Jong-Mu Sun

Jeong DY, et al. J Korean Med Sci. 2027 Mar;42:e63. https://doi.org/10.3346/jkms.2027.42.e63

Purpose: This study evaluated the feasibility and clinical utility of a mobile application-based electronic patient-reported outcome (ePRO) system for longitudinal symptom monitoring in patients with lung cancer receiving systemic therapy.Methods: We developed a mobile application-based ePRO platform for patients with lung cancer receiving chemotherapy and/or immunotherapy in South Korea. Twenty-one treatment- related symptoms were selected from regulatory drug labeling and mapped to Patient- Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE) items. Patients reported symptoms every 3 days or as needed, while clinicians reviewed the summarized data via a web-based interface. The adherence, usability, and concordance between patient- and clinician-reported adverse events (AEs) were assessed.Results: A total of 26 patients used the application, generating 570 symptom reports over a mean follow-up duration of 70.3±64.5 days. The mean adherence rate was 81.9%±21.5%. The most frequently reported symptoms were fatigue (67.7%), shortness of breath (60.1%), decreased appetite (59.9%), insomnia (57.6%), and pain (53.8%), with decreased appetite, fatigue, and shortness of breath being the most common grade ≥2 symptoms. Symptom patterns varied according to the treatment regimen and were consistent with known toxicity profiles. Clinician-documented AEs were primarily limited to laboratory abnormalities, whereas ePRO captured a broader range of subjective symptoms. Longitudinal analysis revealed sustained weekly reporting, regimen-specific temporal symptom trajectories, and higher symptom severity in unscheduled reports than in scheduled reports.Conclusion: Mobile application-based longitudinal ePRO monitoring was feasible, well accepted, and clinically informative for lung cancer care. These findings support further evaluation of mobile ePRO systems in routine practice.

Antitumor activity of JIN-A02 in PC9 cells-driven intracranial tumor models

Changes in EGFR-mutant ctDNA Levels Before and After JIN-A02 Administration in Patients with Stable Disease and Progressive Disease

The EGFR mutation status of patient-derived models using whole exome sequencing analysis

Cell viability curve for treatment of JIN-A02 in Ba/F3 cell lines and tumor cell lines with EGFR activating mutations and containing T790M mutation

Summary of Treatment Related AEs

Area under the curve quantification of TKI efficacy in C797S-negative EGFR-mutant cell lines.

Purpose:Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKI) have revolutionized the treatment of non–small cell lung cancer (NSCLC) with activating EGFR mutations. However, acquired resistance—particularly the EGFR C797S mutation—remains a major clinical challenge. As no approved targeted therapies are available following disease progression on the third-generation EGFR-TKI osimertinib, this study aimed to evaluate JIN-A02, a novel fourth-generation EGFR-TKI, as a therapeutic strategy to overcome C797S-mediated resistance.Experimental Design:JIN-A02, a fourth-generation EGFR TKI, was evaluated for its antitumor efficacy and blood–brain barrier penetration in in vitro and in vivo models of NSCLC harboring EGFR C797S and T790M mutations.Results:JIN-A02 demonstrated potent antiproliferative activity in preclinical NSCLC models harboring EGFR C797S and T790M mutations, with superior inhibition of EGFR signaling compared with osimertinib. In both subcutaneous and orthotopic intracranial xenograft models, JIN-A02 elicited substantial tumor regression, indicating robust in vivo efficacy. The agent was well tolerated throughout the treatment period without notable toxicity. In line with preclinical data, early clinical trial data showed signs of efficacy, including three patients showing partial response.Conclusions:These findings highlight JIN-A02 as a promising therapeutic strategy to overcome C797S- and T790M-mediated resistance in EGFR-mutant NSCLC, including intracranial disease, and support its further clinical development.