Explore the Agenda
8:00 am Check In & Registration
8:45 am Chair’s Opening Remarks
Moving Beyond Small Molecules to Broaden the Therapeutic Options for RAS Driven Cancers
9:00 am Amplifying Anti-Cancer mKRAS Immunity for Improvement of Disease- Free Survival
- Leveraging lymph-node-targeted vaccine technology to activate durable anti-tumour immune responses against KRAS-mutant cancers
- Demonstrating clinical progress with KRAS-directed immunotherapy, including prior Phase 1 data and emerging results from a randomized Phase 2 study in pancreatic cancer
- Advancing immunotherapy beyond small-molecule KRAS inhibition to prevent recurrence in high-risk patients following surgery and chemotherapy
9:30 am Designing a Library of TCR T Cell Therapy Products that Precisely Target Mutant KRAS
- Selecting and validating high value KRAS targets systemized cell biology assays
- Defining potent and selective TCR assets that form the foundation of differentiated TCR T therapy products
- Scaling manufacturing and clinical trial design to enable meet the needs of highly personalized cell therapies
10:00 am Session Reserved for HUB Organoids
10:30 am Morning Break & Networking
11:00 am Moving Beyond Small Molecules: Targeting KRAS-Driven Cancers Through mRNA Vaccination & Adaptive Immune Activation
- Developing AST-1138, an mRNA-based therapeutic cancer vaccine engineered to address KRAS-driven malignancies through precision immune activation, offering a fundamentally distinct and complementary approach to conventional small-molecule inhibitors and targeted protein degraders
- Expanding the breadth of anti-tumor immune recognition by co-targeting both oncogenic mutant KRAS neoepitopes and immunogenic wild-type KRAS domain epitopes, harnessing a proprietary “helper-killer axis” strategy that coordinates MHC Class II–mediated CD4⁺ T helper priming with robust cytotoxic CD8⁺ T cell responses
- Advancing a next-generation immunotherapeutic paradigm powered by the Th-Vac® platform and ASEP AI epitope prediction system, enabling rational, multi-epitope vaccine design that moves beyond the resistance limitations of targeted therapies to establish durable, adaptive anti-KRAS immunity
11:30 am SIL204, an Isoform-Selective Pan-KRAS Silencing Stable siRNA with Dual-Delivery Administration for Pancreatic Cancer: Phase 2 Early Safety Findings & Supporting Preclinical Data
- RNA interference (RNAi) gene-silencing technology offers high locus-level precision, reducing off-target effects with implications for a more favorable safety profile than small-molecule inhibitors
- siRNA directly targets oncogenic gene messengers, enabling intervention earlier in the cellular cancer cascade than other KRAS-directed strategies, with important implications for efficacy
- A unique dual-delivery approach maximizes drug exposure at the primary tumor, overcoming the stromal barrier, while simultaneously targeting micrometastases, two critical disease drivers for locally advanced pancreatic cancer with important efficacy and safety implications
12:00 pm Lunch Break & Networking
Designing the Next-Generation of Drugs by Targeting Alternative RAS Pathways & States to Enhance Therapeutic Efficacy
1:00 pm Next-Generation Pan-KRAS Inhibition: Differentiated Chemistry to Address the Limitations of Contemporary KRAS Therapies
- A novel switch II-targeting scaffold can deliver pseudo-irreversible target engagement with low nanomolar potency across diverse KRAS mutations, addressing the narrow mutational coverage that limits currently approved G12C-specific agents
- Allosteric, non-covalent binding of inactive KRAS, with a slow-off rate and long resident time, can block downstream effector interactions and achieve durable tumor regression in diverse preclinical models
- Oral bioavailability and improved drug-like properties, achievable though a differentiated chemical scaffold, support the translation of these novel pan-KRAS inhibitors toward clinical development
1:30 pm From RAS Biochemistry to Drug Design: How Mutant Cycling & GTP Thresholds Inform Next-Generation RAS Inhibitors
- Revisiting the core biochemistry of RAS mutants to understand how cellular GTP loading and signaling thresholds drive oncogenic transformation
- Examining what first-generation covalent and non-covalent inhibitors revealed about mutant-specific cycling behavior and switch-II pocket accessibility
- Applying biochemical insights from early KRAS inhibitor successes and limitations to guide the design of next-generation RAS-targeted therapies
2:00 pm ETX-929, A Potential Best-In-Class, Oral, Highly Potent & Selective Dual ON / OFF State Pan-KRAS Small Molecule Inhibitor for the Treatment of KRAS Mutant & Wild-type Amplified Cancers
- Kinetic Ensemble platform enabled the development of a mutation agnostic panKRAS inhibitor that engages all KRAS mutant and WT alleles while targeting both active (ON) and inactive (OFF) KRAS states
- Demonstrates how high level drug design choices enable superior selectivity and performance versus competitors restricted to switch II, single state binding
- Optimized drug like properties and exposure profiles to overcome historical bioavailability challenges that limited earlier allele specific KRAS therapies – at IND/Ph1 stage
2:30 pm Afternoon Break & Networking
3:00 pm Expanding the Therapeutic Window in RAS-Driven Cancers: Targeted Degradation via DAC Technology to Enable Safe Pan-KRAS Targeting
- Enabling pan-KRAS/pan-RAS targeting with a potentially improved therapeutic window through antibody-guided DAC technology
- Delivering differentiated biology beyond inhibition by degrading RAS proteins and disrupting downstream signaling pathways
- Advancing toward clinical validation with a growing portfolio of RAS degraders and imminent clinical candidate progression
3:30 pm Achieving Allele Specific KRAS G12D Suppression By Obstructing Oncogene Transcription
- Demonstrating near complete allele specific suppression of KRAS G12D transcription, validated by PCR and confirming precise oncogene shutdown at the source
- Intracellular delivery of oligonucleotide based therapeutics shown directly and indirectly, overcoming one of the major historical barriers for DNA analog modalities
- Debulking tumors in vivo with clear downstream RAS MAPK pathway suppression, establishing strong mechanistic to efficacy alignment in preclinical models