Erasca is a clinical-stage precision oncology company focused on targeting the RAS/MAPK pathway, which is one of the most commonly mutated pathways in cancer, affecting approximately 5.5 million individuals globally each year. The company has developed a robust, modality-agnostic pipeline that includes various therapeutic programs aimed at shutting down this pathway. Their approach encompasses three main strategies: targeting key upstream and downstream signaling nodes, directly inhibiting RAS, and addressing escape routes that cancer cells may utilize to resist treatment. This comprehensive strategy allows Erasca to explore both single-agent and combination therapies, with the goal of improving survival rates for patients with high unmet medical needs across a range of cancers.

Erasca's lead product candidate, naporafenib, is a pan-RAF inhibitor that has shown promise in clinical trials for treating RAS/MAPK-driven solid tumors, including NRAS-mutant melanoma. Additionally, the company is advancing other innovative programs such as ERAS-0015, a pan-RAS inhibitor, and ERAS-4001, a pan-KRAS inhibitor, which are designed to selectively target oncogenic RAS alterations. Other notable candidates include ERAS-007, an ERK1/2 inhibitor, and ERAS-601, a SHP2 inhibitor, both of which are being evaluated for their potential to enhance treatment efficacy in various tumor types. Through these efforts, Erasca aims to deliver transformative therapies to patients suffering from cancers with limited treatment options.

United States

Our mission at Erasca is embedded in our name: To erase cancer.

Energized by recent scientific discoveries and advances in drugging various biological drivers of cancer, we are committed to solving oncology’s hardest problems. We have assembled a proven team and joined forces with world-class collaborators who embrace our ambitious goals.

In addition to our initial programs for undisclosed cancer targets, we seek to expand our pipeline through partnerships with academic scientists and biopharmaceutical companies who have revealed potential new mechanisms for precision oncology. Importantly, Erasca isn’t tied to one form of drug or any singular approach to treating cancer. By keeping an open mind about what is possible, we believe we will achieve the greatest results for patients everywhere.

Cancer

Erasca 

Advanced malignancies

BRAFm Colorectal Cancer

Colorectal cancer

Gastrointestinal stromal tumors

<p class="font_7">ERAS-007 &nbsp;is the most potent ERK inhibitor in development and has the longest &nbsp;target residence time among ERK inhibitors that we are aware of. &nbsp;ERAS-007 has been evaluated as a single agent in a Phase 1 trial in &nbsp;patients with advanced solid tumors. Multiple objective responses were &nbsp;observed in patients with various tumor types, all of which harbor &nbsp;alterations (BRAF, HRAS, and NRAS) in the RAS/MAPK pathway, including &nbsp;melanoma, salivary gland cancer, NSCLC, and thyroid cancer. The adverse &nbsp;event profle was reversible, manageable, and consistent with ERK &nbsp;inhibition. These findings support the development of ERAS-007 as a &nbsp;monotherapy or in combination in diverse, biomarker-selected tumor &nbsp;types. We are pursuing a broad clinical development plan for ERAS-007 &nbsp;across multiple tumor types that includes both monotherapy and &nbsp;combinations with approved and investigational agents, such as RTK, &nbsp;SHP2, RAS, and/or RAF inhibitors. The first series of trials will be &nbsp;four proof-of-concept studies in solid tumors, NSCLC, CRC, and AML. &nbsp;While providing proof-of-concept data, these trials may be expanded to &nbsp;enable potential accelerated approvals in their respective indications.</p>

ERAS-007 w/ encorafenib and cetuximab

RAS Q61X solid tumors

Solid tumor/s

<h3 class="font_3"><strong>Naporafenib (pan-RAF inhibitor)</strong></h3>

Naporafenib w/ Trametinib 

ERAS-0015

ERAS-4001

Glioblastoma

<p class="font_7">ERAS-801: OUR CNS-PENETRANT EGFR INHIBITOR. EGFR-mediated signaling plays a key role in the growth of many tumor types. Targeting of wildtype EGFR (wtEGFR) and mutant variants of EGFR (EGFRm) by small molecules and antibodies has resulted in improved patient outcomes in NSCLC, CRC, and HNSCC. However, the ability of these agents to effectively target wtEGFR and EGFRm in the CNS remains an unmet medical need. The lack of clinical activity is likely multifactorial, but we believe there are two primary reasons why approved EGFR inhibitors are not effective: (1) the molecules do not penetrate the CNS well, and (2) the molecules are weak inhibitors of the EGFRvIII mutant protein as homodimers or heterodimers that include wildtype EGFR. ERAS-801 is designed to be a potent, selective, reversible, and orally available small molecule with both: (1) highly enhanced CNS penetration (3.7:1 brain:plasma ratio in mice) and (2) the ability to target both EGFR alterations such as EGFRvIII, the most common mutant form of EGFR found in GBM, and wtEGFR, which heterodimerizes with EGFRvIII.</p>

ERAS-801/EGFR inhibitor

Head and neck squamous cell carcinoma

<h3 class="font_3">ERAS-601 is a potent, selective oral inhibitor of SHP2, a convergent node for upstream RTK signaling and a critical “on/off switch” that activates GTP-bound RAS signaling. SHP2 also drives tumor cell proliferation and development of resistance. Our SHP2 inhibitor is designed to block oncogenic signal transduction and delay the onset of resistance—thereby potentially serving as a backbone of combination therapy..</h3>

ERAS-601 (SHP2 inhibitor) 

ERAS-007 + ERAS-601

Non-small cell lung carcinoma

<p class="font_8">ERAS-007 &nbsp;is the most potent ERK inhibitor in development and has the longest &nbsp;target residence time among ERK inhibitors that we are aware of. &nbsp;ERAS-007 has been evaluated as a single agent in a Phase 1 trial in &nbsp;patients with advanced solid tumors. Multiple objective responses were &nbsp;observed in patients with various tumor types, all of which harbor &nbsp;alterations (BRAF, HRAS, and NRAS) in the RAS/MAPK pathway, including &nbsp;melanoma, salivary gland cancer, NSCLC, and thyroid cancer. The adverse &nbsp;event profle was reversible, manageable, and consistent with ERK &nbsp;inhibition. These findings support the development of ERAS-007 as a &nbsp;monotherapy or in combination in diverse, biomarker-selected tumor &nbsp;types. We are pursuing a broad clinical development plan for ERAS-007 &nbsp;across multiple tumor types that includes both monotherapy and &nbsp;combinations with approved and investigational agents, such as RTK, &nbsp;SHP2, RAS, and/or RAF inhibitors. The first series of trials will be &nbsp;four proof-of-concept studies in solid tumors, NSCLC, CRC, and AML. &nbsp;While providing proof-of-concept data, these trials may be expanded to &nbsp;enable potential accelerated approvals in their respective indications.</p>

Erasca

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