Day One

• Developing a mechanistically differentiated KRAS G12D inhibitor designed to achieve selective pathway suppression while addressing limitations observed with firstgeneration KRAS targeting approaches
• Exploring rational combination strategies that enhance antitumor activity and delay resistance through complementary pathway modulation
• Demonstrating compelling preclinical efficacy and translational insights supporting clinical advancement in KRAS G12D-driven tumors

• Covering the development of an EGFR-directed RNAi delivery platform
• Discussion on how next generation oligonucleotide chemistries can be utilized for highly specific KRAS mutation selective inhibitors
• Exploration of how newer RNA designs can be used to co-target key combinatorial strategies to enhance efficacy in KRAS mutant cancers

Join our speed networking session tailored for RAS professionals, like yourselves, to connect with

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• Highlighting a fundamental metabolic dependency in mutant RAS cancers by educating audiences on protein scavenging as a shared tumor vulnerability
• Demonstrating efficient tumor delivery and strong safety across multiple RAS-driven models using a protein drug-conjugate platform
• Expanding treatment possibilities by enabling combination and post-resistance strategies alongside next-generation RAS inhibitors

• Comparing mutant-selective versus isoform-selective KRAS inhibitors to evaluate trade-offs between biochemical precision and clinical durability
• Exploring how partial selectivity may extend duration of response and delay resistance in preclinical and clinical models
• Integrating frontline patient data to inform design of next-generation KRAS-targeted therapies that balance efficacy, safety, and real-world performance

• Mapping the global pan-RAS competitive landscape and defining remaining biological and clinical gaps beyond first-generation RAS(ON) and allele-selective inhibitors, highlighting opportunities for differentiated therapeutic strategies
• Leveraging a proprietary molecular-glue discovery platform to identify distinct PPI and enabling identification of differentiated next-generation pan-RAS inhibitors with best-in-class potential
• Demonstrating the therapeutic promise of Healzen Therapeutics’ pan-RAS program through key preclinical insights and program highlights supporting broad activity, improved durability, and competitive differentiation across RAS-driven cancers

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• How does differential targeting influence tolerability and depth of pathway inhibition, and where do selective versus broader approaches ultimately succeed or fail?
• How should mutant-selective versus wild-type-sparing strategies be balanced to deepen inhibition without breaching tolerability limits, especially when layering multi-agent regimens?
• How can safety-first design principles, PK/PD-guided exposure management, mechanism-based toxicity mitigation, and early integration of safety margins, enable continuous pathway suppression and long-term disease control?

• Adaptive resistance to KRAS G12C inhibition: MAPK pathway reactivation remains a key driver limiting depth and durability of response
• Targeting this vulnerability: Combination darlifarnib + adagrasib enhances pathway suppression and overcomes resistance across KRAS G12C preclinical models
• Clinical translation (FIT-001 clinical trial): Early Phase 1a data show manageable safety and encouraging preliminary antitumor activity supporting darlifarnib + KRASi as a combination strategy across solid tumors, including advanced CRC, PDAC and NSCLC

• New Class of Mutant-Targeted Catalytic RAS(ON) Inhibitors
• Exploring strategic combination approaches to amplify efficacy and expand therapeutic reach, building on emerging insights across RAS driven tumor biology
• Showcasing a major year of clinical progress in the field