Erasca, Inc. · NASDAQ:ERAS
Erasca — Investor Presentation (January 2026)
31 slides from Erasca's investor presentation, Jan 12, 2026
Slide 1: On a Journey to Erase Cancer: Erasca Corporate Presentation
On a Journey to Erase Cancer Erasca Corporate Presentation January 2026 Eric and his wife Margaret, inspiring our bold mission to erase cancer Exhibit 99.1
Slide 2: Forward-looking statements
We caution you that this presentation contains forward-looking statements. 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, research and development plan
Slide 3: Our name is our mission: to erase cancer
Our name is our mission: to erase cancer 1 Number of patients alive and free of cancer or free from cancer progression 2 yrs after starting an Erasca regimen, as measured by disease-free survival (adjuvant setting) and progression-free survival (metastatic setting) 2 Unaudited, as of September 30, 2
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 who pioneered development of approaches to inhibit KRAS G12C (RAS-GDP) and active states of RAS (RAS-GTP) Kevan Shokat, PhD Erasca Chair of R&D. World expert in structure-based drug design; former hea
Slide 5: Focused modality-agnostic RAS/MAPK pipeline
large molecule small molecule Focused modality-agnostic RAS/MAPK pipeline Note: Pipeline also includes naporafenib pan-RAF inhibitor for NRASm melanoma (for which we are exploring strategic alternatives, and have ceased the enrollment of new patients in the Phase 3 SEACRAFT-2 trial) 1 Licensor Joyo
Slide 6: Ideal RAS targeting molecules integrate three key attributes
Ideal RAS targeting molecules integrate three key attributes Proprietary Chemical Matter Preclinical Activity RAS Targeting Molecule Bolsters ability to maximize clinical and commercial value in highly competitive market Lower clinically active dose could translate to: Lower risk of solubility-limit
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 TPP: target product profile; OBA: oral bioavailability; IP: intellectual property; FIC: first-in-class; BIC: best-in-class; WT: wildtype; SMi: small molecule inhibitor; MG: molecular glue; 1 in vi
Slide 8: ERAS-0015 and ERAS-4001 exhibit competitive profiles that exceed our TPP
ERAS-0015 and ERAS-4001 exhibit competitive profiles that exceed our TPP Potential first-in-class and best-in-class Pan-KRAS inhibitor Designed to spare H/NRAS WT Wider therapeutic window predicted vs. pan-RAS MG for KRASm solid tumors Designed to address KRASwt activation to prevent resistance vs.
Slide 9: 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 SPR: surface plasmon resonance; KD: equilibrium dissociation constant; ITC: isothermal titration calorimetry 8-21x higher binding affinity to cyclophilin A (CYPA) may enable
Slide 10: ERAS-0015 cell growth inhibition vs RMC-6236 across cell lines
Mutation Tumor type Cell line ERAS-0015 cell growth inhibition (nM) RMC-6236 cell growth inhibition (nM) ERAS-0015:RMC-6236 Fold Potency KRAS G12C NSCLC H358 (adagrasib-resistant) 0.8 3.6 4.5x NSCLC LU99 1.4 5.4 3.9x KRAS G12D NSCLC A-427 13.3 59.2 4.5x CRC SW620 0.2 1.3 6.5x CRC GP2d 0.9 4.6 5.1x P
Slide 11: ERAS-0015 comparable antitumor activity to RMC-6236 at 1/10th dose in KRAS G12D model
ERAS-0015 demonstrated comparable antitumor activity to RMC-6236 at 1/10th of the dose in a sensitive KRAS G12D PDAC CDX model No dose reductions or holidays and no body weight loss for all doses of ERAS-0015 ERAS-0015 and RMC-6236 dosed orally once daily; CDX: cell line-derived xenograft; TGI: tumo
Slide 12: ERAS-0015 comparable antitumor activity at 1/10th dose in KRAS G12V NSCLC model
ERAS-0015 demonstrated comparable antitumor activity to RMC-6236 at 1/10th of the dose in an insensitive KRAS G12V NSCLC CDX model ERAS-0015 was well tolerated at all doses Therapy Dose TGI on Day 22 ERAS-0015 0.3 mg/kg 86% 1 mg/kg 104% 3 mg/kg 105% RMC-6236 1 mg/kg 64% 3 mg/kg 83% 10 mg/kg 104% TGI
Slide 13: ERAS-0015 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 PDAC: pancreatic ductal adenocarcinoma; CDX: cell-line derived xenograft Tumor PK Distribution Assessment in the KRAS G12D PDAC CDX Model, PK-59 Tumor PK Distribution Assessment in the KRAS G12R PDA
Slide 14: 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 IV 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 Vdss (L/kg) 5.3 1.9 1.9 1.9 3.8 3.7 1.8 No Data CL (mL/kg/m
Slide 15: AURORAS-1: First-in-human Phase 1/1b trial of ERAS-0015 in RASm solid tumors
AURORAS-1: First-in-human Phase 1/1b multicenter open-label trial of ERAS-0015 in RASm solid tumors PK: pharmacokinetics Advanced RASm solid tumors Received prior therapy No previous treatment with RAS inhibitor ERAS-0015 Single agent Oral once daily dosing Signs of clinical efficacy Well-behaved PK
Slide 16: ERAS-0015's differentiation potential: clinical responses first observed at 8 mg QD
ERAS-0015’s differentiation potential: Clinical responses first observed at 8 mg QD (1/10th of the dose observed with RMC-6236) coupled with promising safety and PK Preclinical Differentiation Comparable efficacy at 1/10th-1/5th of RMC-6236 dose in multiple mouse models In Vivo Activity PK Propertie
Slide 17: AURORAS-1 case study: confirmed partial response in KRAS G12V NSCLC
Baseline AURORAS-1 case study: Ongoing confirmed partial response in 70-year-old male with KRAS G12V NSCLC treated with ERAS-0015 (8 mg QD) 1 As of January 7, 2026 NSCLC: non-small cell lung cancer; QD: once daily Cycle 3 Diagnosis Stage IV NSCLC; KRAS G12V Prior Therapy Carboplatin/pemetrexed/pembr
Slide 18: ERAS-0015 and ERAS-4001 exhibit competitive profiles that exceed our TPP
ERAS-0015 and ERAS-4001 exhibit competitive profiles that exceed our TPP Potential first-in-class and best-in-class Pan-KRAS inhibitor Designed to spare H/NRAS WT Wider therapeutic window predicted vs. pan-RAS MG for KRASm solid tumors Designed to address KRASwt activation to prevent resistance vs.
Slide 19: ERAS-4001 selectively bound KRAS with high affinities, long residence times
ERAS-4001 selectively bound KRAS with high affinities, long residence times 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-based kinetic biophysical binding characterization of ERAS-4001 SPR =
Slide 20: ERAS-4001 showed potent activity against both GTP- and GDP-bound KRAS
ERAS-4001 showed potent activity against both GTP- and GDP-bound KRAS Assay Class Assay Target ERAS-4001 IC50 (nM) Biochemical Functional RAS-RAF Binding Assay (RBD) RBD KRAS G12D GDP 1.6 RBD KRAS G12D GMPPNP* 6.8 * GMPPNP is a nonhydrolyzable GTP analogue intended to approximate GTP-bound KRAS
Slide 21: 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 KRAS Mutation Tumor type Cell line ERAS-4001 cell growth inhibition (nM) KRAS G12D Pancreatic AsPC-1 1.8 Pancreatic Panc 04.03 1.9 Pancreatic HPAC 1.0 Pancreatic PK-59 2.6 KRAS G12V Lung NCI-H727 3.5 Lung N
Slide 22: ERAS-4001 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 ERAS-4001 was well tolerated at doses up to 300 mg/kg BID for 28 days (i.e., no dose reductions or holidays; no body weight loss or s
Slide 23: ERAS-4001 tumor regressions in 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 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 weight loss or significant health observations) TGI in KRAS G12D PD
Slide 24: ERAS-4001 tumor regression in a pan-KRASi insensitive KRAS G12V NSCLC model
ERAS-4001 achieved tumor regression in a pan-KRASi insensitive KRAS G12V NSCLC CDX model ERAS-4001 was well tolerated at doses ranging from 10 mg/kg p.o. BID to 100 mg/kg p.o. BID (i.e., no dose holidays or mortality) ERAS-4001 at 300 mg/kg p.o. BID showed borderline tolerability with 4 out of 6 mic
Slide 25: 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 IV Dose (mpk) 1.7 2 2.1 C0 (nM) 1,722 1,083 1,669 T1/2 (h) 1.9 3 5.8 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 Oral Dose (mpk) 30.3 30.9 15.3 Cmax (nM) 2,090 584 323 Tmax (h) 1.5
Slide 26: Anticipated key milestones in 2026-2027
Anticipated key milestones in 2026-2027 1 Data to include safety, pharmacokinetics (PK), and efficacy at relevant dose(s) in relevant population(s) of interest Program Mechanism Trial Name Indication Anticipated Milestone ERAS-0015 Pan-RAS molecular glue AURORAS-1 RASm solid tumors H1 2026: Ph 1 mon
Slide 27: 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 Clinical advancement of industry leading RAS-targeting franchise Potential best-in-class/first-in-class RAS progr
Slide 28: Thank you
ERASCA- eek ; SeBati=ay, “Mogg 3 THAN k YOU!
Slide 29: RAS targeting landscape drives importance of identifying FIC or BIC candidates
Note: Select coopetitors shown based on public disclosures; list is not intended to be exhaustive; updated as of January 2026 1 Mutant selective beyond KRAS G12C inhibitors RAS targeting landscape drives importance of identifying development candidates with first-in-class or best-in-class potential
Slide 30: 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 (in vitro and in vivo) Activity1 OBA2 IP3 TPP: target product profile; OBA: oral bioavailability; IP: intellectual property; FIC: first-in-class; BIC: best-in-class; WT: wildtype; SMi: small molecule inhibitor; MG:
Slide 31: 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) Adapted from Lee J., Sivakumar S., Schrock A., et al. “Comprehensive pan-cancer genomic landscape of KRAS altered cancers and real-world outcomes in solid tum