On August 3, 2026 Amplia Therapeutics Limited (ASX:ATX; OTCQB:INNMF), ("Amplia" or the "Company"), reported that it has entered into a Clinical Trial Collaboration and Supply Agreement ("CTCSA") with Eli Lilly & Company ("Lilly"), to evaluate the combination of Amplia’s investigational FAK inhibitor, narmafotinib, with Lilly’s investigational KRAS G12C inhibitor, olomorasib. The Phase 1b/2b clinical trial will evaluate the safety and efficacy of this novel targeted therapy combination as a second line treatment in patients with advanced stage non-small cell lung cancer (NSCLC).
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Under the terms of the CTCSA, Amplia will conduct the study, which is planned to begin in late 2026, at sites in Australia and the USA. Prior to signing the CTCSA, Lilly and Amplia have worked together to finalise an advanced draft clinical study protocol and will now collaborate to finalise both the protocol and other associated clinical study documents.
Dr Chris Burns, Amplia CEO and Managing Director commented: "This collaboration is an exciting new stage in the clinical progression of narmafotinib. We and others have shown that the combination of FAK and KRAS inhibition can lead to improved outcomes, and we are excited to advance with this clinical study to explore the combination potential with olomorasib, Lilly’s leading KRAS G12C inhibitor currently undergoing two global Phase 3 studies in NSCLC."
Strategic significance
The collaboration with Lilly supports and enhances Amplia’s strategy to position narmafotinib as a versatile oncology combination agent with the potential to enhance existing and investigational therapies across several high-value indications.
Leverages narmafotinib’s growing clinical evidence base. This study builds on the promising clinical data from Amplia’s ACCENT study, which has shown that narmafotinib has no significant tolerability burden over chemotherapy alone, together with a range of compelling efficacy signals across responses and survival1.
Expansion into major new indication. The study extends narmafotinib’s clinical development from pancreatic cancer into NSCLC, materially broadening Amplia’s addressable opportunity. The NSCLC market is currently valued at approx. US$31 B and estimated to grow to over US$60 B by 20332. KRAS G12C mutations occur in 13% of patients with NSCLC and 1-3% of patients with other solid tumours.
Capital-efficient growth and enhanced clinical strategy. Lilly’s in-kind supply of olomorasib gives Amplia the ability to efficiently pursue this new program in a high-value indication.
Scientific rationale
Approved KRAS G12C inhibitors such as sotorasib and adagrasib have advanced the treatment of KRAS G12C-mutant NSCLC and are approved for use after prior therapy. However, the clinical benefit of these drugs as single agents is frequently short-lived: response rates are modest and the majority of patients develop resistance, with reported median progression-free survival of only several months. There is therefore a clear and urgent need for strategies that deepen and prolong the benefit of KRAS G12C blockade.
This study combines the potential of Lilly’s potent and highly selective next-generation KRAS G12C inhibitor, olomorasib, with narmafotinib’s role as a suppressor of resistance mechanisms via inhibition of FAK.
Next generation KRAS G12C inhibitor. In studies to date, olomorasib has demonstrated an efficacy and safety profile that has supported later stage clinical development, with Lilly now advancing olomorasib in two separate, global Phase 3 registrational trials.
FAK as a central mediator of resistance to KRAS G12C. A growing body of preclinical and translational research has identified Focal Adhesion Kinase (FAK) as a central mediator of adaptive resistance to KRAS G12C inhibition. This adaptive FAK activation supports tumour cell survival and proliferation, driving resistance through several interconnected mechanisms including FAK-YAP signalling, along with FAK-driven fibrogenesis and remodelling of the tumour microenvironment.
(Press release, Amplia Therapeutics, AUG 3, 2026, View Source [SID1234669619])