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8:00 am Check-In & Light Breakfast
8:50 am Chair’s Opening Remarks
Examining Precision Monotherapies Post-Approval: Learnings from Approved Drugs to Charter the Course for Next-Generation RAS-Targeting
9:00 am Learnings from the RAS-Targeted Therapeutics Clinical Trials of Sotorasib
Synopsis
• Showcasing where the approved KRAS inhibitors are today and how they get there
• Reviewing learnings from the sotorasib development journey
• Exploring what the future of monotherapies and combination regimes hold
9:30 am Overcoming Therapeutic Resistance & Efficacy Challenges in RAS-Mutant Cancers with Certis Oncology Intelligence®
Synopsis
• Exploring CertisAI™ to predict the response of- and identify predictive biomarkers for- RAS-targeted therapies, including novel drug combinations and monotherapies
• Mimicking clinical scenarios, including prior treatment, radiotherapy, acquired drug resistance, metastases and immune response to evaluate resistance mechanisms and design novel strategies for RAS-driven lung, colorectal and pancreatic cancers
• Tracking tumor burden, response, and pathophysiological processes in clinically relevant cancer models, using advanced multi-modality imaging
9:45 am Fulzerasib – A Journey from Second Line to First Line
Synopsis
• From Discovery to IND: Critical criteria to accelerate the pre-clinical development process
• Picking the best partner, at/for the right timing
• Key to survival: Differentiated global clinical development strategy and CMC
10:15 am Leveraging Multi-Omic Testing to Advance RAS-Targeted Cancer Therapies
Synopsis
- Innovations in RAS Mutation Detection and Personalized Treatment: ddPCR™ testing enhances the detection of RAS mutations, facilitating earlier diagnosis, personalized therapy development, and longitudinal monitoring of disease recurrence in RAS-mutant cancers.
- Integrating Proteomics for Comprehensive RAS Targeting: Proteomic testing identifies a patients' immune response to RAS mutant positive cancers, enabling the identification of aggressive cancer phenotypes and informing combination strategies, such as enhanced surveillance, immunotherapy, and chemotherapy for improved patient outcomes.
(Biodesix, Biodesix logo are registered trademarks of Biodesix, Inc. ddPCR is a trademark of Bio-Rad Laboratories, Inc.)
10:45 am Morning Networking Break
TRACK A: Drug Discovery & Pre-Clinical Development
Spearheading the Development of RAS-Targeting PROTACs & Molecular Glues with Improved Selectivity to Overcome Acquired Resistance
11:45 am Development of the Pan-RAF-MEK Molecular Glue NST-628 & Opportunities for RAF Paralog Selective Molecular Glues
12:15 pm Panel : Debating the Therapeutics Utility of PROTACs & Molecular Glues versus Direct Targeting of RAS to Strategies Best-in-Class Therapeutic Interventions
TRACK B: Translation & Clinical Development
Optimizing Therapeutic Dosing & Toxicity Management Across Clinical Phase I-III
11:45 am Divarasib in NSCLC with a KRAS G12C Mutation
12:15 pm Asking More of Small Molecule KRAS Inhibition: Combination with Immunotherapy & Beyond G12C
12:45 pm Lunch & Networking Break
Employing Chemistry & Biology Insights to Improve the Potency & Safety of RAS-Targeting Candidates
1:45 pm Panel : Debating Optimal PK/PD Profiles to Carve Out the Optimal Inhibitor for Targeting RAS
2:30 pm Intercepting Resistance Gene Amplifications in MAPK Pathway-Activated Cancers
Advancing Translational Models to Convey Complex Tumor Microenvironments & Improve Physiological Relevance
1:45 pm In Vivo Modeling of Oncogenic KRAS Signaling Intensity to Elucidate Its Impact on Pancreatic Cancer Tumorigenesis
2:15 pm The Selective WEE1 Inhibitor Azenosertib Shows
2:45 pm Reshaping the Tumor Microenvironment of KRAS G12D Pancreatic Ductal Adenocarcinoma with Combined SOS1 & MEK Inhibition for Improved Immunotherapy Response
3:15 pm Afternoon Networking Break
The Future Outlook on RAS-Targeting: Expanding Beyond NSCLC & G12C to Improve the Standard-of-Care for Patients with Unmet Clinical Need
3:45 pm Inhibiting Phosphocreatine Dependent Energetic Pathway in RAS-Driven Colorectal Cancer by Blocking the SLC6A8 Creatine Transporter by Ompenaclib
Synopsis
• CKB overexpression pathway in RAS mutated mCRC as a therapeutic target
• Ompenaclib – an oral small molecule blocking SLC 6A8 transport of phosphocreatine
• Pre-clinical and clinical data of ompenaclib activity in RAS mutated mCRC
4:15 pm Targeting the RAS-PI3Kα Interaction as an Efficacious & Tolerated Means of Inhibiting the PI3K/AKT Pathway in RAS-Diven Cancers
Synopsis
• Identification and functionalization of C242, unique to p110α, to disrupt RAS-driven activation of PI3Kα
• Pre-clinical models identify disruption of the RAS-PI3Kα interaction as an efficacious and well tolerated means of targeting the PI3K/AKT pathway
• Detailed mechanistic exploration identifies the PI3K/AKT pathway as critical signaling node that drives resistance to direct targeting of KRAS-G12C. In both CDX and PDX models, addition of VVD’s RAS-PI3K disruptors to a KRAS-G12C inhibitor dosing schedule provide more profound and durable responses