Announcement PDF ABN 16 165 160 841 +61 (0) 3 9123 1140 | info@ampliatx.com Level 5, 90 William Street, Melbourne VIC 3000 Australia www.ampliatx.com 9 MARCH 2026 ASX RELEASE POSTER PRESENTATION DEMONSTRATING COMBINATION BENEFIT OF NARMAFOTINIB IN PRECLINICAL KRAS-MUTATED CANCER MODELS 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 tumours is currently an area of intense global activity Melbourne, Australia: 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 included with this announcement. 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 authorised 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. HALLMARK MYC TARGETS (V2) HALLMARK KRAS SIGNALING DOWN PLD ONLY PLD + NARMA PLD ONLY PLD + NARMA PLD ONLY PLD + NARMA HALLMARK DNA REPAIR Combination benefits of Focal Adhesion Kinase Inhibitor Narmafotinib and KRAS inhibitors Terrie-Anne Cock1, Sarah Kinkel1, Han Kyul Cho2, Jiho Park2, Braydon Meyer3, Kendelle Murphy3, David Herrman3, Paul Timpson3, Sang Hyub Lee4, Kyung Min Lee4, Jin Ho Choi4, Jason Lickliter1, Christopher J. Burns1 1Amplia Therapeutics, Melbourne, Australia; 2NEXT&BIO, Seoul, Korea; 3Garvan Institute of Medical Research, Sydney, Australia, 4Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea Best-in-class profile • Highly potent and selective • Oral once-a-day dosing • Good safety and tolerability • Patient population not limited by genetics • Ability to combine with SOC therapies for multiple oncology indications • Confirmed objective response rate of 35% (19/55 patients), including 1 complete response and 1 pathological CR • Median PFS 7.7 m compares favorably to MPACT benchmark study (5.5 m)2 • The combination was well tolerated with no evidence of increased grade ≥3 AEs compared to chemotherapy alone Narmafotinib-related AEs in ≥ 5% of patients, n (%) Severity of Treatment-Related AEs Any grade n (%) Grade ≥ 3 n (%) Nausea 16 (29.1) 2 (3.6) Diarrhea 9 (16.4) 2 (3.6) Vomiting 8 (14.5) 1 (1.8) Fatigue 6 (10.9) 0 Gastroesophageal reflux disease 4 (7.3) 0 Constipation 3 (5.5) 0 Note: investigator read provisional analysis Results shown for n = 55 patients from the Phase 2a cohort1. KRASG12C inhibition has been suggested to hyperactivate FAK signaling, which can lead to fibrosis and reduce the effectiveness of treatment3 PDOs were stabilized for 96h followed by a 96h treatment period. Viability was measured by CellTitre-Glo®2.0. Chris Burns PhD E: Chris@ampliatx.com W: www.ampliatx.com 3. Zhang B, et al. Adv Sci (Weinh). 2021;8(16):e2100250. 1. J Clin Oncol 44, 735(2026) Volume 44, Number 2_suppl 2. Von Hoff DD, et al. N Engl J Med. 2013;369(18):1691-703 *p < 0.05, ** p < 0.01, ***p < 0.001, ****p < 0.0001 Expression profiling showed that narmafotinib monotherapy enhances p53 signaling pathways, while downregulating Wnt signaling The addition of narmafotinib to PLD further disrupts the RAS/ERK/MAPK signaling axis and dampens the downstream Myc responsive proliferation programs Narmafotinib in Phase 2 development for mPDAC in combination with two 1L SOC chemotherapies 1. FOLFIRINOX (AMPLICITY trial NCT07026279) 2. Gem/nab-PTX (ACCENT trial NCT05355298) • Clinically favorable safety and tolerability profile in combination with chemotherapy • Durable and sustained clinical efficacy Improved responsiveness to chemotherapy in preclinical models Combination benefit of narmafotinib with different KRASi NARMAFOTINIB: FAK inhibitor in Phase 2 PDAC Enhanced tumor reductions in ovarian cancer TOV-21G KRASG13C xenograft tumors treated with narmafotinib combined with pegylated liposomal doxorubicin (PLD) reduces KRAS signaling Narmafotinib and gem/nab-PTX combination prolonged inhibition of patient derived TKCC10lo KRASG12V pancreatic tumors Narmafotinib treatment alone inhibits pancreatic cancer patient-derived organoid growth irrespective of KRAS mutation Narmafotinib combined with pan-RAS inhibitor improves tumor growth inhibition Combination treatment with narmafotinib enhanced tumor responsiveness to KRASG12C inhibitor in both sensitive and insensitive xenograft models Pancreatic Capan-1 KRASG12V KRASi sensitive Pancreatic MIA PaCa-2 KRASG12C KRASi insensitive NSCLC NCI-H2122 KRASG12C