NANJING, China, July 9, 2026 /PRNewswire/ -- InxMed Co., Ltd ("InxMed"), a clinical-stage biotechnology company dedicated to developing innovative therapies targeting cancer treatment resistance and metastasis, today announced that the clinical results of ifebemtinib (IN10018), a highly selective focal adhesion kinase (FAK) inhibitor, in combination with garsorasib (D-1553), a potent KRAS^G12C inhibitor in first-line KRAS^G12C-mutant NSCLC, have been published online in The Lancet Respiratory Medicine.

The data were derived from a phase Ib/II trial evaluating the efficacy and safety of ifebemtinib plus garsorasib in KRAS^G12C-mutant solid tumors (NCT06166836/NCT05379946), where ifebemtinib plus garsorasib, as an all‑oral, chemotherapy‑free regimen, demonstrated impressive results in patients with first-line KRAS^G12C-mutant NSCLC.

Promising Antitumor Efficacy and Manageable Safety Profile

33 first-line NSCLC patients with KRAS^G12C-mutation were enrolled in the single-arm phase II cohort and received ifebemtinib (100mg once a day) and garsorasib (600mg twice a day) orally. By data cutoff on September 16, 2025 reported in this paper, the median follow-up duration was 21.5 months. Ifebemtinib in combination with garsorasib demonstrated a high response rate and durable responses in first-line KRAS^G12C-mutation NSCLC, increasing the possibility of a paradigm shift, which, if confirmed in currently ongoing phase 3 trial (NCT07174908), could substantially impact the current treatment options for this patient population.

Key findings published in this paper:

• High Response Rates: Of the 33 enrolled patients, 31 were evaluable. The cORR was 82% (27/33) across all enrolled patients and 87% (27/31) among evaluable patients. And tumor shrinkage was observed in all evaluable patients, even in the patient with best overall response of PD.
• Durable Responses: Among responders, the median Duration of Response (DOR) was Not Reached (NR) (95% CI: 15.2–NE), underscoring the potential of FAK inhibition to prevent or significantly delay treatment resistance.
• Prolonged survival benefit of PFS and overall survival (OS): The mPFS reached an extraordinary 22.3 months (95% CI: 9.6–NE), with 12-month and 18-month PFS rates standing at 67.9% and 58.2%, respectively. The median OS was 27.8 months (95% CI: 27.8–NE), which remained immature as most patients was censored before 27.8 months. The 12-month and 24-month OS rates were 75.8% and 69.7%, respectively.
• Manageable safety profile: All 33 patients experienced treatment-emergent adverse events (TEAE). Most of the TEAE were grade 1 or 2; grade 3 or 4 events occurred in 11 (33%) of 33 patients, of which eight (24%) were related to study drugs. No treatment-related death or treatment-related AEs leading to drug discontinuation were reported.

"The publication of our long-term follow-up data in The Lancet Respiratory Medicine serves as a momentous validation of our translational science," said Dr. Zaiqi Wang, Chairman and Chief Executive Officer of InxMed. "By pairing KRAS^G12C inhibitor with our FAK inhibitor ifebemtinib, we have succeeded in blocking this adaptively resistant pathway. An ORR of 82% and a median PFS of over 22 months in the first-line setting represents a paradigm shift, offering these patients a highly potent, completely chemotherapy-free and all-oral option."

Overcoming Resistance by FAK Inhibition When Targeting KRAS^G12C

KRAS^G12C mutations occur in roughly 12-14% of NSCLC cases. Currently there were six KRAS^G12C inhibitors approved in previously-treated KRAS^G12C-mutant NSCLC, including sotorasib and adagrasib (approved in the USA and Europe) and fulzerasib, garsorasib, glecirasib and sosimerasib (approved in China). However, no KRAS^G12C inhibitors monotherapy or combination regimens were approved in first-line settings partially due to primary or acquired resistance when targeting KRAS^G12C alone. InxMed's translational research showed that KRAS^G12C inhibition alone triggers adaptive hyperactivation of the FAK‑YAP signaling pathway, promotes fibrogenesis in the tumor microenvironment, and thereby enhances tumor cell survival. And FAK inhibition by Ifebemtinib disrupts this resistance mechanism, sensitizing tumor cells to KRAS^G12C inhibition and prolonging the duration of treatment response.

Based on these promising clinical data, ifebemtinib has been granted Breakthrough Therapy Designation (BTD) in first-line NSCLC harboring KRAS^G12C mutation from the China National Medical Products Administration (NMPA). InxMed is progressing its clinical development plan, including an ongoing randomized Phase III confirmatory trial (NCT07174908) intended to support the adoption of this all‑oral, chemotherapy-free regimen as a new standard of care in the front‑line setting.

Based on a robust translational medicine foundation and compelling clinical evidence, Ifebemtinib is poised to become a revolutionary therapeutic that could fundamentally reshape the RAS-targeted treatment paradigm. InxMed is strategically driving a comprehensive development program for Ifebemtinib across RAS-mutant tumors, with combination regimens already initiated or in preparation not only with KRAS G12C inhibitors, but also with KRAS^G12D inhibitors and multi‑RAS inhibitors, among other novel classes, underscoring the company's commitment to transforming the future of RAS-addicted cancers.

About Ifebemtinib (IN10018)

Ifebemtinib (IN10018) is an orally available, highly potent, and selective small-molecule inhibitor of focal adhesion kinase (FAK). InxMed holds exclusive global development and commercialization rights. Clinically, ifebemtinib has demonstrated excellent safety and tolerability in over 700 subjects globally, showing vast potential as a "backbone" combination partner across multiple modalities, including RAS inhibitors, immune checkpoint blockades, and antibody-drug conjugates (ADCs). It has received multiple Breakthrough Therapy Designations from the NMPA and Fast Track Designation from the U.S. FDA.

About InxMed

Founded in 2017, InxMed is a late clinical-stage biotechnology company dedicated to tackling a central challenge in cancer therapy—drug resistance caused by tumor defense mechanisms. Our strategy focuses on critical signaling hubs shared across multiple tumor types, most notably the focal adhesion kinase (FAK) and integrin pathways, which play pivotal roles in tumor cell survival and contribute to treatment failure across various therapeutic modalities. In parallel, we target cancer-associated fibroblasts (CAFs) to dismantle the protective barrier around tumor cells. Through these integrated efforts, we aim to redefine cancer treatment and pioneer new frontiers in therapeutic innovation.  For more information, please visit en.inxmed.com.