Aidixi (disitamab vedotin)

Adjuvant ADC+ICI showed comparable short-term OS and directionally favorable DFS/PFS trends versus GC, with a distinct toxicity profile. These findings are hypothesis-generating and require prospective validation.

First-line disitamab vedotin with tislelizumab and S-1 demonstrated remarkable antitumor activity and a manageable safety profile in HER2-overexpressing advanced G/GEJ adenocarcinoma, warranting validation in randomized controlled trials.

Recent advances in molecular profiling and the development of HER2-directed ADCs have fundamentally reshaped the therapeutic relevance of HER2 in UC, enabling activity even in tumors with heterogeneous or low expression of HER2. This comprehensive narrative review synthesizes current knowledge on HER2 biology in UC, addresses challenges in biomarker assessment, critically appraises the evolving clinical trial landscape of HER2-directed ADCs, explores the interaction between HER2 and other oncogenic alterations and discusses mechanisms of resistance with future directions for HER2-targeted strategies in UC.

Disitamab Vedotin achieved durable partial response (> 8 months PFS) in advanced HER2 2+/FISH- bladder cancer after first-line chemo-immunotherapy progression. This case provides real-world evidence that disitamab vedotin may benefit HER2 2+/FISH- patients, supporting broader HER2 testing and treatment consideration in this subset.

This case suggests that disitamab vedotin combined with toripalimab may have activity in selected patients with advanced urothelial carcinoma, including those with low HER2 expression. However, the findings should be interpreted cautiously, and further studies are needed to clarify the role of this regimen and the value of predictive biomarkers.

P3, N=412, Active, not recruiting, Seagen, a wholly owned subsidiary of Pfizer | Trial primary completion date: Jun 2026 --> Jan 2027

A cross-tumor perspective contrasts GC/GEJ testing and biology with the breast cancer paradigm and summarizes the importance of HER2-low expression in non-gastric malignancies. Finally, we discuss the therapeutic strategies in HER2-low GC/GEJ and highlight key safety and monitoring considerations for HER2-directed ADCs.

P2, N=30, Recruiting, Shanxi Province Cancer Hospital

DS-8201 demonstrates potential as one of the effective salvage therapies following RC48 failure in HER2 altered solid tumors, showing significantly better disease control and a distinct, manageable toxicity profile. These findings highlight the importance of selecting personalized ADCs based on molecular subtypes and toxicity factors and provide a basis for future, larger-scale prospective studies.

In the real-world setting, RC48 shows some clinical efficacy and a manageable safety profile in patients with HER2-expressing advanced gastric cancer. These findings provide useful information for clinical practice.

After initial treatment with transurethral resection of the bladder tumor (TURBT), the patient underwent regular bladder instillations of epirubicin...Due to the patient's renal impairment (baseline creatinine 107.8 µmol/L, glomerular filtration rate (GFR) 79.19 mL/min/1.73m2) and human epidermal growth factor receptor 2 (HER2) overexpression (2+), the decision was made to employ an antibody-drug conjugate (ADC) targeting HER2 (disitamab vedotin, 120 mg intravenously). The report outlines the patient's background, the progression of his disease, the decision-making process behind the use of ADC therapy, and the subsequent response to treatment. The successful control of the disease with ADC therapy in this complex patient population highlights its potential as an effective and less toxic alternative to conventional chemotherapy, particularly in patients with recurrent bladder cancer after renal transplantation.

Time-dependent ROC analysis showed an AUC of 76.3% at 2 years, and decision curve analysis suggested potential clinical utility. These findings indicate that miR-145 may serve as a candidate prognostic biomarker for risk stratification in RC48-treated la/mUC.