Revolution Medicines (RVMD) 8-K Results of Operations and Financial Condition

Exhibit 99.1

On Target to Outsmart CancerTM

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 financial position, business strategy, prospective products, availability of funding, ability to maintain existing collaborations, including with Sanofi, and establish new strategic collaborations, licensing or other arrangements, the scope, progress, results and costs of developing our product candidates or any other future product candidates, the potential market size and size of the potential patient populations for our product candidates, the timing and likelihood of success of obtaining product approvals, plans and objectives of management for future operations, the scope of protection we are able to establish and maintain for intellectual property rights covering our product candidates, future results of anticipated products, and the impact of the COVID-19 pandemic on our business are forward-looking statements. These statements involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Because forward-looking statements are inherently subject to risks and uncertainties, some of which cannot be predicted or quantified and some of which are beyond our control, you should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur and actual results could differ materially from those projected in the forward-looking statements. The information included in these materials is provided as part of an oral presentation on January 11, 2022 and is qualified as such. Except as required by applicable law, we undertake no obligation to update any forward-looking statements or other information contained herein, whether as a result of any new information, future events, changed circumstances or otherwise. For a further description of the risks and uncertainties that could cause actual results to differ from those anticipated in these forward-looking statements, as well as risks relating to the business of Revolution Medicines in general, see Revolution Medicines’ Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission on November 10, 2021, and its future periodic reports to be filed with the Securities and Exchange Commission. This presentation concerns product candidates that are under clinical investigation and which have not yet been approved for marketing by the U.S. Food and Drug Administration (FDA). These product candidates are currently limited by Federal law to investigational use, and no representation is made as to their safety or effectiveness for the purposes for which they are is being investigated.

On Target to Outsmart Cancer HIGH UNMET NEED IN RAS-ADDICTED CANCERS RAS proteins drive 30% of human cancers(1), and are largely unserved by targeted therapeutics STRONG CLINICAL VALIDATION OF RAS AS CANCER DRIVER Proof-of-principle from first-gen KRASG12C inhibitors(2) predicts favorable impact of targeted inhibitors across numerous RAS cancer drivers DEEP SCIENCE-DRIVEN PIPELINE Comprehensive collection of groundbreaking RAS(ON) Inhibitors with best-in-class preclinical profiles and/or first-in-class potential covering RAS space broadly; first candidates planned to enter clinic in 2022 Leading RAS Companion Inhibitors in clinic designed for combination treatment strategies to counter resistance to RAS targeted therapies (1) Prior et al., Cancer Research 2020 (2) Lumakras approved by the FDA in May 2021

Excessive RAS(ON) Signaling Drives 30% of Human Cancers = RAS(OFF) RAS-Addicted Cancers = RAS(ON) Normal RAS Cancer Mutations New patients per year (U.S.)(1) 230,000 All Cell Membrane 67,000 Lung cancer Tightly regulated Excessive control RAS(ON) cell proteins growth RAS(ON) uncontrolled signaling cell growth drives 79,000 Colorectal cancer Exemplary G12C, G12D, G12V, G12R mutations in G13C, G13D 49,000 KRAS, HRAS Pancreatic cancer and/or NRAS Q61H, Q61K, Q61L (1) Estimated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer = non-small cell lung cancer

RAS Deep -Addicted Science- Cancers Driven Pipeline of Targeted Therapies for RAS(ON) Inhibitors RAS Companion Inhibitors 2 Drug expected Candidates to enter 2 Clinical-stage Drug Candidates clinic in 2022 RAS COOPERATING 2 expected Drug Candidates to file RAS(ON) TARGETS 1 IND-ready CANCER Drug Candidate INDs in 2023 DRIVERS 4+ programs Pipeline expansion

RAS(ON) Inhibitors Induce Rapid, Deep Suppression and Sustained of Drivers RAS(ON) Cancer RASMULTI KRASG12C RMC-6236 RMC-6291 RAS(ON) DRIVERS CANCER KRASG12D KRASG13C RMC-9805 RMC-8839

Engine Distinctive Targets RAS Oncogenic Drug Discovery: RAS(ON) Innovation Proteins ) Inhibitory Tri-Complexes Selected compounds Cyclophilin A Binary complex Non-covalent Covalent RAS(ON) Inhibitors Deep and Diverse Collection • Highly potent and selective • Oral and drug-like • Rapid, deep and sustained suppression of RAS(ON) signaling

RMC-6236: First-in-Class RASMULTI(ON) Inhibitor with Broad Potential Against RAS-Addicted Cancers Colorectal 32% Highly Potent and Selective RAS(ON) Inhibitor • Inhibits canonical RAS family members, suppressing Pancreatic the mutant cancer driver and cooperating wild-type 32% RAS proteins 137,000 Robust Anti-tumor Activity in Cancer Models New KRASG12X patients (1) • Deep and sustained inhibition drives durable per year (U.S.) anti-tumor activity in tumors with common RAS variants including KRASG12D, KRASG12V, KRASG12R and KRASG12C 30% Lung Attractive PK/ADME Profile Other 6% • Favorable in vivo oral bioavailability, clearance and concentration in tumors for effective target coverage in RAS-addicted cancer cells KRASG12X includes KRASG12D, KRASG12V, KRASG12R and KRASG12C 8 (1) Calculated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer = non-small cell lung cancer Characterization above is based on RVMD preclinical research

RMC-6236: Highly Active in Vivo Across Cancer Models with KRASG12X Drivers NSCLC PDAC CRC 62% ORR (8/13) 57% ORR (8/14) 38% ORR (5/13) 200 100% DCR (13/13) 200 86% DCR (12/14) 200 54% DCR (7/13) mPD 100 mPD Baseline 100 100 Volume From mPD Tumor 0 mSD 0 0 Mean Change mSD mSD % mPR mPR mPR mCR mCR mCR -100 -100 100 - 2—4 1903—2393—1955 — 2803 H441—1358 H358 KP HPAC GP2D H2122 H2030 — SW620 SW403 CTG LUN352—NCI LUN232 CTG CTG—NCI CTG NCI CTG LUN020 NCI LUN137 PAN022 PAN038 PAN1001 PAN026 PAN020 PAN003 Capan PAN010 PAN031 PAN039 PAN029 PAN009 CRC007 CRC043 CRC078 CRC060 CRC1018 CRC047 CRC051 CRC044 CRC039 CRC1005 KRASG12C KRASG12D KRASG12R KRASG12V Deep Tumor Regressions and Complete Responses Observed Across Cancer Models RMC-6236 RVMD preclinical dosed research, at 25 mg/kg as po of 10/12/21 qd; n = 3-10/group 9 NSCLC = non-small cell lung cancer; PDAC = pancreatic ductal adenocarcinoma; CRC = colorectal cancer Responses assigned according to mRECIST (see appendix) ORR = objective response rate; DCR = disease control rate

RMC-6236: Diverse RAS Highly Drivers Active in Vivo Across Cancer Models with 100 KRASG12X Tumors 75 RMC-6236 Median not reached Control % Tumors for either active Progression- 50 treatment group RAS Pathway Mutant Tumors Median = 9 days Free for both RMC-6236 25 control groups Control 0 0 10 20 30 Days on Treatment Durable Anti-Tumor Benefit Observed in KRASG12X Cancer Models and Beyond RVMD RMC-6236 preclinical dosed research, at 25 mg/kg as po of 10/12/21 qd 10 Progression defined as tumor doubling from baseline over 28 days p<0.0001 by Log-rank test (control vs RMC-6236 treatment) See appendix for composition of KRASG12X Tumors and RAS Pathway Mutant Tumors

RMC with -Checkpoint 6236: Anti-Tumor Inhibitor Immunity in Vivo and Strong Additivity Favorable Transformation of Durable Complete Responses Tumor Immune Microenvironment with Checkpoint Inhibitor Combination CD8+ T Cells M2 M𛉠mMDSCs ) Control RMC-6236 + Anti-PD1 (mm 3 CD45+ Volume of % Tumor 10/10 CR Mean Control RMC-6236 Modulation of the Tumor Microenvironment Primes for Anti-Tumor Immunity in Cancer Models RVMD preclinical research, as of 09/10/2021 Syngeneic tumor model with CT26 cell line engineered to express KRASG12C 11 RMC-6236 dosed at 25 mg/kg po qd; Anti-PD1 dosed at 10 mg/kg ip biw; n = 10/group M2 M𛉠= M2 macrophages; mMDSCs = Monocytic myeloid derived suppressor cells

RMC-6236: Clinical Priorities to Pursue First-in-Class Activity Against KRASG12X Tumors 2022 Further development • Submit IND^ • Define RP2DS • Initiate single agent dose escalation in patients • Single agent expansion cohorts in KRASG12X with cancers with KRASG12X mutations (focused tumors (NSCLC, pancreatic cancer and CRC) on NSCLC, pancreatic cancer and CRC) G12X Activities • Combinations in KRAS tumors (NSCLC, • Include ‘below MTD’ expansion cohorts in pancreatic cancer and CRC) select populations during dose escalation Aims Evidence of first-in-class single agent activity against KRASG12X tumors^ ^See Milestones table KRASG12X may include KRASG12D, KRASG12V, KRASG12R and/or KRASG12C 12 RP2DS = Recommended Phase 2 dose and schedule MTD = maximum tolerated dose NSCLC = non-small cell lung cancer; CRC = colorectal cancer

RMC-6291: Mutant-Selective RAS(ON) Inhibitor with Best-in-Class Potential for KRASG12C Cancers Highly Potent and Selective RAS(ON) Inhibitor Lung 76% • Highly active against KRASG12C • Covalent for irreversible inhibition • Low off-target risk and acceptable safety profile 29,000 Robust Anti-tumor Activity in Cancer Models New KRASG12C patients Rapid, • deep and sustained inhibition drives durable per year (U.S.)(1) anti-tumor effects across multiple KRASG12C tumor types, with complete responses in some models Colorectal 18% Attractive PK/ADME Profile • Favorable in vivo oral bioavailability and clearance Pancreatic for effective target coverage in KRASG12C-addicted 3% Other 3% cancer cells 13 (1) Calculated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer = non-small cell lung cancer Characterization above is based on RVMD preclinical research

RMC-6291: Superior Outcomes in Mouse Clinical Trial with KRASG12C NSCLC Models RMC-6291 Adagrasib 72% (18/25) ORR 52% (13/25) ORR 92% (23/25) DCR 72% (18/25) DCR mPD mPD mSD mSD mPR mPR mCR mCR Best-in-Class Potential in KRASG12C NSCLC RVMD preclinical research as of 10/21/21 Adagrasib NSCLC = Non-small dosed at cell 100 lung mg/kg cancer po qd; RMC-6291 dosed at 200 mg/kg po qd; n = 3 to 10/group 14 Responses assigned according to mRECIST (see appendix)

RMC-6291 May Improve on KRASG12C (OFF) Inhibitor Class Across Three Outcome Measures in NSCLC Increased Rate Of Response(a) Increased Depth Of Response(b) Increased Duration Of Response(c) Volume Tumor in Change % Control RMC-6291 Adagrasib Best-in-Class Potential in KRASG12C NSCLC RVMD preclinical research as of 07/28/21 RMC NSCLC -6291 = Non dosed -small at cell 200 lung mg/kg cancer po qd; Adagrasib dosed at 100 mg/kg po qd 15 PDX Models: (a) LUN055; (b) LXFA-983; (c) CTG-0828 Nichols. Targeting KRASG12C(ON) and Potential Application to Overcoming Drug Resistance in RAS-Addicted Tumors. RAS-Targeted Drug Development Summit. Sept. 22, 2021.

RMC-6291: Clinical Priorities to Pursue Best-in-Class Activity Against KRASG12C Tumors 2022 Further development • Submit IND^ • Define RP2DS • Initiate single agent dose escalation in • Single agent expansion cohorts in KRASG12C KRASG12C tumors NSCLC and pancreatic cancer (RAS inhibitor naïve +/- failure) Activities • Include ‘below MTD’ expansion cohorts in select populations (e.g., NSCLC) during dose • Combinations in KRASG12C NSCLC & CRC escalation Aims Preliminary evidence of superior activity against KRASG12C tumors^ ^See Milestones table RP2DS = Recommended Phase 2 dose and schedule 16 NSCLC MTD = maximum = non-small tolerated cell lung dose cancer; CRC = colorectal cancer

RMC-9805: Mutant-Selective RAS(ON) Inhibitor with Best-in-Class Potential for KRASG12D Cancers Highly Potent and Selective RAS(ON) Inhibitor Pancreatic Colorectal 38% 40% • Highly active against KRASG12D • Covalent for irreversible inhibition • Low off-target risk and acceptable safety profile 55,000 Robust Anti-tumor Activity in Cancer Models New KRASG12D patients • Rapid, deep and sustained inhibition drives durable per year (U.S.)(1) regressions in KRASG12D lung, pancreatic and colorectal cancers Attractive PK/ADME Profile Lung • Favorable in vivo oral bioavailability and clearance Other 14% for effective target coverage in KRASG12D-addicted 8% cancer cells 17 (1) Calculated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer = non-small cell lung cancer Characterization above is based on RVMD preclinical research

RMC-9805: Selective, Covalent and Orally Active with Sustained Inhibition of KRASG12D in Vivo Selective Covalent Single Dose PK/PD Modification of KRASG12D HPAC CDX (PDAC, KRASG12D/WT) PD: Tumor DUSP6 (%) KRAS: WT G12D G13D G12C G13C PK: Unbound plasma conc. (nM) X-linked KRAS 100 KRAS H/NRAS mRNA 100 control 10 to Unbound Potent Inhibition of KRASG12D DUSP6 50 1 Concentration Cancer Cell Growth 125 Tumor relative 0.1 (nM) Plasma 100 % 0 0.5 1 2 4 8 24 48 0.01 %Control) 75 Time point (h) Proliferation 50 CTG, Cell (3D 25 0 -11 -10 -9 -8 -7 -6 -5 Log M [RMC-9805] RVMD RMC-9805 preclinical dosed research, at 100 mg/kg as of po 10/13/2021 18 PDAC = pancreatic ductal adenocarcinoma

RMC-9805: Regressions Tumor in Models of KRASG12D Cancers • First-in-class mutant-selective covalent inhibitor of KRASG12D • Deep and durable anti-tumor responses in vivo in pancreatic and colorectal cancer models • Oral dosing, well tolerated HPAC CDX (PDAC, KRASG12D/WT) 3 ) (mm 3000 Control RMC-9805 Volume 2000 Dosing Tumor 1000 start Mean 0 10 20 30 40 50 Days post-implant Gp2D CDX (CRC, KRASG12D/WT) 3 ) (mm Control RMC-9805 Volume 2000 Dosing 1000 Tumor start Mean 0 10 20 30 40 50 Days post-implant RVMD preclinical research, as of 11/05/2021 RMC-9805 dosed at 100 mg/kg pd qd; n = 10/group (top), 6/group (bottom); PDAC = pancreatic ductal adenocarcinoma; CRC = colorectal cancer

RMC-8839: First-in-Class Mutant-Selective RAS(ON) Inhibitor for KRASG13C Cancers Lung 70% Highly Potent and Selective RAS(ON) Inhibitor • Highly active against KRASG13C • Covalent for irreversible inhibition • Low off-target risk and acceptable safety profile 3,000 Robust Anti-tumor Activity in Cancer Models New KRASG13C patients • Rapid, deep and sustained inhibition drives durable Colorectal (1) G13C 21% per year (U.S.) regressions in KRAS lung cancers Attractive PK/ADME Profile • Favorable in vivo oral bioavailability and clearance Pancreatic for effective target coverage in KRASG13C-addicted 2% Other cancer cells 7% 20 (1) Calculated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer = non-small cell lung cancer Characterization above is based on RVMD preclinical research

RMC-8839: Selective, Covalent and Orally Active with Sustained Inhibition of KRASG13C in Vivo Selective Covalent Single Dose PK/PD Modification of KRASG13C NCI-H1734 (NSCLC CDX, KRASG13C) KRAS: WT G12C G13C PD: Tumor DUSP6 (%) PK: Unbound plasma conc. (nM) X-linked KRAS KRAS H/NRAS Potent Inhibition of KRASG13C Cancer Cell Growth 125 No PD data at 0.5 and 1 hr 100 %Control) 75 Proliferation 50 Cell (CTG, 25 0 -11 -10 -9 -8 -7 Log M [RMC-8839] RVMD RMC-8839 preclinical dosed research, at 100 mg/kg as of po 12/22/2021 21 NSCLC = non-small cell lung cancer

RMC-8839: Regressions Tumor in Models of KRASG13C Cancers • First-in-class mutant-selective covalent inhibitor of KRASG13C • Deep anti-tumor responses in vivo in non-small cell lung cancer models • Oral dosing, well tolerated NCI-H1734 CDX (NSCLC, KRASG13C/WT) Control RMC-8839 ST2822B PDX (NSCLC, KRASG13C/WT) Control RMC-8839 RMC-8839 dosed at 100 mg/kg pd qd; n = 5/group; RVMD preclinical NSCLC = research, Non-small as cell of lung 11/17/2021 cancer

On Pancreatic Target to Cancer Outsmart G12D RMC-6236 Devastating disease 36% RMC-9805 >90% driven by KRAS mutations 49,000 G12V RMC-6236 26% New KRASMUTANT pancreatic cancer patients per year (US)(1) G12R RMC-6236 13% RMC-6291 Dismal survival rates G12C No approved targeted therapies 2% RMC-6236 Other RMC-6236 23% 23 (1) numbers Calculated using using cancer tumor incidence mutation from frequencies ACS Cancer from Facts Foundation and Figures Medicine 2020 (see Insights appendix August for additional 2020 and detail) scaled to estimated patient Our development-stage RAS(ON) Inhibitors • Inhibit >90% of pancreatic cancer drivers (1) in cancer models • Exhibit strong anti-tumor activity in preclinical models of pancreatic cancer

RAS Inhibitors Companion Suppress Cooperating Targets and Sustain Pathways RAS-Addicted that Cancers RMC-4630 SHP2 RMC-5552 RAS (ON) mTORC1 CANCER DRIVERS IMMUNE CHECKPOINTS

RMC-4630: Ongoing and Planned Clinical Combination Studies COMBINED STUDY SPONSOR WITH INDICATION(S) STATUS CodeBreaK 2L+ KRASG12C Amgen sotorasib Ongoing (Phase 1b/2) 101c (U.S.) solid tumors RMC-4630-03 2L+ KRASG12C RevMed sotorasib Ongoing (Phase 2) (Global) NSCLC TCD16210 2L+ KRASG12C Sanofi adagrasib In preparation (Phase 1/2) (Global) NSCLC KRASG12C TBD RevMed RMC-6291 Planning TBD TCD16210 1L PDL1+ Sanofi pembrolizumab Ongoing (Phase 1/2) (Global) NSCLC RMC-4630/SAR442720 under 2018 partnership NSCLC = non-small cell lung cancer

RMC-4630: Clinical Priorities to Pursue Best-in-Class Combination Activity in KRASG12C Tumors 2022 Further development • Registration study in combination with KRASG12C(OFF) inhibitor in KRASG12C NSCLC • Complete enrollment in RMC-4630-03 and • Combination study(ies) with KRASG12C(OFF) preliminary evaluation^ inhibitor in KRASG12C CRC and/or pancreatic Activities cancer • Combination study(ies) with RMC-6291 Evidence of clinical benefit as RAS Companion Inhibitor against KRASG12C NSCLC^ Aims Evidence of clinical benefit as a RAS Companion Inhibitor against additional KRASG12C tumors NSCLC = non-small cell lung cancer 26 RMC-4630/SAR442720 under 2018 partnership CRC = colorectal cancer

Opportunity RMC-5552 Clinical • Potent, selective inhibitor of hyperactivated mTORC1 to reactivate the tumor suppressor 4EBP1 • Designed for combination with RAS(ON) inhibitors in patients with cancers harboring RAS/mTOR pathway co-mutations(1) • >30,000 new patients per year across lung, colorectal and pancreatic cancers (U.S.)(2) • Single agent Phase 1b dose escalation underway, focused on tumor genotypes linked to hyperactivated mTORC1 signaling (1) mTOR pathway co-mutations include genetic changes with likely oncogenic activity in one or more (2) Calculated of PIK3CA, using PTEN, tumor TSC1, mutation TSC2, STK11, frequencies and/or from mTOR Foundation Medicine Insights August 27 2020 and Figures and scaled 2020; to see estimated appendix patient for additional numbers detail using cancer incidence from ACS Cancer Facts Preliminary Evidence of Clinical Activity Best Tumor Change in Efficacy Evaluable Patients Treated with 6 mg IV Weekly# # Preliminary assessments suggest mucositis as the major dose-limiting toxicity. 6 mg weekly was well tolerated. Further enrollment at doses above 6 mg is ongoing to define the RP2DS; *Patient received one dose of 12 mg, followed by weekly doses of 6 mg. Data as of 01/07/2022.

RMC-5552: Clinical Priorities to Pursue Best-in-Class Combination Activity in RASMUTANT/mTORC1-Activated Tumors 2022 Further development • Define single agent RP2DS • Complete single agent dose-escalation • Complete single agent expansion cohorts • Initiate single agent expansion cohorts in • Combinations with RAS(ON) inhibitors from select tumors with mTOR pathway mutations Activities our portfolio in RASMUTANT tumors with mTOR pathway co-mutations Aims Additional evidence of single agent activity against tumors with mTOR pathway mutations^ ^See Milestones table 28 RP2DS = Recommended Phase 2 dose and schedule

Deep Pipeline of Targeted Therapies for Majority of RAS-Addicted Cancers PRECLINICAL IND-ENABLING CLINICAL PHASE 1 CLINICAL PHASE 2 CLINICAL PHASE 3 RAS(ON) INHIBITORS RMC-6236 RASMULTI RMC-6291 KRASG12C RMC-9805 KRASG12D RMC-8839 KRASG13C Additional G12R, G12V, G13D, Q61X, other RAS COMPANION INHIBITORS RMC-4630 SHP2 RMC-5552 mTORC1/4EBP1 RMC-5845(1) SOS1 (1) IND-ready

Anticipated Milestones PROGRAM MILESTONE (EXPECTED TIMING) RAS(ON) INHIBITORS RMC-6236 (RASMULTI) Submit IND (1H22); Provide evidence of first-in-class single agent activity (2023) RMC-6291 (KRASG12C) Submit IND (1H22); Provide preliminary evidence of superior activity (2023) RMC-9805 (KRASG12D) Submit IND (1H23) RMC-8839 (KRASG13C) Submit IND (2H23) Additional RASMUTANT-Selective Inhibitor Nominate development candidate (2H22) RAS COMPANION INHIBITORS Complete enrollment in RMC-4630-03 (2H22); Provide preliminary (2H22) and additional (2023) evidence of RMC-4630 (SHP2) clinical benefit as a RAS Companion Inhibitor from RMC-4630-03 RMC-5552 (mTORC1/4EBP1) Provide additional evidence of single agent activity (2023)

Financial Information Financial Position Cash, cash equivalents and $608.7 million(1) marketable securities @ 9/30/2021 2021 Financial Guidance 2021 GAAP net loss of $170 million to $190 million(2) (1) Expected to fund planned operations to end of 2023 (2) Includes non-cash stock-based compensation expense of approximately $20 million

Focused on serving high unmet needs across numerous cancers driven by diverse RAS mutations Targeted RAS(ON) Inhibitors with compelling preclinical profiles expected to begin entering clinic in 2022 Targeted RAS Companion Inhibitors designed to counter drug resistance have shown initial clinical activity and evaluation continues Development-stage portfolio covers RAS drivers of all major RAS-addicted cancers

Appendix RAS cancer epidemiology statistics are estimated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020: RAS mutations include: KRAS G12(A,C,D,R,S,V), KRAS G13(C,D), KRAS Q61(H, K, L), KRAS A146T, KRAS wild-type amplification, NRAS G12C, NRAS Q61(K,L,R,P), HRAS mutations of known/likely function, BRAF class 3 mutations, NF1 loss of function mutations, PTPN11 mutations of known/likely function. NF1 LOF mutations = 50% of all NF1 mutations of known/likely function. BRAF class 3 mutations = D287H, D594(A,E,G,H,N,V,Y), F595L, G466(A,E,R,V,E,D,R), N581(I,S), S467L,T599I, V459L. Includes 12 major types: non-small cell lung cancer, colorectal, pancreatic adenocarcinoma, renal, gastroesophageal, head and neck squamous cell, ovarian and biliary cancers, acute myeloid leukemia, and advanced melanoma, bladder and uterine/endometrial cancers causing mortality. Est. worldwide annual incidence of RAS-mutated cancers is 3.4 million per Prior et al., Cancer Research 2020 RAS mutations drive 30% of human cancers per Prior et al., Cancer Research 2020 KRASG12X includes KRASG12D, KRASG12V, KRASG12R and KRASG12C Mouse tumor responses on slides 9 and 14 assigned according to mRECIST (modified from Gao et al. Nat Med. 2015): mPD = progressive disease; mSD = stable disease; mPR = partial response; mCR = complete response Kaplan-Meier progression on slide 10 defined as tumor doubling from baseline over 28 days: KRASG12X Tumors, where X = D,V,C, A or R: n = 207 RAS Pathway Mutant Tumors includes KRASG12X and other RAS and RAS pathway mutant tumors: KRASG13C, KRASG13D, KRASK117N, KRASQ61H, NF1LOF, PTPN11E76K or G503V, BRAFClass 3-mutant, and KRASWT-Amp: n = 332 PDX = patient-derived xenograft; CDX = cell line-derived xenograft