On April 27, 2026 Erasca, Inc. (Nasdaq: ERAS), a clinical-stage precision oncology company singularly focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers, reported positive preliminary Phase 1 dose escalation data for its potentially best-in-class, pan-RAS molecular glue ERAS-0015 in patients with RAS-mutant solid tumors.

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The preliminary data are from Erasca’s ongoing AURORAS-1 Phase 1 dose escalation trial in the U.S. and the ongoing JYP0015M101 Phase 1 dose escalation trial in China sponsored by Joyo Pharmatech Co., Ltd. (Joyo), both evaluating ERAS-0015 in patients with RAS-mutant solid tumors.

"We are thrilled with the robust efficacy results demonstrated so far by our pan-RAS inhibitor ERAS-0015 in patients with lung and pancreatic cancer," said Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder. "The magnitude of clinical benefit seen during dose escalation is particularly striking and compares favorably with other pan-RAS, pan-KRAS, or KRAS-mutant selective inhibitors. This efficacy is accompanied by generally well-tolerated safety results, primarily characterized by manageable, low-grade adverse events. Notably, preliminary data support ERAS-0015 may be combined with standard-of-care doses of panitumumab, positioning it as a potential backbone therapy for future combination regimens. Together, we believe these findings support the best-in-class potential of ERAS-0015, and we look forward to continued progress in our Phase 1 monotherapy dose expansion cohorts and combination dose escalation cohorts."

Highlights of Phase 1 Preliminary Results

Pharmacokinetics (PK):
Well-behaved PK, with dose-dependent increase in PK exposure up to the maximum administered dose (MAD) of 40 mg once daily (QD) and no exposure plateau observed
Pharmacologically active dose (PAD) range of 16-32 mg QD defined based on mean steady-state average exposures that exceeded target exposure threshold (based on the insensitive xenograft model)
Pharmacodynamics (PD):
Substantial reductions in KRAS G12X circulating tumor DNA (ctDNA) were observed at the PAD doses (16-32 mg QD), with 100% of patients (14/14) showing at least 75% reduction in KRAS G12X variant allele fraction, including 5 out of 14 patients showing 100% reduction
Efficacy: Robust monotherapy overall response rates (ORR) in patients with KRAS G12X non-small cell lung cancer (NSCLC) and with KRAS G12X pancreatic cancer (PDAC), in each case as of the relevant data cutoff (DCO)1,2:
NSCLC
At PADs of 16-32 mg QD, 62% uORR8wk (N=37) in second line or greater (2L+) KRAS G12X NSCLC, which exceeded comparator by 24 percentage points3,4
At PADs of 16-32 mg QD, 75% uORR8wk (N=16) in post-ICI/platinum (2/3L) KRAS G12X NSCLC, which exceeded comparator by 37 percentage points3,4
At recommended doses for expansion (RDEs) of 24-32 mg QD, 64% uORR8wk (N=25) in 2L+ KRAS G12X NSCLC3
PDAC
At PADs of 16-32 mg QD, 40% uORR14wk (N=20) in 2L KRAS G12X PDAC, which exceeded comparator by 11 percentage points5,6
At RDEs of 24-32 mg QD, 42% uORR14wk (N=12) in 2L KRAS G12X PDAC, which exceeded comparator by 13 percentage points5,6
At RDE of 32 mg QD, 50% uORR14wk (N=2) in 2L KRAS G12X PDAC, which exceeded comparator by 15 percentage points5,7
Multiple ongoing responses: Nearly all responding patients—including all unconfirmed responders—remain on treatment as of the DCO:
NSCLC
23 out of 24 responding patients remain on treatment, including all responders treated at 24-32 mg QD RDEs
PDAC
20 out of 23 responding patients remain on treatment, including all responders treated at 24-32 mg QD RDEs
Safety and Tolerability: Generally well-tolerated with mostly low-grade adverse events (AEs), no dose-limiting toxicities (DLTs), low rate of dose interruptions or reductions due to treatment-related adverse events (TRAEs), and no discontinuations due to TRAEs
Monotherapy RDE: Based on the totality of the preliminary Phase 1 dose escalation data, 24 mg and 32 mg QD were selected as the go-forward monotherapy RDEs
Combinability: ERAS-0015 showed promising clinical potential to combine with panitumumab (anti-EGFR monoclonal antibody)
No DLTs observed through the 31Mar2026 DCO (N=3) with 1 unconfirmed partial response (uPR) in 1 efficacy-evaluable patient with metastatic colorectal cancer (CRC)
1 AURORAS-1 data cutoff (DCO) 4Apr2026; JYP0015M101 data cutoff (DCO) 27Feb2026
2 Pooled data from the Company’s Phase 1 trial (US trial, or AURORAS-1) and Joyo’s Phase 1 trial (China (CN) trial, or JYP0015M101) of ERAS-0015
3 The uORR8wk is the ORR (confirmed and unconfirmed responses) for patients who received first dose of ERAS-0015 at least 8 weeks prior to data cutoff date (US trial) or at least one post-dose tumor assessment (CN trial)
4 Comparator as used in this press release, RMC-6236. Punekar et al. Journal of Thoracic Oncology 2025; data cutoff (DCO) 30Sep2024
5 The uORR14wk is the ORR (confirmed and unconfirmed responses) for patients who received first dose of ERAS-0015 (US, CN) at least 14 weeks prior to data cutoff date
6 Wolpin et al. EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) (ENA) 2024; DCO 23Jul2024
7 Revolution Medicines Press Release (10Sep2025); data cutoff (DCO) 30Jun2025

Key Upcoming and Completed Milestones
The Company initiated ERAS-0015 monotherapy expansion and combination dose escalation cohorts in the US (in Q2 2026 and Q1 2026, respectively), both ahead of previous guidance.

Upcoming milestones include:

AURORAS-1: Phase 1 trial for ERAS-0015 (pan-RAS molecular glue) in patients with RAS-mutant solid tumors
Monotherapy expansion data and combination dose escalation data narrowed to an expected date of H1 2027
BOREALIS-1: Phase 1 trial for ERAS-4001 (pan-KRAS inhibitor) in patients with KRAS-mutant solid tumors
Preliminary Phase 1 monotherapy data expected in the second half of 2026
Initiation of monotherapy expansion cohorts and combination dose escalation cohorts planned for 2027
Conference Call and Webcast Information
Erasca will hold a conference call and webcast Monday, April 27, 2026, at 4:30 pm ET. The webcast link for the conference call is here. The dial-in number is 1-877-407-3982 (U.S./Canada) or 1-201-493-6780 (international) or click the Call me Link. The live webcast and replay may be accessed by visiting Erasca’s website at Erasca.com/events.

About ERAS-0015
ERAS-0015 is an investigational, oral, highly potent pan-RAS molecular glue designed to inhibit RAS signaling with a potential best-in-class profile. Erasca is evaluating ERAS-0015 in the AURORAS-1 Phase 1 trial in patients with RAS-mutant solid tumors. Early dose escalation data in AURORAS-1 demonstrated favorable safety and tolerability results, well-behaved, linear PK, and confirmed and unconfirmed partial responses in multiple patients across multiple tumor types with different RAS mutations, including confirmed and unconfirmed partial responses at doses as low as 8 mg once daily (QD). ERAS-0015 is also designed to prevent resistance against mutant-selective inhibitors through inhibition of RAS wildtype variants. In addition, ERAS-0015 has demonstrated favorable absorption, distribution, metabolism, and excretion (ADME) and pharmacokinetic (PK) properties in multiple animal species.

About ERAS-4001
ERAS-4001 is an investigational, oral, highly potent, and selective pan-KRAS inhibitor with a potential first-in-class and best-in-class profile. Erasca is evaluating ERAS-4001 in the BOREALIS-1 Phase 1 trial in patients with KRAS-mutant solid tumors. ERAS-4001 demonstrated favorable preclinical in vitro potency against KRAS G12X mutations as well as KRAS wildtype amplifications, which may limit treatment resistance mediated through KRAS wildtype activation. No activity was observed for ERAS-4001 against HRAS or NRAS wildtype proteins in preclinical studies, which may enable a better therapeutic window compared to pan-RAS inhibitors. ERAS-4001 showed potent activity against both GTP-bound (active state) and GDP-bound (inactive state) KRAS with single digit nanomolar IC50s. In vivo, ERAS-4001 induced tumor regression in multiple KRAS-mutant models. In preclinical studies, ERAS-4001 showed encouraging ADME and PK properties.

(Press release, Erasca, APR 27, 2026, View Source [SID1234664825])