Ivesa (firmonertinib)

P=N/A, N=42, Not yet recruiting, Guangzhou University of Traditional Chinese Medicine

Firmonertinib plus anlotinib demonstrated preliminary efficacy and manageable safety as first-line treatment among patients with NSCLC harboring EGFR mutations.

P2, N=15, Not yet recruiting, Hunan Cancer Hospital

The EGFR p.V774M/p.The S768I mutation contributed to improving the efficiency of furmonertinib-based therapy for NSCLC.

P2, N=30, Recruiting, Tianjin Medical University Cancer Institute and Hospital

P2, N=28, Not yet recruiting, Peking University Cancer Hospital & Institute

Despite initial responses to first-line firmonertinib-based combination therapy, progression-free survival (PFS) 13 months, the patient developed sequential resistance to subsequent regimens, including liver/brain metastases and treatment-related toxicities. After fourth-line therapy failure and severe intolerance to albumin-bound paclitaxel and bevacizumab, two cycles of ivonescimab-a first-in-class programmed cell death protein receptor-1 (PD-1)/vascular endothelial growth factor-A (VEGF-A) bispecific antibody-induced significant regression of pulmonary target lesions (PR), sustained over six cycles with minimal toxicity...While the rapid PR and favorable safety profile are promising, longer follow-up is required to assess durability and survival benefits. These findings underscore the need for further investigation of bispecific antibodies in precision oncology paradigms for multi-refractory EGFR-driven NSCLC.

Case 1 received osimertinib combined with savolitinib, had 33 months of follow-up, and achieved a partial response. Case 2 received furmonertinib and achieved a complete response. NTRK2 fusion coexisting with EGFR mutations is a rare molecular characteristic of non-small cell lung cancer, accompanied by positive PD-L1 expression, and may serve as a promising biomarker for targeted therapy.

Our integrative single-cell analysis reveals that Furmonertinib therapy induces significant cellular and molecular changes in EGFR-positive LUAD, including TME remodeling, transcriptomic adaptation, and reprogramming of intercellular communication networks. These findings provide insight into the mechanisms of Furmonertinib response and resistance, and may inform strategies to optimize EGFR-TKI therapy.

P=N/A, N=300, Completed, Beijing Tiantan Hospital

P1, N=30, Active, not recruiting, Allist Pharmaceuticals, Inc. | Trial completion date: Aug 2025 --> Feb 2026

P1/2, N=300, Recruiting, Minghui Pharmaceutical (Hangzhou) Ltd