Melbourne, Australia, June 22, 2026 (GLOBE NEWSWIRE) -- Amplia Therapeutics Limited (ASX:ATX | OTCQB:INNMF), (“Amplia” or the “Company”) provides a letter to shareholders from CEO and Managing Director Dr. Chris Burns outlining the potential for the Company’s best-in-class FAK inhibitor narmafotinib in combination with the emerging KRAS inhibitor class following exciting new data presented at the American Society of Clinical Oncology Annual Meeting earlier this month: Dear Fellow Shareholders, The treatment of pancreatic cancer is changing faster than at any point in a generation, and Amplia enters this moment from a position of real strength. Our lead drug, narmafotinib, is advancing on its own merits toward registration in one of medicine's most intractable cancers. The same biology that drives its independent promise also places it at the center of the field's most important new frontier. Few companies our size can make both claims at once. The KRAS opportunity At the 2026 American Society of Clinical Oncology Annual Meeting, investigators presented pivotal Phase 3 data showing that daraxonrasib, an oral KRAS-targeted therapy from Revolution Medicines, roughly doubled overall survival against chemotherapy in previously treated metastatic pancreatic cancer. For the first time, patients with this disease lived a median of more than a year on a targeted treatment. The field's verdict was unambiguous: RAS-targeted therapy is active in pancreatic cancer care and will likely become an integral part of the treatment paradigm. KRAS inhibitors represent a genuine advance, yet they share a well-documented vulnerability. Tumors adapt, resistance emerges, and responses prove less durable than patients need. In March, we presented preclinical data at the AACR Special Conference on RAS Oncogenesis showing that narmafotinib enhances the activity of KRAS inhibitors in preclinical models of pancreatic and lung cancer, and that it blocks the very resistance pathways that limit them. Narmafotinib targets the weakness standing between today's KRAS inhibitors and their full potential. The scientific logic is straightforward. FAK sits at a convergence point for the adaptive signaling that lets tumors escape RAS-pathway blockade, while also driving fibrosis around the tumor limiting any therapy's reach. Adding a FAK inhibitor to a KRAS-targeted backbone can extend both the depth and the durability of response. Both drugs are oral and once-daily, which makes for a rational, patient-friendly combination. At the ASCO plenary, the invited discussant urged that RAS-targeted therapy now anchor trials across pancreatic cancer, whether as monotherapy or in rational combinations. We built narmafotinib for exactly that strategic space. Narmafotinib also stands on its own Pancreatic cancer resists treatment for two stubborn reasons: a dense, fibrotic and immune-suppressed microenvironment around the tumor that walls tumors off from therapyand that suppresses the immune system; and the ability to adapt to, and resist, drug treatment. Narmafotinib, our potent and selective inhibitor of focal adhesion kinase, attacks both. FAK drives the survival, proliferation and chemoresistance of pancreatic tumor cells, and it builds the fibrotic, immunosuppressive barrier that protects them. By inhibiting FAK, narmafotinib breaks down that shield and restores the tumor's sensitivity to chemotherapy. That mechanism carries a decisive advantage: it does not depend on a tumor's mutational profile. Where many targeted therapies reach only the subset of patients who carry a specific mutation, narmafotinib addresses biology common to the great majority of pancreatic cancers. The clinic bears this out. In our ACCENT trial, narmafotinib combined with gemcitabine and nab-paclitaxel (Abraxane®) at their standard dose and schedule, in first-line advanced pancreatic cancer delivered a confirmed response rate of 35%, well above the 23% that chemotherapy alone achieved in the benchmark MPACT study, alongside an interim median progression-free survival of 7.7 months and median overall survival of 11.1 months. Most significantly, five patients recorded confirmed complete responses giving an unprecedented CR rate of 7.8%; with an additional patient achieving a pathological complete response. Patients have tolerated the oral, once-daily regimen well alongside chemotherapy. The U.S. Food and Drug Administration granted narmafotinib both Fast Track and Orphan Drug designation, recognition the agency reserves for therapies that address serious disease with real potential to improve on existing options. We continue to move decisively to convert that promise into an approval path: <ul type="disc"><li style="margin-top:0in; margin-bottom:8pt;">We launched the first stage of a registration-enabling Phase 2b study, advancing a new daily-dosing regimen and laying the groundwork for a Phase 3 program</li><li style="margin-top:0in; margin-bottom:8pt;">We entered an agreement with the Australia New Zealand Gynaecological Oncology Group to study narmafotinib in ovarian cancer, extending its reach into a second fibrotic, FAK-driven malignancy</li></ul> This is a drug with its own destination. Narmafotinib does not depend on any other company's success to create value for shareholders. Turning two opportunities into value The momentum behind KRAS-targeted therapy widens narmafotinib's opportunity rather than defining it. Every KRAS inhibitor advancing through the clinic is a potential combination partner, and we are talking directly with pharmaceutical and biotechnology companies, along with clinicians and other parties working in this field. Our aim is to make narmafotinib the combination partner of choice for the emerging generation of RAS-targeted medicines, in pancreatic cancer and other RAS-driven malignancies, even as we drive our own program toward approval. Looking ahead Execution will define the coming year. We will advance our registration-enabling program, generate the data that supports narmafotinib's combination potential, and pursue the partnership conversations that can accelerate its path to patients. Narmafotinib gives Amplia two ways to win: a lead drug advancing on its own toward a market of urgent need, and a combination opportunity riding the most powerful wave in cancer research. The science has rarely been more compelling, and our position has never been stronger. On behalf of the Board and the entire team, thank you for your continued support. We are building something of real and lasting value, and we are doing it at the moment the field has turned toward us. Sincerely, Christopher Burns, Ph.D. Chief Executive Officer Managing Director Amplia Therapeutics Limited <table style="border-collapse: collapse; width:100%; border-collapse:collapse ;"><tr><td style="vertical-align: top ; "> Investor Contact: Dr Chris Burns Chief Executive Officer <a href="mailto:chris@ampliatx.com" rel="nofollow" target="_blank" title="chris@ampliatx.com">chris@ampliatx.com</a> U.S. Contact: Robert Giordano <a href="mailto:rjgiordano@ggrouplifesciences.com" rel="nofollow" target="_blank" title="rjgiordano@ggrouplifesciences.com">rjgiordano@ggrouplifesciences.com</a> +1 917 327 3938</td><td style="vertical-align: top ; ">Media Contact: Tom Trezona, H^CK Acting MD <a href="mailto:tom@hck.digital" rel="nofollow" target="_blank" title="tom@hck.digital">tom@hck.digital</a> +61 411 235 692 U.S. Media: <a href="mailto:media@ampliatx.com" rel="nofollow" target="_blank" title="media@ampliatx.com">media@ampliatx.com</a> </td></tr></table> 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 <a href="https://www.globenewswire.com/Tracker?data=4wKrox5GyvcrX7L3_7UovtPTjcjYSI85-6GJm0Ll1iKmzxhEOnOQq1OprvuiVZxfrr1GolqX-nvlBnE2yIpWAfOb0nBIRZxn2UNdPLTZDfY=" rel="nofollow" target="_blank" title="">www.ampliatx.com</a> and follow Amplia on <a href="https://www.globenewswire.com/Tracker?data=IJLo9iN45EeXY6TronLoAs1-ah1hmEDEP65wI8myWPbmxh2DxYCY9sEhydPuGthkmT71VaJ4xMDSac3wMHEmjQ==" rel="nofollow" target="_blank" title="">X</a> (@ampliatx) and <a href="https://www.globenewswire.com/Tracker?data=6ay03hQdTwPARJdpB2gCyQ7sMrf2ihSVbc13j8WevrRpzI9DDU8pEBfWLe_ayaM73zAFVvgS1wVc2T760A-z9pm-tEMq9DfsZUvC47WghFMjN2Jmux3N9JvvJY66V2M8" rel="nofollow" target="_blank" title="">LinkedIn</a>. About Narmafotinib Narmafotinib (AMP945) is the company’s best-in-class inhibitor of the protein FAK, a protein over-expressed in pancreatic and other cancers 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 <a href="https://www.globenewswire.com/Tracker?data=twvjQUHE8vVCuaT2cvcDgptRVMhIpBWw-Y26VSFCebkomH2yA-4RlnD3hnv30yx_lahGtvOReGNVmwWHPX-lZw==" rel="nofollow" target="_blank" title="">ACCENT</a> 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 desired outcome in achieving a response rate of 35%, superior to chemotherapy alone and an interim PFS of 7.7 months has been reported. A second trial – AMPLICITY –is being run under an IND at two sites in Australia, investigating the combination of narmafotinib with the chemotherapy FOLFIRINOX in advanced pancreatic cancer patients. <img alt="" src='https://ml.globenewswire.com/media/OGQ3ZGJiZWItYmExOS00ZWFkLWJhMDQtZGFiOGFkNzJmNzliLTUwMDE1NTUyMy0yMDI2LTA2LTIyLWVu/tiny/Amplia-Therapeutics-Limited.png' referrerpolicy='no-referrer-when-downgrade' />

Following Significant Advances at ASCO, Amplia Therapeutics Provides Letter to Shareholders Highlighting the Potential Opportunities for Combination with KRAS Inhibition in Pancreatic Cancer

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