On August 4, 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 finalize an advanced draft clinical study protocol and will now collaborate to finalize 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 tumors.
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 tumor cell survival and proliferation, driving resistance through several interconnected mechanisms including FAK-YAP signaling, along with FAK-driven fibrogenesis and remodeling of the tumor microenvironment.
This ASX announcement was approved and authorized for release by the Board of Amplia Therapeutics and Lilly.

(Press release, Amplia Therapeutics, AUG 4, 2026, View Source [SID1234669682])

On August 4, 2026 Silexion Therapeutics Corp. (NASDAQ: SLXN) ("Silexion" or the "Company"), a clinical-stage biotechnology company pioneering RNA interference (RNAi) therapies for KRAS-driven cancers, reported additional positive preclinical findings from its ongoing translational immuno-oncology program evaluating SIL204 in human KRAS-mutant cancer cells. The new findings further expand SIL204’s therapeutic profile by demonstrating a coordinated immune-sensitizing effect on tumor cells, reinforcing the scientific rationale for combining SIL204 with anti-PD-(L)1 checkpoint inhibitor therapies. In newly reported studies performed across three human cancer cell lines representing three different KRAS mutations, SIL204 treatment produced statistically significant increases in expression of FAS, a well-established immune "death receptor," and statistically significant reductions in expression of HLA-G, an immune checkpoint that tumors use to evade immune surveillance. The findings, generated in human pancreatic (KRAS G12D) and non-small cell lung cancer (NSCLC; KRAS G12V and G12C) cell lines, build on the Company’s previously reported MHC-I upregulation data announced in May 2026, and further support SIL204’s potential to act as a multi-mechanism immune sensitizer in KRAS-driven tumors.

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"These new findings meaningfully extend and reinforce the immuno-oncology profile of SIL204 that we first reported in May," said Ilan Hadar, Chairman and Chief Executive Officer of Silexion Therapeutics. "In one integrated dataset, we are now seeing that SIL204 modulates three of the most important mechanisms by which KRAS-driven tumors evade the immune system – upregulating antigen presentation via MHC-I, upregulating FAS to restore sensitivity to immune-mediated cell death, and downregulating the HLA-G immune checkpoint to remove a key inhibitory signal to immune cells. SIL204 is producing this coordinated immune-sensitizing effect across multiple KRAS mutations and both of the largest KRAS-driven tumor types. We believe this profile supports the rationale for further evaluation of SIL204 in combination with anti-PD-(L)1 checkpoint inhibitor therapies, particularly in indications like pancreatic cancer where these agents have historically shown limited single-agent efficacy."

FAS (also known as CD95) is a cell surface death receptor whose engagement by Fas ligand (FasL) – which is expressed on activated CD8+ T cells and natural killer (NK) cells – triggers programmed cell death of the target cell. Cancer cells, and KRAS-driven tumors in particular, commonly downregulate FAS to evade immune-mediated killing. Recent research published in Developmental Cell (Cell Press) has demonstrated that elimination of oncogenic KRAS in genetic mouse models of pancreatic ductal adenocarcinoma restores FAS expression and enables FasL-expressing CD8+ T cells to eradicate KRAS-driven tumors.¹ In the newly reported Silexion study, SIL204 treatment produced statistically significant, dose-dependent increases in FAS expression at 72 hours in human KRAS G12D-mutant pancreatic cancer cells (PK59; up to approximately 2-fold, P<0.0001 vs. control) and in KRAS G12V-mutant NSCLC cells (CORL23; P<0.05 vs. control).

HLA-G is a non-classical HLA class I molecule that functions as a potent immune checkpoint. When expressed on tumor cells, HLA-G binds inhibitory receptors – including ILT-2 (LILRB1), ILT-4 (LILRB2), and KIR2DL4 – on CD8+ T cells, NK cells, and myeloid immune cells, suppressing their anti-tumor activity and enabling immune escape.² HLA-G is a recognized and increasingly prominent drug target in oncology, with multiple HLA-G-directed programs currently in clinical development in advanced solid tumors. In the newly reported study, SIL204 treatment produced statistically significant, dose-dependent reductions in HLA-G expression in human KRAS G12C-mutant NSCLC cells (NCI-H358; P<0.001 at 24 hours and P<0.01 at 72 hours vs. control at the 200 nM dose), with additional reductions observed in KRAS G12D-mutant pancreatic and KRAS G12V-mutant NSCLC cells.

Taken together with the Company’s previously reported May 2026 findings demonstrating statistically significant upregulation of MHC-I (HLA-ABC) in KRAS G12R-mutant pancreatic cancer cells, these new data support a coordinated immune-sensitization signature across three key immune pathways. The immune-modulatory effects have now been observed across four distinct KRAS mutations (G12D, G12V, G12C, and G12R) in both pancreatic and non-small cell lung cancer models, reinforcing the potential applicability of SIL204’s mechanism across the largest KRAS-driven cancer patient populations.

The findings arrive at a moment when the oncology field is actively exploring combinations of KRAS-directed therapies with immune checkpoint inhibitors, with recent academic and industry work demonstrating that combining KRAS inhibition with anti-PD-1 or anti-PD-L1 agents can produce sustained tumor regression and reprogramming of the tumor microenvironment in KRAS-driven cancers.³ Pancreatic ductal adenocarcinoma and KRAS-mutant NSCLC together represent the largest KRAS-driven patient populations, with KRAS mutations present in approximately 90% of pancreatic cancers and 30–35% of lung adenocarcinomas. Immune checkpoint inhibitors have shown limited single-agent efficacy in pancreatic cancer and variable response rates in KRAS-mutant NSCLC, driving substantial scientific and commercial interest in strategies capable of converting "immunologically cold" tumor phenotypes into more immunotherapy-responsive tumors. The Company believes these findings provide additional translational support for SIL204’s ongoing Phase 2/3 clinical development.

(Press release, Silexion Therapeutics, AUG 4, 2026, View Source [SID1234669681])

On August 4, 2026 Forlong Biotechnology, a clinical-stage biotech company focused on developing transformative cytokine therapies for patients with severe unmet needs, reported approval to initiate a Phase I study of FL115 subcutaneous injection (administered once every three weeks) in patients with advanced solid tumors in Australia. The study has been approved under Australia’s Therapeutic Goods Administration (TGA) Clinical Trial Notification (CTN) scheme, following review by the Human Research Ethics Committee (HREC).

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FL115, an engineered IL-15/IL-15Rα-Fbody fusion protein, has been evaluated as a monotherapy administered via IV infusion in two Phase I studies in patients with advanced solid tumors. These studies demonstrated a favorable safety profile along with preliminary clinical efficacy, supported by significant and sustained expansion of NK and CD8+ T cells, as well as a strong, transient induction of IFN-γ. Clinical benefit has been observed, with 3 patients remaining on treatment (one patient with stable disease and two patients with confirmed partial response) over 12 months.

Compared with IV infusion, subcutaneous administration of FL115 has been shown in preclinical studies to lower Cmax by more than 20-fold while significantly extending meaningful exposure duration, with bioavailability of 60% or higher and no significant gross skin irritation. Such a profile may enhance clinical efficacy through stronger NK and T cell stimulation, while also improving clinical safety by reducing the release of certain cytokines.

"FL115 monotherapy via IV infusion has demonstrated good safety and tolerability, with early signs of potent anti-tumor activity in Phase I studies in patients with heavily-pretreated solid tumors," said Dong Wei, Ph.D., Chief Executive Officer of Forlong Biotechnology. "We expect the subcutaneous formulation of FL115, dosed once every three weeks, to further improve the safety and efficacy profile, as well as convenience for patients — continuing to establish FL115 as a potential best-in-class IL-15 superagonist and, ultimately, bringing new treatment options to cancer patients in need."

About FL115

FL115 is an engineered IL-15/IL-15Rα-Fbody fusion protein designed to enhance anti-tumor immunity through IL-15-mediated signaling on NK and CD8+ T cells, while minimizing the complexity associated with an Fc domain. FL115 has demonstrated significant anti-tumor activity in vivo, both as a monotherapy and in combination therapy, and can be manufactured through a robust, efficient process with excellent product stability. Clinically, FL115 has shown a favorable safety profile and preliminary clinical responses as a monotherapy, and has best-in-class potential to synergize with current and emerging T cell–targeting immunotherapies through combination approaches that could meaningfully improve treatment outcomes for patients.

FL115 is currently being investigated in combination with Bacillus Calmette-Guérin (BCG) in a Phase II clinical trial evaluating safety and preliminary efficacy in patients with non-muscle invasive bladder cancer (NMIBC), and in combination with an anti-PD-1 monoclonal antibody in a Phase I clinical trial evaluating safety and preliminary efficacy in patients with advanced solid tumors. A Phase I clinical trial of FL115 subcutaneous injection is also being initiated in Australia.

(Press release, Forlong Biotechnology, AUG 4, 2026, View Source [SID1234669680])

On August 4, 2026 enGene Therapeutics Inc. (Nasdaq: ENGN, "enGene" or the "Company"), a clinical-stage, non-viral genetic medicines company, reported that it will host a virtual key opinion leader (KOL) event on Tuesday, August 11, 2026 at 11:00 AM ET featuring Neal Shore, MD, FACS (Carolina Urologic Research Center; Atlantic Urology Clinics). Dr. Shore will join management to provide insights into the evolving NMIBC treatment landscape and the various considerations driving treatment selection.

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The event will provide an overview of:

The future treatment paradigm in NMIBC and how sequencing therapies may evolve
Insights on community urology practices and how treatment considerations and choice drivers vary
Pricing and reimbursement dynamics
A live question and answer session will follow the formal presentations.

To register for the webinar, please click here. The live webinar and subsequent replay of the event can also be accessed on the "Events and Presentations" page under the "Investors" section of the enGene website at www.engene.com.

Featured Speaker

Neal Shore, MD, FACS is the Medical Director for START-Carolinas Research (formerly Carolina Urologic Research Center) in Myrtle Beach, SC, USA, and the Global Director of GU Oncology for START Cancer Research. He is actively involved with the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Guidelines Committee for Bladder Cancer and has served on the boards of the Bladder Cancer Advocacy Network, the APCCC Scientific Steering Committee, Maple Tree Cancer Alliance, and the Duke Global Health Institute.

Dr. Shore has conducted over 500 clinical trials, primarily in genitourinary oncology, and has authored more than 400 peer-reviewed publications along with numerous book chapters. He is Chair of both the Prostate Cancer Academy and the Bladder/Kidney Cancer Academy, and co-Chair of the annual AUA International Prostate Cancer Forum. He has served or continues to serve on the editorial boards of Urology Times, Chemotherapy Advisor, OncLive, PLOS ONE, Urology Practice, JUOP, Everyday Urology, Oncology, and World Journal of Urology. He is the Editor-in-Chief of Reviews in Urology.

Dr. Shore graduated from Duke University and Duke University Medical School. He completed his general surgery and urology residency at New York Hospital-Cornell Medical Center/Memorial Sloan Kettering Cancer Center. He is a Fellow of the American College of Surgeons and a Certified Physician Investigator.

(Press release, enGene Therapeutics, AUG 4, 2026, View Source [SID1234669679])

On August 4, 2026 CEL-SCI Corporation (NYSE American: CVM) reported the publication of its study, "A Novel Neoadjuvant Immunotherapy Confers Improved Overall Survival in Oral Cancer Patients with Low Tumor PD-L1 Expression: The IT-MATTERS Clinical Trial – Prognostic Role of Tumor PD-L1 Expression," in the internationally recognized journal Oral Oncology.

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The peer-reviewed publication provides scientific evidence supporting the biomarker strategy that forms the foundation for selecting patients in CEL-SCI’s upcoming global Confirmatory Registration Study of Multikine (Leukocyte Interleukin, Injection)*. The Oral Oncology published study identifies low and zero tumor PD-L1 expression (TPS <10%) and the absence of lymph node involvement (N0) as prognostic biomarkers for selecting patients most likely to achieve substantial survival benefit from Multikine administered before surgery.

In this biomarker-selected patient population, patients receiving the Multikine treatment regimen prior to surgery followed by standard of care achieved a 73.4% five-year overall survival (OS) rate compared with 45.8% for patients receiving surgery followed by standard of care alone, corresponding to a hazard ratio of 0.34 (p=0.0012) and a 28.6% absolute improvement in five-year survival. The published study also demonstrated a statistically significant improvement in progression-free survival (PFS), with a 49% reduction in the risk of disease progression or death (PFS hazard ratio 0.51; p=0.0197) compared to control in the same patient population.

Importantly, the peer-reviewed publication concludes that these biomarkers can be used prospectively to identify patients most likely to benefit from Multikine and guide future clinical studies in head and neck (squamous cell carcinoma) cancer.

"Publication of these findings in Oral Oncology represents an important peer-reviewed acceptance of the science behind our Multikine development program," said Geert Kersten, CEO of CEL-SCI. "The results not only confirm the remarkable overall and progression free survival benefit observed in the selected population analyzed in our Phase 3 trial, but they also provide strong support for the biomarker selection strategy we are implementing for our Confirmatory Registration Study. It is important to note that when Keytruda was approved by the FDA in the same indication, based on event free survival, it had not established overall survival benefit. As awareness of the Multikine data grows within the global oncology community, we believe Multikine will become increasingly recognized as a differentiated immunotherapy."

The publication in Oral Oncology notes that currently approved checkpoint inhibitor therapies are generally directed toward patients with higher PD-L1 expression, while Multikine’s unique mechanism of action enables it to benefit patients whose tumors express low (TPS <10%), as well as zero (0%) PD-L1. This creates the potential for a treatment approach that specifically targets the underserved low and zero PD-L1 patient population.

CEL-SCI is preparing to commence enrollment in its global 212-patient Confirmatory Registration Study, which will evaluate Multikine in newly diagnosed, previously untreated, locally advanced resectable head and neck oral cancer patients with low and zero (TPS <10%) PD-L1 tumor expression and no lymph node involvement—the same patient population reported on in the newly published study in Oral Oncology. The trial is designed with approximately 97% statistical power to confirm the previously observed overall survival benefit.

About Multikine

Multikine is a novel cancer immunotherapy administered before surgery as a treatment for newly diagnosed previously untreated locally advanced head and neck cancer. Its goal is to activate a person’s immune system to fight cancer before the ravages of surgery, radiation and chemotherapy have weakened the immune system. In the world’s largest head and neck cancer Phase 3 study, Multikine increased the 5-year survival rate of the target patient population to 73% vs 45% in patients treated with standard of care alone and halved the risk of death from 55% to 27%.

(Press release, Cel-Sci, AUG 4, 2026, View Source [SID1234669678])