Racura Oncology has received approval to escalate the dosage of its drug RC220 in the HARNESS-1 trial, aimed at treating EGFR-mutant lung cancer, marking a significant step in cancer research.

Therapeutic strategies after progression on third-generation EGFR tyrosine kinase inhibitors (EGFR-TKIs) remain suboptimal in EGFR-mutant non-small cell lung cancer (NSCLC). We investigated whether co...

Read the full paper: Targeting ABCA3 impedes tumor progression and EGFR-TKI resistance in EGFR-mutant LUAD

ArriVent’s Firmonertinib Fails in First-Line EGFR-Mutant NSCLC Trial

Phase II study shows promise in setting of third-generation EGFR TKI resistance

Firmonertinib did not significantly improve BICR-assessed PFS vs platinum/pemetrexed chemotherapy in first-line EGFR exon 20–mutant NSCLC in FURVENT trial.

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This study shows that osimertinib reduces brain metastasis risk differences seen between two common EGFR lung cancer mutation subtypes.

Early cranial stereotactic radiotherapy (SRT) administered with first-line osimertinib was associated with improved intracranial control and survival outcomes in patients with EGFR-mutant non-small cell lung cancer (NSCLC) and limited brain metastases, according to research presented at the International Association for the Study of Lung Cancer (IASLC) 2026 World Conference on Lung Cancer (WCLC).

Dr. Doroshow transitions to MET-directed resistance and invites Dr. Patel to lead. He describes MET amplification or overexpression as a resistance pathway in roughly 15% of EGFR-mutated metastatic non-small cell lung cancer (NSCLC) patients. Amivantamab-based regimens, which target both EGFR and MET, may reduce MET-driven resistance though not eliminate it. Testing must distinguish DNA-level events (MET amplification, by copy number) from protein-level overexpression (by immunohistochemistry [IHC]). Telisotuzumab vedotin (Teliso-V), a MET-directed antibody-drug conjugate (ADC) with a monomethyl auristatin E (MMAE) payload, is an option for 3+ MET protein overexpression in more than 25% of cells. For genomic MET amplification, small molecule combinations — savolitinib (a CNS-penetrant third-generation MET inhibitor with peripheral edema and hepatotoxicity), capmatinib, or tepotinib paired with osimertinib or lazertinib — are standard.

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Read the full paper: Mesenchymal stem cell-induced metabolic reprogramming of EGFR-wild-type tumor cells drives therapeutic resistance in EGFR-mutant non-small cell lung cancer

A new preclinical study has demonstrated that combining HER3-DXd with olaparib significantly improves treatment responses in lung cancer models.

BlossomHill Therapeutics (Nasdaq: BLSM) announced that the U.S. FDA has granted Fast Track designation to BH-30643 for treating adult patients with advanced or metastatic EGFR C797S-positive non-small cell lung cancer (NSCLC) after prior third-generation EGFR TKI therapy. BH-30643, a novel, orally bioavailable, non-covalent, macrocyclic, brain-active, mutant-selective OMNI-EGFR inhibitor, is being studied in SOLARA, a global Phase 1/2 first-in-human trial at more than 40 sites in 10 countries, including C797S resistance cohorts in TKI-pretreated and TKI-naïve settings.According to BlossomHill Therapeutics, Fast Track status enables more frequent FDA interactions and potential eligibility for rolling review, Accelerated Approval, and Priority Review if criteria are met. The company’s pipeline also includes BH-30236 for R/R AML or HR-MDS and BH-501284, a preclinical pan-KRAS Switch II inhibitor.

Creixell et al. map the early signaling networks triggered by AXL during EGFR inhibition in lung cancer cells. They reveal that AXL activates FAK1, SFK/Abl1, and downstream YAP to promote cell survival and migration. Co-inhibition of these pathways eliminates drug-tolerant persister cells.

Topline global pivotal Phase 3 data for firmonertinib in first-line EGFR exon 20 insertion mutant NSCLC expected 2H 2026 ARR-217, a CDH17 targeted ADC for gastrointestinal malignancies, advanced to Phase 1b dose optimization Dosing of first patient with ARR-002, a dual-targeting MUC16/NaPi2b