Scientific Paper Detailing Preclinical Studies of Narmafotinib in Pancreatic Cancer Now Online

HIGHLIGHTS

• A manuscript describing comprehensive preclinical studies of narmafotinib in models of pancreatic cancer is now available online.
• The findings provide further evidence of narmafotinib’s ability to target several important drivers of pancreatic cancer progression, including fibrosis, chemotherapy resistance and metastatic spread.

Melbourne, Australia, July 31, 2026 (GLOBE NEWSWIRE) — Amplia Therapeutics Limited (ASX:ATX; OTCQB:INNMF), (“Amplia” or the “Company”), announces that a scientific manuscript detailing extensive preclinical studies of narmafotinib in pancreatic cancer has been made publicly available on the biology preprint server bioRxiv and can be accessed via this link¹.

The manuscript describes research conducted by Professor Paul Timpson and colleagues at the Garvan Institute of Medical Research, Sydney, and provides further insight into the multiple mechanisms through which narmafotinib may act to improve outcomes in pancreatic cancer.

Key findings reported in the manuscript include:

• Reduction of tumour fibrosis, a hallmark of pancreatic cancer that contributes to treatment resistance and impaired drug delivery;
• Enhanced anti-tumour activity when combined with chemotherapy across multiple preclinical pancreatic cancer models;
• Reduced cancer dissemination and metastatic spread in a model of metastatic pancreatic cancer; and
• Downregulation of multiple genes associated with chemotherapy resistance, further supporting the biological rationale for combining narmafotinib with chemotherapy and other drugs.

Dr Chris Burns, CEO and Managing Director of Amplia commented, “We are delighted that the extensive research conducted by Professor Timpson’s team at the Garvan Institute over recent years is now being shared with the broader scientific community. Importantly, these studies strengthen the scientific rationale for the clinical development of narmafotinib, and provides further insight into the multifaceted mechanisms through which narmafotinib can act in the treatment of this devastating disease.”

The publication represents one of the most comprehensive preclinical evaluations of narmafotinib undertaken to date and further supports Amplia’s ongoing clinical development program in pancreatic cancer.

This ASX announcement was approved and authorised for release by the Board of Amplia Therapeutics.

About Amplia Therapeutics Limited

Amplia Therapeutics Limited is an Australian pharmaceutical company advancing a pipeline of Focal Adhesion Kinase (FAK) inhibitors for cancer and fibrosis. FAK is an increasingly important target in the field of cancer and Amplia has a particular development focus in fibrotic cancers such as pancreatic and ovarian cancer. FAK also plays a significant role in a number of chronic diseases, such as idiopathic pulmonary fibrosis (IPF). For more information visit www.ampliatx.com and follow Amplia on X (@ampliatx) and LinkedIn.

About Narmafotinib

Narmafotinib (AMP945) is the company’s best-in-class inhibitor of the protein FAK, a protein over-expressed in pancreatic cancer and a drug target gaining increasing attention for its role in solid tumours. The drug, which is a highly potent and selective inhibitor of FAK, has shown promising data in a range of preclinical cancer studies. Narmafotinib is currently undergoing a clinical trial (the ACCENT trial) where it is dosed in combination with the chemotherapies gemcitabine and Abraxane in first-line patients with advanced pancreatic cancer. The trial has achieved its desired outcome in achieving a response rate of 36%, superior to chemotherapy alone, and a mOS of 11.1 months has been reported. A second trial in pancreatic cancer (AMPLICITY) is being run at sites in Australia investigating the combination of narmafotinib with the chemotherapy FOLFIRINOX in advanced pancreatic cancer patients, while a trial in ovarian cancer (PRROSE) examining a combination of narmafotinib with standard-of-care chemotherapy will open shortly.

¹ https://www.biorxiv.org/content/10.64898/2026.07.23.740234v1