Explore the Agenda
8:00 am Registration Opens & Morning Welcome Coffee
8:50 am Chair’s Opening Remarks
Deep Diving into the Potential of Pan RAS Targeting & Liquid Biopsy Strategies to Advance Effective Inhibitors for Treating a Wide Array of Cancers
9:00 am Targeting Oncogenic RAS with Tri-Complex RAS(ON) Inhibitors
- RAS(ON) inhibitors selectively target the active GTP-bound form of oncogenic RAS and lead to deep and durable responses in preclinical models of RAS-driven tumors
- RAS(ON) mutant- and multi-selective inhibition has demonstrated anti-tumor activity in RAS addicted PDAC and NSCLC
- Potential combination strategies to forestall/address emerging resistance mechanisms to RAS(ON) inhibition are being explored
9:30 am A Series of Clinically Applied Small Molecule Pan-KRAS Inhibitors Arrest the KRAS GTPase Cycle to Drive Robust Anti-Tumor Efficacy in KRAS Mutant Tumor Models
- Pfizer’s Pan-KRASi series arrests the KRAS GTPase Cycle and blocks the interaction of KRAS with its effectors (including RAF) and interactors, including Guanine Nucleotide Exchange factor (GEFs), SOS-1
- Pfizer’s Pan-KRASi series demonstrates robust in vitro and in vivo activity across all major KRAS mutant alleles, in models representative of multiple tumor types
- Overcoming Receptor Tyrosine Kinase (RTK)-driven adaptive resistance to Pan-KRAS inhibition drives more durable ERK-MAPK pathway suppression and deeper efficacy in KRAS mutant tumor models
10:00 am Rapid Turnaround Liquid Biopsy Testing in the Evaluation of RAS Mutational Status During Treatment
- Advances in targeted biomarker testing have progressed in parallel with RAS inhibitor innovation ddPCR is a highly sensitive, targeted, and economical alternative to NGS during longitudinal monitoring of RAS alterations in clinical studies
- Biodesix has demonstrated utility of rapid, high-throughput sample testing from blood samples across multiple cancer types leading to more informed and accelerated decisions by biopharma partners.
10:30 am Morning Break & Speed Networking
This session is your opportunity to get face-to-face with many of the brightest minds working in the RAS-targeting field and establish meaningful business relationships to pursue for the rest of the conference. Also, don’t forget to enjoy some refreshments before we split off into the 2 different tracks: Drug Discovery & Preclinical Development and Translation & Clinical Development.
TRACK A: Drug Discovery & Preclinical Development
TRACK A: Drug Discovery & Preclinical Development
Optimizing Small Molecule Inhibitors for More Selective & Potent Therapeutics to Treat KRAS-Mutant Cancers
11:30 am Discovery of Potential Best-in-Class Small Molecule Inhibitors Targeting Various KRAS Mutations for Cancers
- Introduction of Abbisko’s KRAS inhibitors franchise
- Discovery of KRAS G12D inhibitor ABSK141 with potential best-in-class oral bioavailability
- Discovery and extensive profiling of pan-KRAS inhibitor ABSK211 with potential best-in-class potency
12:00 pm AZD0022: a Potent, Oral KRASG12D-Selective inhibitor that Drives Robust Anti-Tumor Activity in KRASG12D Models
- Disclosure of AZD0022 as a potent, selective, oral KRASG12D inhibitor which inhibits GDP- and GTP- bound KRASG12D
- AZD0022 drives robust RAS pathway inhibition in vitro and in vivo and displays significant antitumour activity in NSCLC, CRC and PDAC pre-clinical models
- These preclinical data are supportive of the ongoing ALAFOSS-1 Ph1/2 Clinical trial initiated in 2024 in NSCLC, CRC and PDAC patients
TRACK B: Translation & Clinical Development
TRACK B: Translation & Clinical Development
Unraveling Innovative Biomarker & Modelling Strategies for Accurate Assessment of RAS-Targeted Therapeutics Fast-Tracking More Clinical
Successes
11:30 am Developing Multi-Omic Biomarker Strategies for Assessing Sensitivity of RASTargeting Drugs for More Efficacious Therapies
- Uncovering the impact of genomics on RAS inhibitor sensitivity
- Highlighting how transcriptional signatures may affect sensitivity to RAS targeting drugs
- Predicting RAS sensitivity through proteomic biomarkers and pathway analysis to advance more effective RAS-targeting drugs and combinations
12:00 pm Session Details to be Revealed
12:30 pm Lunch & Networking Break
TRACK A: Drug Discovery & Preclinical Development
Evaluating Next Generation Targeting Modalities for Improving RASTargeted Drug Efficacy to Minimize Cancer Progression
1:30 pm D3S-001, a KRAS G12C Inhibitor with Rapid Target Engagement Kinetics, Overcomes Nucleotide Cycling, & Demonstrates Robust Preclinical & Clinical Activities
- The discovery journey of D3S-001 and the unique target engagement kinetics of this nextgeneration KRAS G12C inhibitor
- How its novel mode of action enables the compound to overcome EGF-mediated nucleotide exchange and some of the known resistance mechanisms
- Translating the preclinical features of D3S-001 into the clinic and exploring combination strategies with internal assets (novel IO bispecific antibody and small molecule) to enhance anti-tumor activity and overcome resistance
2:00 pm Roundtable Discussion: Comparing On vs. Off-State Approaches in the Targeting of RAS for Achieving More Durable & Efficacious Responses
- How to achieve high specificity and affinity given the highly dynamic and flexible structures of the on- and off-states of RAS?
- Does targeting active or inactive states of RAS lead to more durable and tolerable treatments of cancer?
- Investigating the key challenges of targeting the active vs inactive states of RAS
2:30 pm Small Molecule Direct Degraders for Cancer Driver Proteins
- PI3Kalpha mutant and isoform specific degraders
- Positive selection screening strategy for KRAS G12D degraders
- Development of novel KRAS degraders
TRACK B: Translation & Clinical Development
Enhancing Cancer Therapy Response Rates by Uncovering Mutation Specific Impacts & Eliminating RAS for Greater Durability
1:30 pm Panel Discussion: Reducing Non-Responsiveness of RAS-Targeted Therapies by Delving into Mutation & Tissue Specific Impacts to Improve Drug Efficac
• Uncovering factors within the tumor microenvironment which may result in non-responsiveness to
RAS-targeted therapies
• How do tissue specific interactions influence efficacy of RAS-targeting drugs?
• How do you successfully overcome or delay resistance to RAS-targeting therapies?
2:30 pm Emerging Cancer Therapeutic Approach to Overcome Challenges of Targeted Therapeutics & Treat RAS-Driven Cancers
- Uncovering a new technology to eliminate RAS and cancer driver genes by fatty acid oxidation (FAO) inhibition
- Overcoming overcome drug resistance and reversing high-fat diet induced tumor growth promotion by FAO inhibition
- Highlighting phase 1 results and movement into phase 2 clinical trial
3:00 pm Afternoon Networking Break & Scientific Poster Session
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!
TRACK A: Drug Discovery & Preclinical Development
Leveraging Biologic Strategies for More Effective Drugs to Treat Resistant Cancer Populations
4:00 pm Spearheading the Development of TCR-Based Approaches for Inhibition of RAS-Driven Cancers in Resistant Patient Populations
- Identifying and quantifying precise HLA-peptide targets for TCR-based therapies
- Novel specificity analysis of TCR to avoid off-target toxicities
- Focused clinical trial designs to integrate with existing standard of care for RAS-driven malignancies
4:30 pm T Cell Engagers Targeting Drug-Induced Synthetic Neoantigens Address KRAS-G12C Inhibitor Resistance
- Development of engineered bispecific T cell engagers that recognize KRAS covalent inhibitor–modified peptide-MHC complexes with high affinity and specificity, enabling selective targeting of resistant tumor cells
- Companion immunotherapy approach designed to complement KRASG12C inhibitors by resistant cancer populations, with demonstrated efficacy in vitro and in vivo
- Cross-HLA binding and structural insights supporting broad patient coverage and the molecular basis for recognition of hapten-modified targets
TRACK B: Translation & Clinical Development
Improving Preclinical Testing & Patient Stratification Strategies to Enhance Response Rates for Effective RAS Inhibitors
4:00 pm Pan-Raf-MEK Non-Degrading Molecular Glue NST-628: Pre-Clinical Modelling & Incorporation of PD, ctDNA & Circulating Tumor Markers in Guiding Dose Escalation & Patient Selection in the FIH Clinical Study
- Design of Phase 1 NST-628 first-in-human clinical study
- Approach to modelling of target NST-628 exposures based on tumor growth inhibition and surrogate PD markers in xenografts
- Dose dependence of NST-628 effect on ctDNA, PD and circulating tumor markers and application for patient selection
4:30 pm Ensuring the Right Patients Receive the Right Treatments by Improving Patient Stratification with Tumor Profiling, Genetic Testing & More
- Leveraging tumor profiling and genetic testing for identifying reliable predictive biomarkers for patient stratification
- Managing tumor diversity and ensure optimal patient selection
- Uncovering innovative approaches, such as liquid biopsy techniques, to improve patient stratificatio