Poster Presentation Demonstrating Combination Benefit of Narmafotinib in Preclinical Kras-Mutated Cancer Models

Rhea-AI Summary

Amplia Therapeutics (OTCQB:INNMF) reported preclinical poster data on March 6, 2026 showing its FAK inhibitor narmafotinib enhances the activity of kRAS inhibitors across pancreatic, lung and ovarian cancer models. The data suggest narmafotinib can block resistance pathways and may improve efficacy and durability of kRAS therapies.

The findings were presented at the AACR Special Conference: RAS Oncogenesis and Therapeutics; a copy of the poster is available from the company.

HIGHLIGHTS

• Amplia’s lead drug narmafotinib enhances the activity of kRAS inhibitors in multiple preclinical cancer models presented at US conference
  
  
• Data showing narmafotinib activity in preclinical models of pancreatic cancer, lung cancer and ovarian cancer are presented
  
  
• The development of kRAS inhibitors for different types of solid tumors is currently an area of intense global activity

Melbourne, Australia, March 09, 2026 (GLOBE NEWSWIRE) -- Amplia Therapeutics Limited (ASX:ATX; OTCQB:INNMF), (“Amplia” or the “Company”), announces that compelling data describing new clinical opportunities for its lead drug narmafotinib was presented at the AACR Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics in Los Angeles, California on Friday March 6.

The poster presentation discloses preclinical data demonstrating that the Company’s best-in-class FAK inhibitor narmafotinib enhances the activity of a new class of drugs called kRAS inhibitors in various models of cancer. In particular, the data indicates that narmafotinib blocks resistance pathways that can emerge with kRAS inhibitor treatment, thereby enhancing efficacy and durability of response.

A copy of the poster is available on the Company’s website.

Inhibitors of mutant kRAS proteins are an exciting new class of drug in development for the treatment of lung, colon and pancreatic cancer, amongst others. There are currently over 50 different kRAS inhibitors undergoing clinical studies across the globe. Despite promising mid-stage clinical data, however, side-effects of these drugs can be significant and treatment-emergent resistance is commonplace.

Dr Chris Burns, CEO of Amplia, commented, "We are excited to present our research findings at this specialist conference focused on RAS inhibition in cancer. We believe there is significant clinical potential in combining narmafotinib with kRAS inhibitors and will be discussing our findings with pharma and biotech companies actively working in this space."

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

Investor Contact: Dr Chris Burns Chief Executive Officer chris@ampliatx.com U.S. Contact: Robert Giordano rjgiordano@ggrouplifesciences.com +1 917 327 3938

Media Contact: H^CK Director, Haley Chartres haley@hck.digital +61 423 139 163 U.S. Media: media@ampliatx.com

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 tumors. 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 already achieved its primary endpoint in achieving a confirmed response rate of 35%, superior to 23% reported in the benchmark MPACT study for gemcitabine and Abraxane alone. An interim median PFS of 7.7 months has also been reported. A second trial – AMPLICITY – has recently opened and is being run under an IND at sites in Australia and the US, investigating the combination of narmafotinib with the chemotherapy FOLFIRINOX in advanced pancreatic cancer patients.

FAQ

What did Amplia (INNMF) present about narmafotinib at AACR on March 6, 2026?

The company presented preclinical poster data showing narmafotinib enhances kRAS inhibitor activity in multiple cancer models. According to Amplia, the poster indicates narmafotinib blocks resistance pathways and may increase efficacy and durability when combined with kRAS inhibitors.

Which cancer types did Amplia (INNMF) report narmafotinib activity in?

Narmafotinib showed activity in preclinical models of pancreatic, lung and ovarian cancer. According to Amplia, these models demonstrated enhanced responses when narmafotinib was combined with kRAS inhibitors and evidence of resistance pathway suppression.

How might narmafotinib affect resistance to kRAS inhibitors, according to Amplia (INNMF)?

Amplia reported narmafotinib appears to block resistance pathways that emerge with kRAS inhibitor treatment. According to Amplia, this blockade could improve treatment durability and enhance overall efficacy in preclinical models.

Does Amplia (INNMF) claim clinical trial results for narmafotinib with kRAS inhibitors?

No, the announcement describes preclinical poster data, not clinical trial outcomes. According to Amplia, the results are preclinical findings presented to inform further discussions with pharma and biotech partners.

Where can investors find the narmafotinib poster presented by Amplia (INNMF)?

A copy of the poster is available on Amplia's website for review. According to Amplia, the poster was presented at the AACR Special Conference in RAS Oncogenesis and Therapeutics on March 6, 2026.