SEOUL, South Korea, Feb. 12, 2026 — J INTS BIO, Inc. has announced the publication of research on its investigational fourth-generation EGFR tyrosine kinase inhibitor (TKI), JIN-A02, in the prominent oncology journal Clinical Cancer Research. The journal, published by the American Association for Cancer Research (AACR), holds an Impact Factor of 10.2 as per the latest Journal Citation Reports (2025), underscoring its significance in translational and clinical cancer research.

The research details a therapeutic strategy aimed at overcoming the EGFR C797S mutation, a key resistance mechanism that often develops after treatment with the third-generation EGFR inhibitor Tagrisso. By combining extensive preclinical data with initial clinical evidence, the study proposes a potential new treatment pathway for EGFR-mutant non-small cell lung cancer (NSCLC) patients with few options following Tagrisso failure.

EGFR-mutant NSCLC is fueled by abnormal EGFR signaling. Although EGFR-targeted therapies have significantly enhanced patient outcomes in the last ten years, acquired resistance eventually occurs in nearly all patients. The C797S mutation is a primary resistance mechanism that renders current third-generation EGFR therapies ineffective, and no approved treatments specifically target it. JIN-A02 is an oral, fourth-generation EGFR inhibitor designed to selectively attack resistance mutations like C797S and T790M while sparing the wild-type EGFR. In preclinical models using tumor samples from patients with Tagrisso-resistant, EGFR E19del/T790M/C797S mutant NSCLC, JIN-A02 showed strong antitumor effects. It achieved a maximum tumor growth inhibition (TGI) of 168.2%, far surpassing Tagrisso’s effect under identical conditions and signifying actual tumor shrinkage, not just stalled growth.

Analyses of tumor tissue revealed substantial decreases in phosphorylated EGFR (p-EGFR) and the proliferation marker Ki-67 after JIN-A02 treatment, verifying successful blockade of EGFR-driven signaling pathways. In models of brain metastases, JIN-A02 led to swift and durable decreases in tumor burden, indicating its potential to cross the blood-brain barrier (BBB) at therapeutic levels.

The publication also includes early results from an ongoing Phase 1/2 clinical trial (NCT05394831) involving EGFR-mutant NSCLC patients who had progressed on prior EGFR therapies and chemotherapy. At the data cutoff, 23 patients had received JIN-A02, with several showing partial responses or stable disease. One patient in the 300 mg group achieved a partial response, with a 39.7% reduction in lung lesion size by the start of the third treatment cycle. This response continued through the seventh cycle, with a maximum reduction of 44.9%. Furthermore, this patient’s brain metastases shrank by 25% by the fifth cycle, and the benefit was maintained through the seventh cycle.

For this patient, blood-based circulating tumor DNA (ctDNA) analysis indicated the complete elimination of the EGFR C797S mutation and the exon 19 deletion, plus a reduction exceeding 90% in the T790M mutation. These results suggest that JIN-A02’s molecular target inhibition successfully produced a tangible clinical benefit.

Professor Sun Min Lim from the Division of Medical Oncology at Severance Hospital, the study’s corresponding author, commented, “JIN-A02 has shown promising preclinical activity and early clinical signs of efficacy against C797S-mediated resistance, an area with very limited options after third-generation EGFR therapy fails. The activity seen in brain metastases, coupled with the reduction of EGFR mutations in plasma ctDNA, offers crucial validation for advancing its clinical development.”

J INTS BIO intends to speed up the clinical development of JIN-A02, concentrating on optimizing the dose, gathering more data from patients with brain metastases, and confirming molecular biomarkers of response. The ultimate objective is to provide a new therapeutic choice for EGFR-mutant NSCLC patients who have run out of standard treatment options.

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