Revolution Medicines, Inc. · NASDAQ:RVMD

Revolution Medicines — Investor Presentation (August 2026)

99 slides from Revolution Medicines's investor presentation, August 2026

1. Slide 1: On Target to Outsmart Cancer

   On Target to Outsmart Cancer August 2026 © 2026 Revolution Medicines, Inc.

2. Slide 2: Legal Disclaimer

   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 fina

3. Slide 3: Our Vision: Industry-Leading Global Targeted Medicines Franchise

   Our Vision | Creating Industry-Leading Global Targeted Medicines Franchise for Patients with RAS-Addicted Cancers e r De v DISCOVER DEVELOP DELIVER ve D isco Continuous innovation Broad clinical development Bringing transformative lop through unique platform across tumor types and targeted medicines

4. Slide 4: Uniquely Positioned to Change Global Standards of Care in RAS-Addicted Cancers

   Uniquely Positioned | Aiming to Change Global Standards of Care for Patients with Common RAS-Addicted Cancers Product Pipeline Targets RAS Variants Among RAS Pancreatic adenocarcinoma Mutant Solid Tumors • >90% are RAS-driven(1) Daraxonrasib (multi-selective) Non-small cell lung cancer RMC-5127 • ~3

5. Slide 5: 2026: A Transformational Year Across Discovery, Development and Delivery

   2026: A Transformational Year Across Discovery, Development and Delivery Discovery: proprietary tri-complex platform underlies extensive portfolio of innovative, oral inhibitors targeting the oncogenic r De (“ON”) state of RAS v e ve Disco lop Development: deep late-stage pipeline of investigational

6. Slide 6: Develop

   De ve lop © Revolution Medicines

7. Slide 7: Advancing Broad and Differentiated Pipeline of RAS(ON) Inhibitors

   Advancing Broad and Differentiated Pipeline of RAS(ON) Inhibitors Phase 3 Registrational Trials Molecule Target Trial Treatment Setting Regimen Status Daraxonrasib MULTI 2L metastatic Mono Completed Mono & Daraxonrasib MULTI 1L metastatic Ongoing Combo PDAC Daraxonrasib MULTI Adjuvant in resectable

8. Slide 8: PDAC

   PDAC © Revolution Medicines

9. Slide 9: RASolute 302: Unprecedented Overall Survival Benefit in Previously Treated Pancreatic Cancer

   RASolute 302 | Unprecedented Overall Survival Benefit in Patients with Previously Treated Metastatic Pancreatic Cancer Oral, once-daily daraxonrasib demonstrated statistically significant and clinically meaningful improvements in PFS and OS compared with SOC IV chemotherapy Daraxonrasib outcomes in

10. Slide 10: Pancreatic Cancer: Aim to Redefine Standard of Care Across Continuum of Disease

    Pancreatic Cancer | Aim to Redefine Standard of Care Across Continuum of Disease Previously Treated Excessive RAS(ON) signaling underlies all stages of PDAC • Unprecedented Phase 3 results establish daraxonrasib as potential new standard of care First Line • Multiple registrational programs expandin

11. Slide 11: Executing Rapidly Following Landmark RASolute 302 Results

    Executing Rapidly Following Landmark RASolute 302 Results in Pancreatic Cancer – Daraxonrasib Enters Delivery Stage Expanding Patient Access Advancing Toward Global Registration • Robust Expanded Access Program active across • NDA accepted for review by U.S. FDA the U.S. • Phased review of MAA under

12. Slide 12: Zoldonrasib + Chemotherapy Initial Activity in First-Line RAS G12D PDAC

    Zoldonrasib + Chemotherapy Demonstrated Promising Initial Activity in First- Line RAS G12D PDAC Zoldonrasib 1200 mg QD + mFFXa Zoldonrasib 1200 mg QD + GnPa (N=22) (N=31) ORR % (95% CI)b 82 (60–95) ORR % (95% CI)b 61 (42–78) DCR % (95% CI) c 96 (77–100) DCR % (95% CI)c 90 (74–98) Data cutoff: 8 Feb

13. Slide 13: Zoldonrasib + Chemotherapy Safety Profile in First-Line RAS G12D PDAC

    Zoldonrasib + Chemotherapy Safety Profile Supports Development in First- Line Treatment for RAS G12D PDAC Zoldonrasib 1200 mg QD + mFFX Zoldonrasib 1200 mg QD + GnP (N=41) (N=40) Any Grade Grade ≥3 Any Grade Grade ≥3 Any study drug-related AE, n (%) 40 (98) 25 (61) Any study drug-related AE, n (%) 4

14. Slide 14: Zoldonrasib + Daraxonrasib Doublet Initial Antitumor Activity in Previously Treated PDAC

    Zoldonrasib + Daraxonrasib Doublet Demonstrated Compelling Initial Antitumor Activity in Previously Treated RAS G12D PDAC Zoldonrasib 1200 mg QD + Daraxonrasib 300 mg QD 2L PDAC (N=30)a 3L+ PDAC (N=30)a ORR % (95% CI)b 50 (31–69) 47 (28–66) c DCR % (95% CI) 97 (83–100) 90 (74–98) Data cutoff: 9 Feb

15. Slide 15: Zoldonrasib + Daraxonrasib Doublet Preliminary Durability

    Zoldonrasib + Daraxonrasib Doublet Demonstrated Compelling Preliminary Durability in Previously Treated RAS G12D PDAC Zoldonrasib 1200 mg QD + Zoldonrasib 1200 mg QD + Daraxonrasib 300 mg QD Daraxonrasib 300 mg QD 2L PDAC (N=30) 3L+ PDAC (N=30) 2L PDAC (N=30) 3L+ PDAC (N=30) mPFS (95% CI), months 9.

16. Slide 16: Zoldonrasib + Daraxonrasib Doublet Safety and Tolerability Profile

    Zoldonrasib + Daraxonrasib Doublet Demonstrated Manageable Safety and Tolerability Profile Zoldonrasib 1200 mg QD + Daraxonrasib 300 mg QD All 2L+ PDAC Treated (N=60) Any Grade Grade ≥3 Any study drug-related AE, n (%) 58 (97) 21 (35) a TRAEs occurring in ≥10% of all patients, n (%) Rashb 54 (90) 7

17. Slide 17: NSCLC

    NSCLC © Revolution Medicines

18. Slide 18: NSCLC: Layered Development Strategy Targeting RAS Tumor Drivers

    Non-Small Cell Lung Cancer | Layered Development Strategy Targeting RAS Tumor Drivers NSCLC treatment defined RAS(ON) RAS(ON) by classes of oncogenic Multi-Selective Inhibition Mutant-Selective Inhibition drivers; increasingly by for treatment across for treatment by individual specific tumor mutati

19. Slide 19: Daraxonrasib: Establishing the Foundation in Previously Treated RAS Mutant NSCLC

    Daraxonrasib | Establishing the Foundation in Previously Treated RAS Mutant NSCLC Recognition of Clinical Registrational Development Future Potential Opportunities Global Phase 3 registrational FDA Breakthrough trial (RASolve 301) in Broad clinical development Therapy Designation in previously treat

20. Slide 20: NSCLC: RAS(ON) Mutant-Selective Portfolio for Genetically Segmented Landscape

    Non-Small Cell Lung Cancer | RAS(ON) Mutant-Selective Portfolio Designed for Treatment Landscape Segmented by Genetic Cause Three RAS Variants Dominate RAS Mutant NSCLC1 Promising Clinical Portfolio of RAS(ON) Mutant- Selective Inhibitors G12C • Clinical-stage mutant-selective inhibitors address >70

21. Slide 21: Zoldonrasib + Pembrolizumab + Chemotherapy: Baseline Patient Characteristics

    Zoldonrasib + Pembrolizumab + Chemotherapy: Baseline Patient Characteristics Zoldonrasib 1200 mg QD + Pembrolizumab + Pemetrexed + Platinum (N=38) Median age, years (range) 64 (28, 84) Sex - Male, n (%) 20 (53%) ECOG PS 1, n (%) 17 (45%) Current/Past Smoker, n (%) 28 (74%) Metastatic at initial diag

22. Slide 22: Zoldonrasib + Pembrolizumab + Chemotherapy: Manageable Safety Profile

    Zoldonrasib + Pembrolizumab + Chemotherapy: Manageable Safety Profile with Minimal Added Toxicity Zoldonrasib 1200 mg + Pembrolizumab + Pemetrexed + Platinum (N=38) TRAEs generally consistent with the Any Grade Grade >= 3 established safety profile of SOC Any TRAE, n (%) 34 (89%) 9 (24%) pembrolizum

23. Slide 23: Zoldonrasib + Pembrolizumab + Chemotherapy: Encouraging Antitumor Activity

    Zoldonrasib + Pembrolizumab + Chemotherapy: Encouraging Antitumor Activity Zoldonrasib 1200 mg + Pembrolizumab TPS ORR + Pemetrexed + Platinum TPSd <1% ORR 60% (6/10) (N=28) a Best % Change in SOD from Baseline in TPS 1-49% ORR 92% (11/12) ORR: % (95% CI) b 82% (63, 94) DCR: % (95% CI) c 100% (88, 1

24. Slide 24: Elironrasib + Pembrolizumab + Chemotherapy: Baseline Patient Characteristics

    Elironrasib + Pembrolizumab + Chemotherapy: Baseline Patient Characteristics Elironrasib 200 mg BID + Pembrolizumab + Pemetrexed + Platinum (N=39) Median age, years (range) 66 (40, 84) Sex - Male, n (%) 16 (41%) ECOG PS 1, n (%) 19 (49%) Current/Past Smoker, n (%) 38 (97%) Metastatic at initial diag

25. Slide 25: Elironrasib + Pembrolizumab + Chemotherapy: Manageable Safety Profile

    Elironrasib + Pembrolizumab + Chemotherapy Manageable Safety Profile with Minimal Added Toxicity Elironrasib 200 mg BID + Pembrolizumab + Pemetrexed + Platinum (N=39) TRAEs generally consistent with the Any Grade Grade ≥3 established safety profile of SOC Any TRAE 38 (97%) 20 (51%) pembrolizumab and

26. Slide 26: Elironrasib + Pembrolizumab + Chemotherapy: Encouraging Antitumor Activity

    Elironrasib + Pembrolizumab + Chemotherapy: Encouraging Antitumor Activity Elironrasib 200 mg BID + Pembrolizumab + Pemetrexed + TPS ORR Platinum (N=39) a TPS <1% 50% (2/4) Best % Change in SOD from Baseline in ORR: % (95% CI) b 85% (70, 94) TPS 1-49% 85% (22/26) DCR: % (95% CI) c 97% (87, 100) PFS

27. Slide 27: CRC

    CRC © Revolution Medicines

28. Slide 28: Colorectal Cancer: Exploring Combinations in Genetically Heterogeneous Disease

    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-selective Evaluating multiple potential inhibitors as part of

29. Slide 29: Discover

    er v Disco © Revolution Medicines

30. Slide 30: Discover: Continuous Innovation Through Unique Platform and Insights

    Discover | Continuous Innovation Through Unique Platform and Insights to Sustain Leadership Position and Impact Highly productive, Singular focus on creating Continuing investment industry leading drug novel targeted therapies for leveraging proprietary discovery capabilities patients with RAS-addic

31. Slide 31: Deliver

    Deliver © Revolution Medicines

32. Slide 32: Deliver: State-of-the-Art Organization and Capabilities for Commercialization

    Deliver | State-of-the-Art Organization and Capabilities to Enable Successful Commercialization Launch-ready U.S. commercial Patient services program, commercial capabilities positioned for supply, and distribution network are daraxonrasib in PDAC ready Experienced leadership team with a Global laun

33. Slide 33: Financial Summary

    Financial Summary © Revolution Medicines

34. Slide 34: Strong Financial Position Enables Broad Execution

    Strong financial position Creating Industry-Leading Global Targeted enables broad execution Medicines Franchise for Patients with RAS- across compelling opportunities Addicted Cancers to serve unmet needs De $3.9 billion er in cash and investments as of June 30, 2026 v ve D is co + lop $1.5 billion

35. Slide 35: Corporate Updates

    Corporate Updates © Revolution Medicines

36. Slide 36: Tracking Expected Impact

    Tracking Expected Impact Pancreatic Cancer Non-Small Cell Lung Cancer 1H 2026 Readout for RASolute 302 (daraxonrasib in 2L) 1H 2026 Initiate RASolve 308 (zoldonrasib combination in 1L) Initiate RASolute 305 (zoldonrasib + chemo combination Q4 2026 Initiate RASolve 307 (elironrasib combination in 1L)

37. Slide 37: Our Why: Building on Strong Pillars for Growing Transformative Patient Impact

    Our Why | Building on Strong Pillars for Growing Transformative Patient Impact Our Mission Our mission is to revolutionize treatment globally for patients with RAS-addicted cancers through the discovery, development and delivery of innovative, targeted medicines. Published: February 28, 2025 Publish

38. Slide 38: On Target to Outsmart Cancer

    On Target to Outsmart Cancer ®

39. Slide 39: Appendix

    Appendix © Revolution Medicines

40. Slide 40: Reference Data Tables for Current Therapies Across PDAC, NSCLC and CRC

    Reference Data Tables for Current Therapies Across PDAC, NSCLC and CRC © Revolution Medicines

41. Slide 41: PDAC is an Aggressive Disease - Cytotoxic Chemotherapy is Global Standard of Care

    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% Locally advanc

42. Slide 42: Adjuvant: High Unmet Need for Patients with Resectable PDAC

    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 metastatic

43. Slide 43: 1L PDAC: Significant Need for Improved Treatment(s)

    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 Rate (%)

44. Slide 44: 2L+ PDAC: Significant Need for Improved Treatment(s)

    2L+ PDAC: Significant Need for Improved Treatment(s) Reported Efficacy Median PFS Median OS Study Regimen Treatment line No. of patients ORR (%) (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 (4) FOL

45. Slide 45: 2L+ NSCLC: Significant Need for Improved Treatment(s)

    2L+ NSCLC: Significant Need for Improved Treatment(s) Reported Efficacy Timing relative to CPI Median PFS Median OS Study Treatment arm No. of patients ORR (%) 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 9.4 OAK(3)

46. Slide 46: Later Line CRC: Significant Need for Improved Treatment(s)

    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 3L 246

47. Slide 47: Daraxonrasib

    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 Designatio

48. Slide 48: Daraxonrasib Clinical Data

    Daraxonrasib Clinical Data © Revolution Medicines

49. Slide 49: RASolute 302: Overall Survival in the Overall Study Population

    RASolute 302: Overall Survival in the Overall Study Population Daraxonrasib Chemotherapy (n=248) (n=252) mOS, months (95% CI) 13.2 (10.0–NE) 6.7 (5.8–8.0) HR (95% CI)a 0.40 (0.30–0.53) P-valueb p=4.6×10−11 Data previously presented at the © 2026 ASCO, Inc. Reused with permission. All rights reserved

50. Slide 50: RASolute 302: Overall Survival Benefit Consistent Across Subgroups

    RASolute 302: Overall Survival Benefit Consistent Across Subgroups Events/N Favors Favors Population Daraxonrasib Chemotherapy Daraxonrasib Chemotherapy HR (95% CI)a Overall 79/248 141/252 0.42 (0.32–0.55) Age, years <65 37/114 68/121 0.41 (0.27–0.61) ≥65 42/134 73/131 0.43 (0.29–0.63) Sex Male 45/1

51. Slide 51: RASolute 302: Progression-Free Survival in the Overall Study Population

    RASolute 302: Progression-Free Survival in the Overall Study Population (by BICR) Daraxonrasib Chemotherapy (n=248) (n=252) mPFS, months (95% CI) 7.2 (5.7–7.5) 3.6 (2.9–4.2) HR (95% CI)a 0.49 (0.38–0.64) P-valueb p=5.2×10−8 Data previously presented at the © 2026 ASCO, Inc. Reused with permission. A

52. Slide 52: RASolute 302: Patient-Reported Outcomes (Overall Population)

    RASolute 302: Patient-Reported Outcomes (Overall Population) Daraxonrasib Chemotherapy HR (95% CI) 12 0.51 (0.37–0.71) • EORTC QLQ-PAN26 and EORTC QLQ-C30 Median time to deterioration, p<0.0001 10 HR (95% CI) questionnaires were administered on day 0.60 (0.46–0.79) 1 of each cycle and at end of trea

53. Slide 53: RASolute 302: Safety Overview

    RASolute 302: Safety Overview Daraxonrasib Chemotherapy (n=241) (n=214) Median time on 6.2 1.5-3.2a treatment, (0.03-14.1) (0.03-12.9) • Median dose intensity: months (range) • 93% with daraxonrasib Any TEAEs, n (%) 241 (100) 209 (97.7) • 65-95%a across chemotherapy regimens Any TRAEs, n (%) 236 (97

54. Slide 54: 1L PDAC: Daraxonrasib Monotherapy Promising Initial Antitumor Activity

    1L PDAC: Daraxonrasib (300 mg) Monotherapy Demonstrated Promising Initial Antitumor Activity in Patients with RAS Mutations All RAS (n=38)b 100 ORRc, % (95% CI) 47 (31, 64) Best % change in SOD from baseline in target tumor DCRd, % (95% CI) 92 (79, 98) 50 6-month PFSe, % (95% CI) 71 (53, 83) 6-month

55. Slide 55: 1L PDAC: Daraxonrasib Monotherapy Generally Well Tolerated

    1L PDAC: Daraxonrasib (300 mg) Monotherapy Generally Well Tolerated All RAS n (%) (n=40) Any grade Grade ≥3 Patients with any TRAE 38 (95) 15 (38) Patients with serious TRAE 4 (10) 3 (8) TRAEs occurring in ≥15% of patients Rasha 35 (88) 4 (10) Diarrhea 25 (63) 4 (10) Stomatitis 25 (63) 4 (10) Nausea

56. Slide 56: 1L PDAC: Daraxonrasib Monotherapy Dose Modification and Dose Intensity

    1L PDAC: Daraxonrasib (300 mg) Monotherapy Demonstrated Acceptable Rate of Dose Modification and Favorable Dose Intensity All RAS (n=40) Patients with dose modification due to TRAEs, n (%) 28 (70) Dose interruption 24 (60) Dose reduction 16 (40) Patients with dose discontinuation due to TRAEs, n (%)

57. Slide 57: 1L PDAC: Daraxonrasib + GnP Encouraging Initial Antitumor Activity

    1L PDAC: Daraxonrasib + GnP Demonstrated Encouraging Initial Antitumor Activity in Patients with RAS Mutations All treated (n=40)a 100 ORRb, % (95% CI) 58 (41, 73) → On treatment Best Percentage Change in SOD From * Unconfirmed DCRc, % (95% CI) 90 (76, 97) Baseline in Target Tumor Burden 50 6-month

58. Slide 58: 1L PDAC: Daraxonrasib + GnP Acceptable Safety/Tolerability

    1L PDAC: Daraxonrasib + GnP Demonstrated Acceptable Safety/Tolerability All treated patients (n=40) Any grade Grade ≥3 TRAEs (any drug), n (%) 40 (100) 29 (73) Serious TRAEs, n (%) 11 (28) 10 (25) TRAEs occurring in ≥30% of patients, n (%) Rasha 36 (90) 6 (15) Diarrhea 30 (75) 6 (15) Fatigue 28 (70)

59. Slide 59: 1L PDAC: Daraxonrasib + GnP Dose Modification and Dose Intensity

    1L PDAC: Daraxonrasib + GnP Demonstrated Acceptable Rate of Dose Modification and Favorable Dose Intensity for Daraxonrasib All treated patients (n=40) Daraxonrasib GnP Patients with dose modification due to TRAEs, n (%) 24 (60) 30 (75) Dose interruption 24 (60) 21 (53) Dose reduction 14 (35) 23 (58

60. Slide 60: Daraxonrasib + GnP Improved Depth and Durability in Preclinical PDAC Models

    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 1500 ** 100 Mean tumor volume (mm3) %Tumors progression-free G12X WT 10 PDAC 10 PDAC models models (7 KRAS G12X(7 KRAS WT

61. Slide 61: Regimens of Daraxonrasib and GnP for RASolute 303 Combination Arm

    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 generally Daraxonrasib 160–300 mg 200 mg well tolerated in 2L PDAC Sched

62. Slide 62: 2L/3L NSCLC: Encouraging Durability with Daraxonrasib 120-220 mg

    2L/3L NSCLC: Encouraging Durability in Patients with RAS G12 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) Median follow-up is 10.8 months. RMC-6236-001: 2L/3L patients with RAS G12X NSCLC treated with dar

63. Slide 63: 2L/3L NSCLC: Daraxonrasib Generally Well Tolerated at 120-220 mg

    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, n (%) Ras

64. Slide 64: 2L/3L NSCLC: Daraxonrasib Favorable Dose Intensity at 120-220 mg

    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 leading to

65. Slide 65: Daraxonrasib Registrational Study Designs

    Daraxonrasib Registrational Study Designs © Revolution Medicines

66. Slide 66: 2L Metastatic PDAC: Design of RASolute 302 Trial

    2L Metastatic PDAC: Design of RASolute 302 Trial Primary Endpoints N = 500 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 SOC (All Patients) • ECOG PS

67. Slide 67: 1L Metastatic PDAC: Design of RASolute 303 Trial

    1L Metastatic PDAC: Design of RASolute 303 Trial Daraxonrasib Primary Endpoints Key Eligibility Criteria N ~ 900 (300 mg) • Confirmed metastatic PDAC, • PFS, OS regardless of RAS status R Daraxonrasib Daraxonrasib • No prior systemic therapy for 1:1: 1 (200 mg) + GnP(1) (300 mg) metastatic disease •

68. Slide 68: Adjuvant Therapy in Resectable PDAC: Design of RASolute 304 Trial

    Adjuvant Therapy in Resectable PDAC: Design of RASolute 304 Trial N=500 Primary Key Eligibility Daraxonrasib Endpoint Surgery Criteria No radiologic 300 mg PO QD • DFS + evidence of • Confirmed PDAC Duration 2 years R Perioperative disease • R0 or R1 resection* 1:1 chemotherapy Secondary • ECOG PS 0

69. Slide 69: Previously Treated NSCLC: Design of RASolve 301 Trial

    Previously Treated NSCLC: Design of RASolve 301 Trial Key Eligibility Criteria • Locally advanced or metastatic NSCLC Primary Endpoints N=590 Daraxonrasib (RAS G12X-C)(1) • RAS genotypes: RAS G12X-C (core population), G12C, G13X or Q61X 200 mg PO QD • PFS, OS • Prior therapies: 1 or 2 prior lines of

70. Slide 70: Zoldonrasib

    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 © Revolution Medicines

71. Slide 71: Zoldonrasib Clinical Data

    Zoldonrasib Clinical Data © Revolution Medicines

72. Slide 72: Zoldonrasib Monotherapy Initial Activity in Previously Treated KRAS G12D PDAC

    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, Pharmacokinetics,

73. Slide 73: Zoldonrasib Monotherapy: Generally Well Tolerated Across Indications

    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 (33%

74. Slide 74: Zoldonrasib Monotherapy Initial Activity in Previously Treated KRAS G12D NSCLC

    Promising Initial Activity of Zoldonrasib Monotherapy in Previously Treated Patients with KRAS G12D NSCLC ICI and Platinum Chemo Treated 100 (No Prior Docetaxel) On treatment Zoldonrasib 1200 mg PO QD (N = 27) * Unconfirmed ORRa, % (95% CI) 52 (32, 71) Best % Change in SOD from Baseline 50 DCRa, % (

75. Slide 75: Initial Durability Data for Zoldonrasib Monotherapy in KRAS G12D NSCLC

    Encouraging Initial Durability Data for Zoldonrasib Monotherapy in Previously Treated Patients with KRAS G12D NSCLC ICI and Platinum Chemo Treated ICI and Platinum Chemo Treated (No Prior Docetaxel) (No Prior Docetaxel) Zoldonrasib 1200 mg PO QD (N = 27) Zoldonrasib 1200 mg PO QD (N = 27) mPFS, mont

76. Slide 76: Zoldonrasib Monotherapy Generally Well Tolerated in KRAS G12D NSCLC

    Zoldonrasib Monotherapy Generally Well Tolerated in Previously Treated Patients with KRAS G12D NSCLC All Patients with NSCLC Treated with Zoldonrasib 1200 mg PO QD (N = 40) Maximum Severity of Treatment-Related AEs Grade 1 Grade 2 Grade 3a Any Grade Any TRAE, n (%) 23 (58) 8 (20) 5 (13) 36 (90) TRAE

77. Slide 77: Zoldonrasib Monotherapy Minimal Dose Modifications and Discontinuations

    Zoldonrasib Monotherapy Led to Minimal Dose Modifications and Discontinuations with Favorable Dose Intensity Maintained All NSCLC Treated 1200 mg TRAEs Leading to Zoldonrasib Action Taken PO QD (N = 40) Dose modification, n (%) Dose interruption 6 (15) Dose reduction 1 (3) Dose discontinuation, n (%

78. Slide 78: Zoldonrasib Registrational Study Designs

    Zoldonrasib Registrational Study Designs © Revolution Medicines

79. Slide 79: 1L Metastatic RAS G12D PDAC: Design of RASolute 305 Trial

    1L Metastatic RAS G12D PDAC: Design of RASolute 305 Trial Zoldonrasib (1200 mg QD) + mFOLFIRINOX or Primary Endpoints Key Eligibility Criteria N = 670 Gemcitabine/Nab-paclitaxel • Confirmed metastatic (n=335) • PFS, OS pancreatic adenocarcinoma • No prior systemic therapy for R metastatic disease 1:

80. Slide 80: 1L Metastatic RAS G12D PDAC: Design of RASolute 309 Trial

    1L Metastatic RAS G12D PDAC: Design of RASolute 309 Trial Zoldonrasib (1200 mg QD) + Primary Endpoints Key Eligibility Criteria N = 400 Daraxonrasib (300 mg QD) • Confirmed metastatic (n=200) • PFS, OS pancreatic adenocarcinoma • No prior systemic therapy for R metastatic disease 1:1 Secondary Endpo

81. Slide 81: 1L Metastatic RAS G12D NSCLC: Design of RASolve 308 Trial

    1L Metastatic RAS G12D NSCLC: Design of RASolve 308 Trial Primary Endpoints Key Eligibility Criteria N = 430 • Confirmed metastatic non- Zoldonrasib (1200 mg) + • PFS (per BICR) 2 squamous NSCLC KN-189 (N=215) • No prior systemic therapy for R 1:1 Secondary Endpoints metastatic disease • Documented

82. Slide 82: Elironrasib

    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 © Revolution Medicines

83. Slide 83: Elironrasib Clinical Data

    Elironrasib Clinical Data © Revolution Medicines

84. Slide 84: Elironrasib Monotherapy: Antitumor Activity and Durability in Previously Treated RAS G12C NSCLC

    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 Baseline Sc

85. Slide 85: Elironrasib Monotherapy in RAS G12C NSCLC Previously Treated with G12C(OFF) Inhibitor

    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 follow-up, months (range): 17.6 (10.3, 24.6) and 17.4 (14, 28.5). Median duration of

86. Slide 86: Elironrasib Monotherapy: Encouraging Durability After G12C(OFF) Inhibitor

    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) OS Probability PFS Probability NSCLC, non-s

87. Slide 87: Elironrasib Monotherapy: Generally Well Tolerated in RAS G12C NSCLC

    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%) 0 Electr

88. Slide 88: Elironrasib + Daraxonrasib RAS(ON) Inhibitor Doublet Background

    Elironrasib + Daraxonrasib RAS(ON) Inhibitor Doublet Background © Revolution Medicines

89. Slide 89: Elironrasib and Daraxonrasib Combination Benefit in Preclinical NSCLC Models

    Elironrasib and Daraxonrasib Show Combination Benefit and Synergize with Anti-PD-1 in Preclinical NSCLC Models Elironrasib and Daraxonrasib Show Combination RAS(ON) Inhibitor Doublet Sensitizes Benefit in a NSCLC Model Immune-Refractory NSCLC to Anti-PD-1 Control Daraxonrasib Control Elironrasib+ant

90. Slide 90: Elironrasib + Daraxonrasib Doublet Activity in 2L+ NSCLC

    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 treated

91. Slide 91: Elironrasib + Daraxonrasib: Generally Well Tolerated in 2L+ NSCLC

    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% of pati

92. Slide 92: Limited Monotherapy Activity of Daraxonrasib or Elironrasib in CRC

    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) Previo

93. Slide 93: Elironrasib + Daraxonrasib Doublet Activity in Previously Treated CRC

    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 first dose

94. Slide 94: RM-055 Preclinical Data

    RM-055 Preclinical Data © Revolution Medicines

95. Slide 95: RM-055: New Class of Mutant-Targeted Catalytic RAS(ON) Inhibitors

    RM-055, Exemplifying Innovative New Class of Mutant-Targeted Catalytic RAS(ON) Inhibitors, Designed to Mimic the Activity of Natural GAPs A Single CYPA:RM-055 Binary Complex Inactivates RM-055 Markedly Stimulates Hydrolysis of Multiple RAS Proteins RAS-GTP to RAS-GDP G12V mutant RAF RBD CYPA:TCI G12

96. Slide 96: RM-055 Drives Deep and Durable Tumor Regressions in G12 Mutant KRAS Models

    RM-055 Drives Deep and Durable Tumor Regressions in G12 Mutant KRAS Preclinical Models PDAC NSCLC CRC (KRAS G12D)1 (KRAS G12C)2 (KRAS G12V)3 2000 Mean tumor volume (mm3) 2000 Mean tumor volume (mm3) Control Control Control RM-055 0.3 mg/kg po qd 1500 RM-055 10 mg/kg po qd 1500 RM-055 10 mg/kg po qd

97. Slide 97: New Class of RAS(ON) Inhibitors Designed to Overcome Drug Resistance

    Innovative New Class of RAS(ON) Inhibitors Designed to Overcome RAS-Driven Drug Resistance and Extend Clinical Benefit Standard Models Resistant Models3 Post-Progression Treatment 2000 2000 Mean tumor volume (mm3) Mean tumor volume (mm3) 2000 Mean tumor volume (mm3) Control (NSCLC, KRAS G12C)2 1500

98. Slide 98: Royalty Pharma Partnership

    Royalty Pharma Partnership © Revolution Medicines

99. Slide 99: Royalty Pharma Partnership Provides $2 Billion in Flexible Committed Capital

    Royalty Pharma Partnership Bolsters Already Strong Financial Position by Providing $2 Billion in Flexible Committed Capital Received $2 Billion Committed June 2025 Scheduled* Scheduled* Received May 2026 approval Synthetic Term Debt ($0.75 B) RVMD discretion* Royalty RVMD discretion* ($1.25 B) 3 Tra

Revolution Medicines — Investor Presentation (August 2026) on 6ix