Slide 1: On a Journey to Erase Cancer
On a Journey to Erase Cancer Erasca Corporate Presentation August 2026 Eric and his wife Margaret, inspiring our bold mission to erase cancer
Slide 2: Disclaimer: Forward Looking Statements & Market and Clinical Data
Disclaimer: Forward Looking Statements & Market and Clinical Data We caution you that this presentation contains forward-looking statements. All statements other than statements of historical facts contained in this presentation are forward-looking statements, including statements regarding: our fut
Slide 3: Our name is our mission: to erase cancer
Our name is our mission: to erase cancer Vision to one day erase cancer1 in at least 100,000 patients annually as a leading global oncology company Experienced leadership team and SAB with track record of serial successes • Founded by Jonathan Lim, MD & Kevan Shokat, PhD around disruptive idea to ta
Slide 4: SAB includes world’s leading experts in the RAS/MAPK pathway
SAB includes world’s leading experts in the RAS/MAPK pathway Erasca co-founder. World expert in RAS Erasca Chair of R&D. World expert in World expert in functional cancer who pioneered development of approaches structure-based drug design; former head of genetics and identifying new drug to inhibit
Slide 5: Focused modality-agnostic RAS/MAPK pipeline
Focused modality-agnostic RAS/MAPK pipeline Program Target Modality Indication Discovery IND-enabling Phase 1 Phase 2 Phase 3 Worldwide Rights ERAS-0015 RAS RASm solid tumors AURORAS-1 ERAS-4001 KRAS KRASm solid tumors BOREALIS-1 small molecule small molecule molecular glue Note: Pipeline also inclu
Slide 6: Ideal RAS targeting molecules integrate three key attributes
Ideal RAS targeting molecules integrate three key attributes • Lower clinically active dose could Preclinical translate to: Activity Preclinical Activity - Lower risk of solubility-limited absorption and exposure plateau observed with the most advanced pan-RAS MG in development RAS Targeting - Bette
Slide 7: ERAS-0015 and ERAS-4001 exhibit competitive profiles that exceed our TPP
ERAS-0015 and ERAS-4001 exhibit competitive profiles that exceed our TPP Preclinical Activity1 OBA2 IP3 ERAS-0015 • In vitro: 0.2 – 13.8 nM IC50 in KRAS G12D/V/C/X, G13D, WT; • 38 – 48% in small • IP exclusivity expected through Pan-RAS activity in H/NRAS animal species 2043 Molecular • In vivo: Tum
Slide 8: ERAS-0015: Potential best-in-class pan-RAS molecular glue
ERAS-0015: Potential best-in-class pan-RAS molecular glue Preclinical Differentiation1 Comparable anti-tumor activity at 1/10th-1/5th of RMC-6236 In Vivo Activity ERAS-0015 dose in multiple mouse models Pan-RAS • Higher oral bioavailability (improved %F) Molecular Glue PK Properties • Lower CL, long
Slide 9: US Trial: Dose-dependent increase in PK exposure up to 40 mg MAD with no exposure plateau
US Trial: Dose-dependent increase in PK exposure up to 40 mg MAD with no exposure plateau observed; PAD defined based on steady-state exposures that exceeded target threshold • PK exposure increased with dose with low-to- moderate PK variability • Pharmacologically active dose (PAD) range: Ceff base
Slide 10: US Trial PD: Greater KRAS G12X ctDNA reduction at PAD doses
US Trial PD: Greater KRAS G12X ctDNA reduction at PAD doses (16-32 mg) vs. below PAD (2-8 mg) Change in solid tumor ctDNA KRAS G12X VAF from C1D1 to C3D1: Below PAD (2-8 mg) vs at PAD range (16-32 mg) 100% of patients (19/19) at PAD showed at least 75% reduction of KRAS G12X variant allele fraction,
Slide 11: Predicted sensitivity of Big 3 tumor types to pan-RAS inhibition
Predicted sensitivity of Big 3 tumor types to pan-RAS inhibition NSCLC PDAC CRC Relative anticipated sensitivity in the clinic to pan-RAS inhibition High Med Low Up to 50% of patients may exhibit Primary and adaptive resistance, often delayed RECIST responses Pan-RAS response dynamics Faster, deeper
Slide 12: CN Trial: Encouraging preliminary efficacy signal in 2L+ KRAS G12X NSCLC
CN Trial: Encouraging preliminary efficacy signal observed for ERAS-0015 in 2L+ KRAS G12X NSCLC Within pharmacologically active dose range 2L+ KRAS G12X 16 mg QD 24 mg QD1 ALL 2L+ KRAS G12X Post-ICI/platinum (2/3L) NSCLC (N=6) (N=21) (N=27) NSCLC KRAS G12X Dose 16-24 mg QD1 16-24 mg QD1 CR, n (%) 0
Slide 13: CN trial: Most patients with 2L+ KRAS G12X NSCLC remain on treatment
CN trial: Most patients with 2L+ KRAS G12X NSCLC remain on treatment suggesting potentially favorable safety and tolerability1 100% of responders – including all patients with uPRs – remain on treatment Reinforces the safety, 6 months tolerability and durability of response of ERAS-0015 DCO Feb 2026
Slide 14: US trial: Encouraging preliminary ERAS-0015 efficacy data in 2L+ KRAS G12X NSCLC
US trial: Encouraging preliminary ERAS-0015 efficacy data in patients with 2L+ KRAS G12X NSCLC consistent with data from CN trial Responses observed throughout the dose range indicate sensitivity of NSCLC to pan-RAS inhibition 60% uORR observed at the PAD 71% uORR observed in post-ICI/platinum (2/3L
Slide 15: US trial: Most patients with 2L+ KRAS G12X NSCLC remain on treatment
US trial: Most patients with 2L+ KRAS G12X NSCLC remain on treatment as of DCO 6 out of 7 responders—including all patients with uPRs—remain on treatment Reinforces the safety, tolerability 6 months and potential durability of response of ERAS-0015 DCO Apr2026; NSCLC=non-small-cell lung cancer; PD=p
Slide 16: ERAS-0015: Preliminary NSCLC data suggest differentiated preclinical properties could drive improved clinical activity
ERAS-0015: Preliminary NSCLC data suggest differentiated preclinical properties could potentially drive improved clinical activity, consistent with KRAS G12Ci precedent First-in-class molecules Potentially best-in-class molecules 37% 43% 59% Sotorasib ORR1 Adagrasib ORR2 KRAS G12Ci’s Divarasib ORR3
Slide 17: CN trial: Encouraging preliminary efficacy data for ERAS-0015 in 2L+ KRAS G12X PDAC
CN trial: Encouraging preliminary efficacy data for ERAS-0015 in 2L+ KRAS G12X PDAC Within pharmacologically active dose range (PAD) ERAS-0015 2 mg QD 16 mg QD 24 mg QD 32 mg QD ALL 2L+ KRAS ERAS-0015 (N=1) (N=11) (N=32) (N=10) (N=54) G12X PDAC1 CR, n (%) 0 0 0 0 0 2L+ KRAS 2L KRAS G12X PR, n (%) 0
Slide 18: CN trial: Most patients with 2L+ KRAS G12X PDAC remain on treatment
CN trial: Most patients with 2L+ KRAS G12X PDAC remain on treatment suggesting potentially favorable safety and tolerability1 84% (16/19) of responders – including all uPRs at 24-32 mg – remain on treatment Reinforces the safety, tolerability and durability of response of ERAS-0015 6 months DCO Feb
Slide 19: US trial: Encouraging preliminary ERAS-0015 efficacy data in 2L+ KRAS G12X PDAC
US trial: Encouraging preliminary ERAS-0015 efficacy data in patients with 2L+ KRAS G12X PDAC, including 57% uORR at 32 mg ERAS-0015 2L+ 8 mg QD 16 mg QD 24 mg QD 32 mg QD 40 mg QD KRAS G12X N=9 N=8 N=8 N=7 N=2 PDAC1 Of the patients treated at uORR1 , n (%) 1 (11) 0 2 (25) 4 (57) 1 (50) RDEs of 24 m
Slide 20: US trial: Time on treatment for patients with 2L+ KRAS G12X PDAC
US trial: Time on treatment for patients with 2L+ KRAS G12X PDAC All patients with either confirmed or unconfirmed responses remain on treatment 6 months At RDE of 32 mg QD, 6 of 7 enrolled patients remained on treatment; at RDE of 24 mg QD, 6 of 8 enrolled patients remained on treatment DCO 25May20
Slide 21: US trial: ERAS-0015 shows promising clinical potential to combine with SOC in CRC
US trial: ERAS-0015 shows promising clinical potential to combine with SOC in CRC ERAS-0015 + panitumumab1 Initiated ERAS-0015 (at 16 mg QD) plus 24 mg ERAS-0015 plus panitumumab (at anti-EGFR mAb (at approved dose) approved dose) combo cohort enrolling combo cohort in Q1 2026 No DLTs observed in th
Slide 22: US trial: ERAS-0015 was generally well-tolerated with mostly low-grade TRAEs
US trial: ERAS-0015 was generally well-tolerated with mostly low-grade TRAEs and no discontinuations Summary of TRAEs occurring in ≥10% of patients Patients with RASm NSCLC and PDAC Treated at PAD (16-32mg) ERAS-0015 (N=72) TRAEs, n (%) Grade 1 Grade 2 Grade 31 Grade 4 All Grades Rash2, n (%) 37 (51
Slide 23: US trial: ERAS-0015 was generally well-tolerated with mostly low-grade TRAEs and no discontinuations
US trial: ERAS-0015 was generally well-tolerated with mostly low-grade TRAEs and no discontinuations Summary of TRAEs occurring in ≥10% of patients Patients with RASm NSCLC and PDAC Treated at PAD (16-32mg) ERAS-0015 (N=72) 16 mg QD 24 mg QD 32 mg QD 16-32 mg TRAEs, n (%) (N=16) (N=28) (N=28) (N=72)
Slide 24: US trial: Relative Dose Intensity supports tolerability of doses across the PAD
US trial: Relative Dose Intensity supports tolerability of doses across the PAD Relative Dose Intensity (RDI) Patients with RASm NSCLC and PDAC Treated at PAD (16-32mg) ERAS-0015 (N=72) 16 mg QD 24 mg QD 32 mg QD 16-32 mg QD (N=16) (N=28) (N=28) (N=72) RDI of ERAS-0015 (%) n1 16 27 27 70 Mean (SD) 1
Slide 25: Valuable investigator insights on safety and tolerability
Valuable investigator insights on safety and tolerability • Close engagement with ERAS-0015 investigators helps optimize our development approach • To date, feedback on ERAS-0015 has been highly encouraging:1 “There’s Grade 2 rash that's tolerable and intolerable. I get the sense at least from my pa
Slide 26: Emerging efficacy differentiation from Ph 1 clinical data
Emerging efficacy differentiation from Ph 1 clinical data strengthens rationale for potential registration-enabling trials in PDAC and NSCLC PDAC NSCLC ERAS-0015 Apr 2026 25 May 2026 Dose N uORR N uORR 24 mg (2L+) 7 14% 8 25% ERAS-0015 32 mg (2L+) 4 50% 7 57% ~40-57% Apr 2026 75% 40 mg (2L+) 2 0% 2
Slide 27: Emerging safety and tolerability differentiation from Ph 1 clinical data
Emerging safety and tolerability differentiation from Ph 1 clinical data strengthens rationale for potential registration-enabling trials in PDAC and NSCLC ERAS-0015 RMC-6236 Ph 1 16-32 mg Ph 1 16-32 mg Ph 1 ≥80mg Ph 1 160-300mg Ph 1 300mg Ph 1 All doses Ph 3 300 mg Apr 2026 25 May 2026 (ESMO 2023)1
Slide 28: ERAS-4001 selectively bound KRAS with high affinities, long residence times
ERAS-4001 selectively bound KRAS with high affinities, long residence times SPR-based kinetic biophysical binding characterization of ERAS-4001 Target KD (nM) t1/2 (s) KRAS G12D 0.0006 273,079 KRAS G12V 0.0069 30,159 KRAS G12C 0.016 7,724 KRAS WT 0.058 3,409 HRAS WT 117 18.1 NRAS WT 2,660 1.2 SPR =
Slide 29: ERAS-4001 showed potent activity against both GTP- and GDP-bound KRAS
ERAS-4001 showed potent activity against both GTP- and GDP-bound KRAS ERAS-4001 Assay Class Assay Target IC50 (nM) RBD KRAS G12D GDP 1.6 Biochemical Functional RAS-RAF Binding Assay (RBD) RBD KRAS G12D GMPPNP* 6.8 * GMPPNP is a nonhydrolyzable GTP analogue intended to approximate GTP-bound KRAS 29
Slide 30: ERAS-4001 potently and selectively inhibited cell growth in KRAS cell lines
ERAS-4001 potently and selectively inhibited cell growth in KRAS G12X, G13D and WT cell lines ERAS-4001 cell growth KRAS Mutation Tumor type Cell line inhibition (nM) Pancreatic AsPC-1 1.8 Pancreatic Panc 04.03 1.9 KRAS G12D Pancreatic HPAC 1.0 Pancreatic PK-59 2.6 Lung NCI-H727 3.5 Lung NCI-H441 0.
Slide 31: ERAS-4001 achieved tumor regression in a KRAS G12D PDAC CDX model
ERAS-4001 achieved tumor regression in a KRAS G12D PDAC CDX model at doses at or above 100 mg/kg BID KRAS G12D CDX Panc 04.03 TGI curves from 28 day repeat dose study TGI, PD (pERK) and PK (AUC0-last) Summary pERK AUC0-last TGI on Therapy Dose Inhibition Day 28 (nmol/L·h) at 8 hr 30 mg/kg 97% 17% 1,
Slide 32: ERAS-4001 achieved tumor regressions in sensitive KRAS G12D and G12V CDX models
ERAS-4001 achieved tumor regressions in sensitive KRAS G12D and G12V CDX models at doses as low as 30 mg/kg BID TGI in KRAS G12D PDAC CDX PK-59 TGI in KRAS G12V Ovarian CDX RKN • ERAS-4001 was well tolerated in both studies at doses up to 300 mg/kg BID (i.e., no dose reductions or holidays; no body
Slide 33: ERAS-4001 achieved tumor regression in a pan-KRASi insensitive KRAS G12V NSCLC CDX model
ERAS-4001 achieved tumor regression in a pan-KRASi insensitive KRAS G12V NSCLC CDX model TGI in KRAS G12V NCI-H727 % Body Weight Change TGI Summary Therapy Dose TGI on Day 21 10 mg/kg 3% 30 mg/kg 30% ERAS-4001 100 mg/kg 77% 300 mg/kg 101% • ERAS-4001 was well tolerated at doses ranging from 10 mg/kg
Slide 34: ERAS-4001 showed promising PK in mouse, rat, and dog
ERAS-4001 showed promising PK in mouse, rat, and dog PK Parameter Mouse Rat Dog Dose (mpk) 1.7 2 2.1 C0 (nM) 1,722 1,083 1,669 T1/2 (h) 1.9 3 5.8 IV Vd (L/kg) 5.16 10.1 14.1 CL (mL/kg/min) 45.5 70.9 53.1 AUC0-last (nM·h) 938 615 827 Dose (mpk) 30.3 30.9 15.3 Cmax (nM) 2,090 584 323 Tmax (h) 1.5 4 0.
Slide 35: Anticipated key milestones in 2026-2027
Anticipated key milestones in 2026-2027 Program Trial Name Anticipated Milestones Mechanism Indication • 1H27: - Monotherapy expansion data - Combination dose escalation data, including panitumumab combination ERAS-0015 AURORAS-1 to -3 - Initiate potentially registration-enabling trial in 2L+ NSCLC
Slide 36: Compelling investment thesis
Compelling investment thesis EXPERIENCED TEAM WITH TRACK RECORD OF SERIAL SUCCESSES Seasoned drug developers who have advanced multiple programs from discovery to IND to global approvals WORLD-CLASS SCIENTIFIC ADVISORY BOARD Includes leading pioneers in the RAS/MAPK pathway (Shokat, UCSF; Lito, MSKC
Slide 37: THANK YOU!
THANK YOU!
Slide 38: RAS targeting landscape drives importance of identifying development candidates
RAS targeting landscape drives importance of identifying development candidates with first-in-class or best-in-class potential Pan-RAS AN9025 GF-276 RO7673396 ERAS-0015 RMC-6236 KST-6051 AMG-410 JAB-23E73 ERAS-4001 Pan-KRAS PF-07934040 BBO-11818 (G12X) ALTA-3263 RG6620/GDC-7035 RNK08954 (G12D) LY396
Slide 39: ERAS-0015 early clinical differentiation vs. comparator pan-RAS molecular glue
ERAS-0015 early clinical differentiation vs. comparator pan-RAS molecular glue RMC-6236 benchmark ERAS-0015 Preliminary Phase 1 Data FPD to DCO3: 16 months FPD to DCO6: ~9.5 months (US) – 10.5 months (CN) Potential differentiation attributes Efficacy in Pts with PDAC and NSCLC Efficacy in Pts with P
Slide 40: ERAS-0015’s higher CYPA binding affinity may be a differentiator from RMC-6236
ERAS-0015’s higher CYPA binding affinity may be a differentiator from RMC-6236, demonstrating potential best-in-class profile Binding affinity Assay ERAS-0015 RMC-6236 difference: (nM) (nM) ERAS-0015/ RMC-6236 SPR KD 4.5 92 21x ITC KD 5.3 44.1 8x 8-21x higher binding affinity to cyclophilin A (CYPA)
Slide 41: ERAS-0015 demonstrated significantly more potent inhibition of cell growth vs. RMC-6236
ERAS-0015 demonstrated significantly more potent inhibition of cell growth across KRAS mutant cell lines vs. RMC-6236 ERAS-0015 cell growth RMC-6236 cell growth ERAS-0015:RMC-6236 Mutation Tumor type Cell line inhibition (nM) inhibition (nM) Fold Potency H358 (adagrasib- NSCLC 0.8 3.6 4.5x KRAS G12C
Slide 42: ERAS-0015 demonstrated comparable antitumor activity to RMC-6236 at lower doses
ERAS-0015 demonstrated comparable antitumor activity to RMC-6236 at 1/10th to 1/5th of the dose in multiple in vivo mouse models Dose achieving tumor regression1 Model KRAS Mutation Tumor Origin ERAS-0015 RMC-6236 PK-59: CDX G12D PDAC 0.3 mg/kg 3 mg/kg NCI-H727: CDX G12V NSCLC 1 mg/kg 10 mg/kg SW620
Slide 43: ERAS-0015 demonstrated preferential tumor distribution and longer residence time vs. RMC-6236
ERAS-0015 demonstrated preferential tumor distribution and longer residence time vs. RMC-6236 in vivo Tumor PK Distribution Assessment in the Tumor PK Distribution Assessment in the KRAS G12D PDAC CDX Model, PK-59 KRAS G12R PDAC CDX Model, PSN-1 ERAS-0015 RMC-6236 ERAS-0015 RMC-6236 PDAC: pancreatic
Slide 44: ERAS-0015 showed promising PK in mouse, rat, dog, and monkey
ERAS-0015 showed promising PK in mouse, rat, dog, and monkey Mouse Rat Dog Monkey ERAS-0015 RMC-6236 ERAS-0015 RMC-6236 ERAS-0015 RMC-6236 ERAS-0015 RMC-6236 Dose (mpk) 1 1 1 1 1 1 1 No Data T1/2 (h) 5.0 1.7 5.7 1.5 24.5 7.6 15.2 No Data IV Vdss (L/kg) 5.3 1.9 1.9 1.9 3.8 3.7 1.8 No Data CL (mL/kg/m
Slide 45: CN and US Trials: Similar trial designs support generalizability between them
CN and US Trials: Similar trial designs support generalizability between them China Trial (JYP0015M101) FPD to DCO ~10.5 months1 US Trial (AURORAS-1) FPD to DCO ~9.5 months2 Phase Ia: Dose Escalation3 Phase Ib: Dose Expansion Part 1: Dose Escalation3 Primary Endpoints: DLTs, Safety assessments Prima
Slide 46: CN and US Trials: Baseline characteristics (PDAC and NSCLC)
CN and US Trials: Baseline characteristics (PDAC and NSCLC) RASm PDAC RASm NSCLC1 PDAC KRAS G12X/G13X NSCLC3 CN Trial (JYP0015M101) US Trial (AURORAS-1)2 (2, 8, 16, 24, 32, 40 mg) (16, 24, 32 mg) (2, 4, 8, 16, 24, 32, 40 mg) (8, 16, 24, 32, 40 mg) N=78 N=42 N=42 N=22 Median Age (range) 64.5 years (3
Slide 47: Single-dose PK data between CN and US trials have been largely comparable
Single-dose PK data between CN and US trials have been largely comparable CN Trial (JYP0015M101)1 US Trial (AURORAS-1)2 1Data generated by Joyo Pharma 05Jan2026 2Data generated by Erasca 02April2026 Note: see Disclaimer slide regarding Cross-Study Comparisons 47
Slide 48: KRAS alterations found most commonly in CRC, PDAC and NSCLC
KRAS alterations found most commonly in CRC, PDAC and NSCLC Estimated number of patients affected by KRAS mutant tumors in the US (thousands) 74.3 G12C G12D G12V G12A G12R Other Multiple 55.0 50.1 16.1 12.7 9.9 8.2 4.5 0.4 CRC NSCLC PDAC Urinary Endometrial Other GI Unknown Other GU Other Primary Ad
Slide 49: Erasca believes that the claims in RVMD’s April 24, 2026 letter are without merit
Erasca believes that the claims in RVMD’s April 24, 2026 letter1 are without merit Claim 1: Patent Infringement Claim 2: Trade Secret Misappropriation by a under the Doctrine of Equivalents Third Party (not Erasca) Medshine2 is one of several companies that filed patent applications following the pu