Revolution Medicines, Inc. · NASDAQ:RVMD
Revolution Medicines — Q4 2025 Earnings Presentation
76 slides from Revolution Medicines's earnings presentation, Feb 25, 2026
Slide 1: On Target to Outsmart Cancer
On Target to Outsmart Cancer February 2026 © 2026 Revolution Medicines, Inc.
Slide 2: Legal Disclaimer
2 Legal Disclaimer This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act. All statements other than statements of historical facts contained in this presentation, including statements regarding our future results of operations and fi
Slide 3: Our Mission
3 Our Mission | Revolutionize Treatment Globally for Patients with RAS-Addicted Cancers through the Discovery, Development and Delivery of Innovative, Targeted Medicines 2500+ patients treated with one or more of our RAS(ON) inhibitors 8 randomized Phase 3 registrational trials • active and planned
Slide 4: Uniquely Positioned
4 Uniquely Positioned | Aiming to Change Global Standards of Care for Patients with Common RAS-Addicted Cancers Pancreatic ductal adenocarcinoma Product Pipeline Targets RAS Variants • >90% are RAS-driven(1) Among RAS Mutant Solid Tumors Daraxonrasib Non-small cell lung cancer (multi-selective) RMC-
Slide 5: Industry-Leading Capabilities
5 Industry-Leading Capabilities | Advancing Targeted Treatment Regimens Based on RAS(ON) Inhibitors Proprietary tri-complex discovery platform targeting the oncogenic (or “ON”) state of RAS Robust clinical development programs and expertise to maximize impact for patients Expanding commercialization
Slide 6: © 2023 Revolution Medicines Confidential
6 © 2023 Revolution Medicines Confidential
Slide 7: Pipeline Led by Four Pioneering, Clinical-Stage, RAS(ON) Inhibitors
Pipeline Led by Four Pioneering, Clinical-Stage, RAS(ON) Inhibitors 7 COMPOUND FOCUS STUDY DETAILS EARLY CLIN. DEVELOPMENT REGISTRATIONAL TRIAL 2L metastatic PDAC 1L metastatic Adjuvant in resectable Daraxonrasib (MULTI) 2L/3L metastatic NSCLC 1L metastatic Planning ongoing + SOC, RAS(ON) inhibitor
Slide 8: Pancreatic Cancer: Registrational Trials Across Disease Settings
8 Pancreatic Cancer | Registrational Trials to Maximize Potential Across Early- to Late-Stage Disease Settings Clinical Evidence Registrational Trials Daraxonrasib | MULTI Daraxonrasib | MULTI • Unprecedented clinical profile across treatment lines, • 2L metastatic (RASolute 302): daraxonrasib RAS m
Slide 9: Pancreatic Cancer: Registrational Trials and Strategic Drivers
9 Pancreatic Cancer | Registrational Trials Maximize Potential Across Early- to Late-Stage Disease Settings Registrational Trials Strategic Drivers Daraxonrasib | MULTI RASolute 302: Urgent need, fastest entry point into PDAC, • 2L metastatic (RASolute 302): daraxonrasib opportunity to establish OS
Slide 10: Advancing Zoldonrasib in 1L PDAC
10 Advancing Zoldonrasib in 1L PDAC | Encouraging Initial Results in Combination with FOLFIRINOX Zoldonrasib 1200 mg + mFFX1 (N=19) % (95% CI) Safety/Tolerability Summary ORR2 63% (38, 84) DCR3 95% (74, 100) • Initial safety and tolerability profile of the combination was largely consistent with the
Slide 11: Non-Small Cell Lung Cancer
11 Non-Small Cell Lung Cancer | Broad Potential Across Lines of Therapy with Multi- and Mutant-Selective Approaches Clinical Evidence Registrational Trials Daraxonrasib | MULTI • Compelling monotherapy clinical results in previously treated • 2L/3L metastatic (RASolve 301) patients, including ORR, P
Slide 12: Colorectal Cancer
12 Colorectal Cancer | Exploring Combinations to Maximize Clinical Impact in Genetically Heterogeneous Disease Clinical Evidence Enabling Registrational Trials Daraxonrasib | MULTI • Evaluating daraxonrasib in combination with RAS(ON) mutant- Evaluating multiple potential selective inhibitors as par
Slide 13: © 2023 Revolution Medicines Confidential
13 © 2023 Revolution Medicines Confidential
Slide 14: Discover
14 Discover | Continuous Innovation Through Unique Platform and Insights to Sustain Leadership Position and Impact Highly productive, Singular focus on Continuing investment industry leading drug creating novel targeted leveraging proprietary discovery capabilities therapies for patients platform an
Slide 15: Daraxonrasib Demonstrates Encouraging Durability in RAS Mutant PDAC
15 Daraxonrasib Demonstrates Encouraging Durability in RAS Mutant PDAC in Clinical and Preclinical Settings 2L PDAC Patients – Overall Survival Preclinical Models of RAS G12X PDAC (!! !"#$%&'&*+',"%-."# T1.812,,9./:;122 D& 5-064.1, &! Median, Months %& OS (95% CI) !"#$%&'(')# RAS G12X 13.1 (10.9, NE
Slide 16: Innovative New Class of RAS(ON) Inhibitors Designed to Overcome Resistance
16 Innovative New Class of RAS(ON) Inhibitors Designed to Overcome RAS-Driven Drug Resistance and Extend Clinical Benefit; FIH in 2026 Standard Models Resistant Models3 Post-Progression Treatment D!!! D!!! 23).,/M4-5,6-7M43,844"9 23).,/M4-5,6-7M43,844"9 D!!! 23).,/M4-5,6-7M43,844"9 !"#A%"C (NSCLC, K
Slide 17: © 2023 Revolution Medicines Confidential
17 © 2023 Revolution Medicines Confidential
Slide 18: Deliver
18 Deliver | Building State-of-the-Art Organization and Capabilities to Enable Successful Commercialization Scaling the commercialization Core capabilities established in organization in preparation for the US and building underway in daraxonrasib launch readiness priority international regions Expe
Slide 19: Strong Financial Position
19 Strong financial position Creating Industry-Leading Global enables broad execution Targeted Medicines Franchise for Patients with RAS-Addicted Cancers across compelling opportunities to serve unmet needs $2.0 billion in cash and investments as of December 31, 2025 + $1.75 billion in additional co
Slide 20: Tracking Expected Impact
20 Tracking Expected Impact Pancreatic Cancer Non-Small Cell Lung Colorectal Cancer & Program Cancer Program RVMD-Led Collaborations • Readout for • Initiate RASolve 308 • Update on combination CRC RASolute 302 (daraxonrasib) (zoldonrasib combination) 1L data 2L registrational trial registrational t
Slide 21: Our Why
21 Our Why | Building on Strong Pillars for Growing Transformative RAS-addicted cancers are among the Patient Impact most common and difficult-to-treat cancers in need of new targeted medicines Extensive clinical evidence has shown that RAS(ON) inhibitors have the potential to improve outcomes and c
Slide 22: On Target to Outsmart Cancer
22 On Target to Outsmart Cancer ®
Slide 23: Appendix
23 Appendix © 2023 Revolution Medicines Confidential
Slide 24: Reference Data Tables for Current Therapies Across PDAC, NSCLC and CRC
24 Reference Data Tables for Current Therapies Across PDAC, NSCLC and CRC © 2023 Revolution Medicines Confidential
Slide 25: PDAC is an Aggressive Disease
PDAC 25 PDAC is an Aggressive Disease - Cytotoxic Chemotherapy is Global Standard of Care Across Lines of Therapy 56,000 new diagnoses annually (US) 1L chemotherapy 2L chemotherapy Resectable Surgery and adjuvant Metastatic disease chemotherapy No treatment (eligibility or choice) ~ 40% ~ 60% Locall
Slide 26: Adjuvant: High Unmet Need for Patients with Resectable PDAC
PDAC 26 Adjuvant: High Unmet Need for Patients with Resectable PDAC Resectable and borderline resectable disease accounts for ~15-25% of newly diagnosed patients with pancreatic cancer in the US.(1,2) While surgery with perioperative chemotherapy offers the possibility of a cure, ~80% advance to met
Slide 27: 1L PDAC: Significant Need for Improved Treatment(s)
PDAC 27 1L PDAC: Significant Need for Improved Treatment(s) Reported Efficacy and Safety Gemcitabine-based 5FU-based Gemcitabine/ mFOLFIRINOX or nab-Paclitaxel NALIRIFOX Efficacy (1-7) ORR (%)* 23-43 32-42 DCR (%) 50-76 62-70 mPFS (mo) 5.5-7.1 6.4-8.0 mOS (mo) 8.5-11.7 11.1-11.7 Safety (4) G3+ TRAE
Slide 28: 2L+ PDAC: Significant Need for Improved Treatment(s)
PDAC 28 2L+ PDAC: Significant Need for Improved Treatment(s) Reported Efficacy No. of Median PFS Median OS Study Regimen Treatment line ORR (%) patients (months) (months) NAPOLI 1(1) 5-FU+LV+Nal-IRI 2L+ 117 8 3.1 6.1 SWOG S1513(2) FOLFIRI 2L 58 10 2.9 6.5 SWOG S1115(3) FOLFOX 2L 62 7 2.0 6.7 SEQUOIA
Slide 29: 2L+ NSCLC: Significant Need for Improved Treatment(s)
NSCLC 29 2L+ NSCLC: Significant Need for Improved Treatment(s) Reported Efficacy Timing relative to Median PFS Median OS Study Treatment arm No. of patients ORR (%) CPI approval in 1L (months) (months) REVEL(1) prior Docetaxel, 2L+ 625 14% 3.0 9.1 CheckMate 057(2) prior Docetaxel, 2L+ 290 12% 4.2 9.
Slide 30: Later Line CRC: Significant Need for Improved Treatment(s)
CRC 30 Later Line CRC: Significant Need for Improved Treatment(s) Reported Efficacy Treatment No. of Median PFS Median OS Study Regimen ORR (%) DCR (%) line patients (months) (months) (1) RECOURSE Trifluridine/tipiracil 3L+ 534 2% 44% 2.0 (1.9–2.1) 7.1 (6.5–7.8) (2) Trifluridine/tipiracil SUNLIGHT 3
Slide 31: Daraxonrasib
31 Daraxonrasib RAS(ON) Multi-Selective Inhibitor Active against: • Diverse RAS driver mutations • Multiple drug resistance mechanisms, including secondary RAS mutations and wild- type RAS FDA granted: • Commissioner’s National Priority Voucher • Orphan Drug Designation • Breakthrough Therapy Design
Slide 32: Daraxonrasib Clinical Data
32 Daraxonrasib Clinical Data © 2023 Revolution Medicines Confidential
Slide 33: 2L PDAC: Daraxonrasib (300 mg) Demonstrated Compelling Clinical Activity
PDAC 33 2L PDAC: Daraxonrasib (300 mg) Demonstrated Compelling Clinical Activity in Patients with RAS Mutations RAS G12X RAS Mutant(4) N=26 N=38(3) ORR(1), % (n) 35% (9) 29% (11) DCR(2), % (n) 92% (24) 95% (36) (4) Median (range) follow-up is 16.7 (10.3, 24.6) months and 17.4 (10.3, 24.6) months for
Slide 34: 2L PDAC: Encouraging Progression-Free Survival and Overall Survival
PDAC 34 2L PDAC: Daraxonrasib (300 mg) Demonstrated Encouraging Progression-Free Survival and Overall Survival Median PFS, Months (95% CI) Median OS, Months (95% CI) RAS G12X 8.5 (6.7, 10.5) RAS G12X 13.1 (10.9, NE) RAS Mutant 8.1 (5.9, 10.1) RAS Mutant 15.6 (10.9, NE) PFS Probability OS Probability
Slide 35: 2L+ PDAC: Daraxonrasib at 300 mg Daily Generally Well Tolerated
PDAC 35 2L+ PDAC: Daraxonrasib at 300 mg Daily Generally Well Tolerated N=83 Any Grade Grade ≥3 Patients with Any TRAE, N (%) 80 (96%) 28 (34%) TRAEs occurring in ≥15% of patients, N (%) Rash* 75 (90%) 6 (7%) Stomatitis/mucositis* 45 (54%) 3 (4%) Diarrhea 43 (52%) 3 (4%) Nausea 32 (39%) 0 Vomiting 3
Slide 36: 2L+ PDAC: Acceptable Dose Modification and Dose Intensity Achieved
PDAC 36 2L+ PDAC: Acceptable Dose Modification and Dose Intensity Achieved in Patients Receiving Daraxonrasib at 300 mg Daily N=83 Patients with dose modification due to TRAEs, N (%) 40 (48%) Dose interruption 36 (43%) Dose reduction 25 (30%) Patients with dose discontinuation due to TRAEs, N (%) 0
Slide 37: 1L PDAC: Daraxonrasib Monotherapy Demonstrated Promising Initial Antitumor Activity
PDAC 37 1L PDAC: Daraxonrasib (300 mg) Monotherapy Demonstrated Promising Initial Antitumor Activity in Patients with RAS Mutations N=38(1,4) ORR(2), % (n) 47% (18) DCR(3), % (n) 89% (34) Two treatment-naïve patients who are included in the safety analysis are excluded from the waterfall and ORR/DCR
Slide 38: 1L PDAC: Daraxonrasib Monotherapy Generally Well Tolerated
PDAC 38 1L PDAC: Daraxonrasib (300 mg) Monotherapy Generally Well Tolerated N=40 Any Grade Grade ≥3 Patients with any TRAE, N (%) 38 (95%) 14 (35%) TRAEs occurring in ≥15% of patients, N (%) Rash* 35 (88%) 3 (8%) Diarrhea 23 (58%) 4 (10%) Stomatitis/mucositis* 23 (58%) 3 (8%) Nausea 20 (50%) 1 (3%)
Slide 39: 1L PDAC: Daraxonrasib Monotherapy Acceptable Dose Modification
PDAC 39 1L PDAC: Daraxonrasib (300 mg) Monotherapy Demonstrated Acceptable Rate of Dose Modification and Favorable Dose Intensity N=40 Patients with dose modification due to TRAEs, N (%) 25 (63%) Dose interruption 21 (53%) Dose reduction 13 (33%) Patients with dose discontinuation due to TRAEs, N (%
Slide 40: Daraxonrasib Combination with GnP Improved Responses in Preclinical PDAC Models
PDAC 40 Daraxonrasib Combination with GnP Demonstrated Improved Depth and Durability of Responses in Preclinical Models of PDAC Capan-1 (PDAC, KRAS G12V / G12V) 10 PDAC Xenograft Models1 &D!! TWKC a-b-@A<BTWKC WX-8D<!-M"S=CG->?-@A<B WX-8D<!-M"S=CG->?-@A<B Fd a-b-@A<BFde e ** "!! 23).,/M4-5,6-7M43,84
Slide 41: Highly Active Regimens of Daraxonrasib and GnP in RASolute 303
PDAC 41 Highly Active Regimens of Daraxonrasib and GnP to be Deployed in Combination Arm of RASolute 303 Phase 3 1L PDAC Trial RASolute 303 Treatment Target Ranges Rationale for Selection Combination Arm Dose: Dose: • Highly active and 160–300 mg 200 mg generally well tolerated in Daraxonrasib 2L PD
Slide 42: 1L PDAC: Daraxonrasib + GnP Encouraging Initial Antitumor Activity
PDAC 42 1L PDAC: Daraxonrasib + GnP Demonstrated Encouraging Initial Antitumor Activity in Patients with RAS Mutations N=31(1,4) ORR(2), % (n) 55% (17) DCR(3), % (n) 90% (28) Median (range) follow-up is 6.9 (4.3, 9.7) months. (1) All treated 1L PDAC patients received a first dose 200 mg QD of daraxo
Slide 43: 1L PDAC: Daraxonrasib + GnP Acceptable Safety/Tolerability
PDAC 43 1L PDAC: Daraxonrasib + GnP Demonstrated Acceptable Safety/Tolerability (N=40) Any Grade Grade ≥3 Patients with any TRAE, N (%) 39 (98%) 23 (58%) TRAEs occurring in ≥30% of Patients, N (%) Rash* 34 (85%) 5 (13%) Fatigue 27 (68%) 5 (13%) Diarrhea 27 (68%) 5 (13%) Nausea 25 (63%) 2 (5%) Vomiti
Slide 44: 1L PDAC: Daraxonrasib + GnP Acceptable Rate of Dose Modification
PDAC 44 1L PDAC: Daraxonrasib + GnP Demonstrated Acceptable Rate of Dose Modification and Favorable Dose Intensity for Daraxonrasib (N=40) Daraxonrasib GnP Patients with dose modification due to TRAEs, N (%) 21 (53%) 22 (55%) Dose interruption 21 (53%) 15 (38%) Dose reduction 9 (23%) 17 (43%) Patien
Slide 45: 2L/3L NSCLC: Encouraging Durability with Daraxonrasib at 120-220 mg Daily
NSCLC 45 2L/3L NSCLC: Encouraging Durability in Patients with RAS G12X Mutations Treated with Daraxonrasib at 120-220 mg Daily Median PFS, Months Median OS, Months (95% CI) (95% CI) 9.8 (6, 12.3) 17.7 (13.7, NE) RMC-6236-001: 2L/3L patients with RAS G12X NSCLC treated with daraxonrasib at 120-220 mg
Slide 46: 2L/3L NSCLC: Daraxonrasib Generally Well Tolerated at 120-220 mg Daily
NSCLC 46 2L/3L NSCLC: Daraxonrasib Generally Well Tolerated in Patients Treated at 120-220 mg Daily 120-300 mg 120-220 mg 300 mg (N=124) (N=73) (N=51) Any Grade Grade ≥3 Any Grade Grade ≥3 Any Grade Grade ≥3 Any TRAE 121 (98%) 33 (27%) 71 (97%) 12 (16%) 50 (98%) 21 (41%) TRAEs in ≥ 10% of patients,
Slide 47: 2L/3L NSCLC: Favorable Dose Intensity Maintained at 120-220 mg
NSCLC 47 2L/3L NSCLC: Daraxonrasib Favorable Dose Intensity Maintained at 120-220 mg 120-300 mg 120-220 mg 300 mg (N=124) (N=73) (N=51) TRAEs leading to dose modification, n (%) 64 (52%) 30 (41%) 34 (67%) Dose interruption 59 (48%) 25 (34%) 34 (67%) Dose reduction 34 (27%) 15 (21%) 19 (37%) TRAEs le
Slide 48: 1L NSCLC: Daraxonrasib + Pembrolizumab +/- Chemotherapy Antitumor Activity
NSCLC 48 1L NSCLC: Daraxonrasib + Pembrolizumab +/- Chemotherapy Demonstrated Encouraging Preliminary Antitumor Activity Daraxonrasib 200 mg + Daraxonrasib 100-200 mg + TPS Subgroup1 TPS Subgroup1 Pembrolizumab (N=7)2,3 Pembrolizumab + Chemotherapy (N=10)2 ORR4, % (n) 86% (6) ORR4, % (n) 60% (6) TPS
Slide 49: 1L NSCLC: Daraxonrasib + Pembrolizumab +/- Chemotherapy Generally Well Tolerated
NSCLC 49 1L NSCLC: Daraxonrasib + Pembrolizumab +/- Chemotherapy Generally Well Tolerated Daraxonrasib 200 mg + Daraxonrasib (100-200 mg) + Pembrolizumab (N=10) Pembrolizumab + Chemotherapy (N=13) Median follow-up, mo (range) 2.3 (0.9, 6.2) 2.6 (0.7, 5.6) Preferred Term Any Grade Grade ≥ 3 Any Grade
Slide 50: 1L NSCLC: Combination Supports Favorable Dose Intensity
NSCLC 50 1L NSCLC: Daraxonrasib + Pembrolizumab +/- Chemotherapy Combination Supports Favorable Dose Intensity Daraxonrasib (100-200 mg) + Daraxonrasib 200 mg + Pembrolizumab + Pembrolizumab (N=10) Chemotherapy (N=13) Daraxonrasib-related AEs: Leading to daraxonrasib dose reduction 1 (10%) 1 (8%) Le
Slide 51: Daraxonrasib Registrational Study Designs
51 Daraxonrasib Registrational Study Designs © 2023 Revolution Medicines Confidential
Slide 52: 2L Metastatic PDAC: Design of RASolute 302 Trial
PDAC 52 2L Metastatic PDAC: Design of RASolute 302 Trial Primary Endpoints N = 460 Daraxonrasib (RAS G12X) Key Eligibility Criteria 300 mg PO QD • PFS, OS • Confirmed PDAC R (N=230) • 1 prior line of therapy in the metastatic setting 1:1 Secondary Endpoints Investigator’s Choice (All Patients) • ECO
Slide 53: 1L Metastatic PDAC: Design of RASolute 303 Trial
PDAC 53 1L Metastatic PDAC: Design of RASolute 303 Trial Key Eligibility Criteria Daraxonrasib Primary Endpoints N ~ 900 (300 mg) • Confirmed metastatic PDAC, regardless of RAS • PFS, OS status R Daraxonrasib Daraxonrasib • No prior systemic therapy 1:1:1 (200 mg) + GnP(1) (300 mg) for metastatic di
Slide 54: Adjuvant Therapy in Resectable PDAC: Design of RASolute 304 Trial
PDAC 54 Adjuvant Therapy in Resectable PDAC: Design of RASolute 304 Trial N=500 Primary Key Eligibility Endpoint Daraxonrasib Surgery Criteria No 300 mg PO QD • DFS + radiologic • Confirmed PDAC Duration 2 years R Perioperative evidence of • R0 or R1 resection* 1:1 chemotherapy disease • ECOG PS 0 o
Slide 55: Previously Treated NSCLC: Design of RASolve 301 Trial
NSCLC 55 Previously Treated NSCLC: Design of RASolve 301 Trial Key Eligibility Criteria • Locally advanced or metastatic Primary Endpoints NSCLC N=420 Daraxonrasib (RAS G12X-C)(1) • RAS genotypes: RAS G12X-C 200 mg PO QD (core population), G12C, G13X or • PFS, OS Q61X R (N=210) • Prior therapies: 1
Slide 56: Elironrasib
56 Elironrasib RAS(ON) G12C-Selective Covalent Inhibitor Active against • Primary RAS G12C mutation • Tumors in patients naïve to, or previously treated with, first-generation KRAS(OFF) inhibitors FDA granted: • Breakthrough Therapy Designation © 2023 Revolution Medicines Confidential
Slide 57: Elironrasib Clinical Data
57 Elironrasib Clinical Data © 2023 Revolution Medicines Confidential
Slide 58: Elironrasib Monotherapy: Antitumor Activity and Durability in Previously Treated RAS G12C NSCLC
NSCLC 58 Elironrasib Monotherapy: Encouraging Antitumor Activity and Durability in Patients with Previously Treated RAS G12C NSCLC Elironrasib (200 mg BID) (N=36) Elironrasib (200 mg BID) (N=36) ORR1, % (n) 56% (20) Median PFS 9.9 (6.2, NE) DCR2, % (n) 94% (34) Months (95% CI) on treatment # Post Ba
Slide 59: Elironrasib Monotherapy: Activity After a G12C(OFF) Inhibitor
NSCLC 59 Elironrasib Monotherapy: Encouraging Antitumor Activity in Patients with RAS G12C NSCLC Previously Treated with a G12C(OFF) Inhibitor Elironrasib (200 mg BID) (N=24) ORR1, % (n) 42% (10) DCR2, % (n) 79% (19) Median (range) follow-up is 17.6 (10.3, 24.6) months and 17.4 (14, 28.5) months. Me
Slide 60: Elironrasib Monotherapy: Durability After a G12C(OFF) Inhibitor
NSCLC 60 Elironrasib Monotherapy: Encouraging Durability in Patients with RAS G12C NSCLC Previously Treated with a G12C(OFF) Inhibitor PFS, mo (CI) 6.2mo (4.0, 10.3) Median OS, mo (CI) NE (6.7, NE) 6-mo PFS rate, % (CI) 53% (31-71) 12-mo OS rate, % (CI) 62% (40-78) PFS Probability OS Probability NSC
Slide 61: Elironrasib Monotherapy: Generally Well Tolerated in RAS G12C NSCLC
NSCLC 61 Elironrasib Monotherapy: Generally Well Tolerated in Patients with Previously Treated RAS G12C NSCLC Elironrasib 200 mg BID (N=36) Maximum Severity of Treatment-Related AEs Any Grade Grade ≥3 Any TRAE 28 (78%) 7 (19%) TRAEs in ≥ 15% of patients, n (%) Diarrhea 11 (31%) 2 (6%) Nausea 8 (22%)
Slide 62: Elironrasib + Pembrolizumab: Preliminary Antitumor Activity in 1L RAS G12C NSCLC
NSCLC 62 Elironrasib + Pembrolizumab: Promising Preliminary Antitumor Activity in Patients with 1L RAS G12C NSCLC Elironrasib 200 mg BID + Pembrolizumab in TPS1 ≥ 50% (N=5)2 ORR3, % (n) 100% (5) DCR4, % (n) 100% (5) on treatment # Post 1 2 1 1 2 Baseline Scans (1) Tumor proportion score (TPS) is bas
Slide 63: Elironrasib + Pembrolizumab: Well Tolerated with Favorable Dose Intensity
NSCLC 63 Elironrasib + Pembrolizumab: Generally Well Tolerated with Favorable Dose Intensity in Patients with 1L RAS G12C NSCLC Elironrasib 200 mg BID + Pembrolizumab (N=8) Median time on treatment, mo (range) 2.7 (0.7-3.2) Any Grade Grade ≥3 Any TRAE 6 (75%) 2 (25%) TRAEs in ≥ 15% of patients, n (%
Slide 64: Elironrasib + Daraxonrasib RAS(ON) Inhibitor Doublet Background
64 Elironrasib + Daraxonrasib RAS(ON) Inhibitor Doublet Background © 2023 Revolution Medicines Confidential
Slide 65: Elironrasib and Daraxonrasib Show Combination Benefit and Synergize with Anti-PD-1
NSCLC 65 Elironrasib and Daraxonrasib Show Combination Benefit and Synergize with Anti-PD-1 in Preclinical NSCLC Models Elironrasib and Daraxonrasib Show RAS(ON) Inhibitor Doublet Sensitizes Combination Benefit in a NSCLC Model Immune-Refractory NSCLC to Anti-PD-1 Control Daraxonrasib Control Eliron
Slide 66: Elironrasib + Daraxonrasib: Antitumor Activity in 2L+ NSCLC
NSCLC 66 Elironrasib + Daraxonrasib: Doublet Shows Encouraging Antitumor Activity in Patients with 2L+ NSCLC Previously Treated with KRAS(OFF) G12C Inhibitor Elironrasib + Daraxonrasib (N=26)(1) ORR(2), % (n) 62% (16) DCR(3), % (n) 92% (24) # Post Baseline Scans The combination arm includes patients
Slide 67: Elironrasib + Daraxonrasib: Generally Well Tolerated in 2L+ NSCLC
NSCLC 67 Elironrasib + Daraxonrasib: Generally Well Tolerated in 2L+ NSCLC Patients Previously Treated with G12C(OFF) Inhibitor Elironrasib 200 mg BID + Daraxonrasib 100-200 mg QD (N=33) Median time on treatment, mo (range) 3.61 (0.20-8.67) Any Grade Grade ≥3 Any TRAE 31 (94%) 15 (43%) TRAEs in ≥ 20
Slide 68: Limited Monotherapy Activity of Daraxonrasib or Elironrasib in CRC
CRC 68 Limited Monotherapy Activity of Either Daraxonrasib in RAS Mutant CRC or Elironrasib in CRC Previously Treated with KRAS G12C(OFF) Inhibitor ORR RAS Inhibitor Population n/N (%) Daraxonrasib in RAS Mutant CRC(1,3) RAS inhibitor naive 2/22 (9%) 300 mg QD Elironrasib in KRAS G12C Mutant CRC(2)
Slide 69: Elironrasib + Daraxonrasib: Antitumor Activity in Previously Treated CRC
CRC 69 Elironrasib + Daraxonrasib: Doublet Shows Encouraging Antitumor Activity in Patients with CRC Previously Treated with KRAS(OFF) G12C Inhibitor Elironrasib + Daraxonrasib(1) (N=12) ORR(2), % (n) 25% (3) DCR(3), % (n) 92% (11) # Post Baseline Scans Analyses include all patients who received fir
Slide 70: Zoldonrasib
70 Zoldonrasib RAS(ON) G12D-Selective Covalent Inhibitor Active against: • Primary RAS G12D mutation • Most common RAS driver in RAS-addicted solid tumors FDA granted: • Breakthrough Therapy Designation © 2023 Revolution Medicines Confidential
Slide 71: Zoldonrasib Clinical Data
71 Zoldonrasib Clinical Data © 2023 Revolution Medicines Confidential
Slide 72: Zoldonrasib Monotherapy in Previously Treated KRAS G12D PDAC
PDAC 72 Encouraging Initial Activity of Zoldonrasib Monotherapy in Previously Treated Patients with KRAS G12D PDAC Tumor Response for PDAC Patients Treated with 1200 mg Daily Dose (QD, N=20 or BID, N=20)1 ORR2, % (n) 30% (12) DCR3, % (n) 80% (32) David S. Hong et al., Preliminary Safety, Pharmacokin
Slide 73: Zoldonrasib Monotherapy in Previously Treated KRAS G12D NSCLC
NSCLC 73 Encouraging Initial Activity of Zoldonrasib Monotherapy in Previously Treated Patients with KRAS G12D NSCLC Tumor Response for Patients with NSCLC Treated with 1200 mg QD (N=18)1 ORR2, % (n) 61% (11) DCR3, % (n) 89% (16) # Post Baseline Scans All patients with NSCLC who received first dose
Slide 74: Zoldonrasib Monotherapy: Generally Well Tolerated Across Indications
74 Zoldonrasib Monotherapy: Generally Well Tolerated Across Indications Patients Treated with 1200 mg QD Zoldonrasib (N=90)(1) Maximum Severity of Treatment-Related AEs Grade 1 Grade 2 Grade 3 Any Grade Any TRAE 49 (54%) 16 (18%) 2 (2%) 67 (74%) TRAEs occurring in ≥10% of patients, n (%) Nausea 30 (
Slide 75: Royalty Pharma Partnership
75 Royalty Pharma Partnership © 2023 Revolution Medicines Confidential
Slide 76: Royalty Pharma Partnership Bolsters Already Strong Financial Position
76 Royalty Pharma Partnership Bolsters Already Strong Financial Position by Providing $2 Billion in Flexible Committed Capital $2 Billion Committed Received Scheduled* Scheduled* positive readout approval Synthetic Term Debt RVMD discretion* ($0.75 B) RVMD discretion* Royalty ($1.25 B) 3 Tranches Ma