:45 am Unveiling the Potential of RAS-Targeted Vaccines as a Durable & Versatile Immunotherapy Solution
12:15 pm RAS Mutant Targeting TCR-T Development & Manufacturing
12:45 pm Development of an Arenavirus-Based Immunotherapy for Treatment of KRAS Mutant Cancer
TRACK B: Translation & Clinical Development
Striving for Best-in-Class by Elevating the Potency & Selectivity of Next Generation RAS Inhibitors
11:45 am Taking a Direct Approach: FMC-376, a Direct Inhibitor of ON+OFF KRAS G12C, Overcomes the Primary Drivers of Both Innate & Acquired Resistance
12:15 pm Roundtable Discussion: Improving the Oral Bioavailability of RAS-Targeting Inhibitors to Maintain Coverage of the Target & Increase the Depth of Treatment
12:45 pm Targeting Beyond G12C in RAS-Addicted Cancers: Opportunities Using RAS(ON) Tri-Complex Inhibitors
1:15 pm Lunch & Networking Break
Expanding the Treatable Patient Population by Overcoming Hurdles in Drug Discovery Beyond G12C Point Mutations
2:15 pm Addressing mKRAS Inhibitor Resistance with Hetero-Bifunctional mKRAS-HSP90 CHAMPs
2:45 pm Designing Novel Pan-mut-KRAS Inhibitors
3:15 pm Genialis(TM) krasID: a First-in-Class Biomarker to Predict Response & Benefit of KRAS Inhibitors
Developing Next-Generating Inhibitors to Non-Canonical Targets to Overcome Resistance
2:15 pm KO-2806, a Farnesyl transferase Inhibitor, Re-sensitizes KRASG12C NSCLC Tumors to KRASG12C Mutant-Specific Inhibitors
2:45 pm Nano-Antibody (SBT-100) Inhibits KRAS and STAT3, & Penetrates the Blood-BrainBarrier
3:15 pm Panel Discussion: Exploring Model Types with Improved Predictive Value for RASDriven Tumors: Advantages, Challenges & Clinical Translation
3:45 pm Afternoon Break & Poster Session
Synopsis
As the research, discovery, and development into RAS-targeted therapies continues to progress from strength to strength, it is more important than ever to collaborate and learn with your peers, as we continue to advance these therapies to patients in need. Join our dedicated session to share your latest data and have the first look on what your peers are working on!
Exploring Innovations in Vertical Pathway Targeting to Comprehensively Suppress Tumorigenic Activity & Overcome Mechanistic Resistance
4:15 pm Ulixertinib, a Clinically Proven Safe & Effective ERK1/2 Inhibitor with Combination Therapy Potential for Overcoming Resistance via Reactivation of the MAPK Pathway
Synopsis
• Safe and effective targeting of ERK1/2 in humans is possible with ulixertinib
• ERK inhibition provides the backbone for vertical combination treatment to overcome numerous MAPK reactivating resistance mechanisms
• ERK inhibition remains a critical option to be explored for patient benefit, both as first-line and to overcome RAS inhibitor resistance
4:45 pm ONCO Prime – A Comprehensive Platform for Identification of KRAS-Specific Synthetic Lethal Targets Using Patient-Derived Cells
Synopsis
• Showcasing Ryvu’s cutting-edge drug discovery platform, uniquely combining high throughput capabilities with the precision and translational impact traditionally associated with later, lower throughput stages
• Leveraging human stem cell-derived model cells (PDC), patient-derived xenografts (PDXs) and clinical samples to create a groundbreaking approach to identify synthetic lethal (SL) targets specific to oncogenic pathways
• In conjunction with our novel ranking algorithm, these models have successfully identified potential drug targets in KRAS-mutant cells—targets that remained undetected in immortalized CRC cell lines, likely due to genetic and epigenetic alterations accumulated over years of cell culture