Revolution Medicines, Inc. · NASDAQ:RVMD
Revolution Medicines — Technical Presentation (March 2025)
10 slides from Revolution Medicines's technical presentation, March 2025
Slide 1: RAS(ON) G12D-Selective Inhibitor Zoldonrasib Synergizes with Anti-PD-1 in KRAS G12D Models
The RAS(ON) G12D-Selective Inhibitor Zoldonrasib (RMC-9805) Synergizes with Anti-PD-1 to Extend Durability of Antitumor Activity in KRAS G12D-Driven Preclinical Cancer Models Marie Menard, Ph.D. Revolution Medicines, Redwood City CA
Slide 2: Disclosure Information
Disclosure Information Marie Menard I have the following relevant financial relationships to disclose: Employee and Stockholder of Revolution Medicines
Slide 3: Zoldonrasib (RMC-9805) is a RAS(ON) G12D-Selective, Tri-Complex Inhibitor
Zoldonrasib (RMC-9805) is a RAS(ON) G12D-Selective, Tri-Complex Inhibitor • Oral, mutant-selective, covalent inhibitor targeting the ON (active, GTP-bound) state of RAS G12D • Induces deep and durable responses in a mouse clinical trial with KRAS G12D xenograft models of PDAC, NSCLC, and CRC(1) • Pr
Slide 4: RAS(ON) G12D-Selective Inhibition Drives Durable Responses in an Immune Cell-Dependent Manner
RAS(ON) G12D-Selective Inhibition Drives Durable Responses in an Immune Cell-Dependent Manner in KRAS G12D Models Durability of response Regressions and durable responses dependent on immune cells 100 % Tumors Progression-Free 200 Mean Tumor Volume Change 150 75 % From Baseline 100 50 50 0 25 -50 0
Slide 5: Zoldonrasib Induces Profound Changes in both Tumor Cells and TME
Zoldonrasib Induces Profound Changes in both Tumor Cells and TME NK cells T cells Macrophages DC Fibroblasts B cells Neutrophils Endothelial cells Tumor cells KPCY 2838c3 (KrasG12D/+, Trp53R172H/+ GEMM-derived PDAC) tumors were treated with vehicle or Zoldonrasib at 100 mg/kg po qd for 9 days and co
Slide 6: Primes the TME for Combination with Immunotherapy by Promoting T Cell Infiltration
Zoldonrasib Primes the TME for Combination with Immunotherapy by Promoting T Cell Infiltration Increase in lymphoid to myeloid ratio in the TME Increase in CD8+ T cells Vehicle Zoldonrasib Vehicle Zoldonrasib CD8 4000- Cell Numbers 2000- CD8 IHC staining and quantification in KPCY 2838c3 tumors trea
Slide 7: Promotes Tumor Recognition by Increasing Antigen Presentation on Tumor Cells
Zoldonrasib Promotes Tumor Recognition by Increasing Antigen Presentation on Tumor Cells Increased expression of antigen processing and Cancer cell-intrinsic modulation of MHC presentation genes in tumor cells expression on cell surface In Vivo Vehicle Zoldonrasib 3.0×104 In Vitro MHC-I (MFI) 2.0×10
Slide 8: Combination of Zoldonrasib with Anti-PD-1 Induces Deeper and More Durable Responses
Combination of Zoldonrasib with Anti-PD-1 Induces Deeper and More Durable Responses Representative ultrasound images Vehicle Zoldonrasib Anti-PD-1 Zoldonrasib + Anti-PD-1 at day 14 of treatment Vehicle Vehicle Anti-PD1 Anti-PD-1 300 % Tumor Volume Change 200 100 RMC-9805 Zoldonrasib RMC-9805 ++Anti-
Slide 9: Preclinical Studies Provide Strong Rationale for Combination of RAS(ON) Inhibitors with Anti-PD-1
Preclinical Studies Provide Strong Rationale for Combination of RAS(ON) Inhibitors with Anti-PD-1 RAS(ON) • TME Remodeling • Enhanced Antigen Presentation Inhibitor • Increased TCR Repertoire Diversity + • Reversal of T Cell Exhaustion Anti-PD-1 • Expansion of Tumor-Specific CTL • Promotion of Epito
Slide 10: Acknowledgments
Acknowledgments • Revolution Medicines Research and Development Teams • Ben Stanger, Bob Vonderheide, Margo Orlen (University of Pennsylvania) and our other Academic Collaborators • •
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