On October 14, 2025 GNTbm (stock code: 7427, Taiwan) reported the preclinical data on GNTbm-TKI, a novel multi-receptor tyrosine kinase inhibitor for cancer immunotherapy. GNTbm-TKI will be presented as posters at the 2025 European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Annual Meeting, which is held in Berlin, Germany, from Oct 17 to 21, 2025.

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Abstract: 2242
Title:Preclinical development of GNTbm-TKI, a novel multi-receptor tyrosine kinase inhibitor, while combined with GNTbm-38 showing potent induced tumor microenvironment remodeling activity in cancer immunotherapy
Session Date/Time: 10/19/2025, 12:00-12:45 CEST
Poster Board Number: 1577P

Currently, although there are many options for cancer immunotherapy, they still cannot meet the needs of clinical treatment, especially for advanced solid tumors defined as ‘cold tumors’. Genetic alterations of certain receptor tyrosine kinases (TKs), including TAM (TYRO3, AXL, and c-MER), are critical in creating environment conducive to tumor development in several cancers such as HNSCC, CRC, HCC, and RCC. GNTbm-TKI is a novel multi-targeted TKI, showing induction of immune activation in the tumor microenvironment (TME), that indicates the potential application in cancer immunotherapy for unmet medical needs.

The results of the study show that GNTbm-TKI strongly inhibited the activities of TYRO3, AXL, c-MER, BTK, ROS1, NTRK2, MET, and VEGFR2 at nanomolar level. GNTbm-TKI showed anti-proliferation activity in NCI-60 human cancer cell lines with low GI50 values. GNTbm-TKI showed a superior in vivo efficacy in WT mice compared to immune-deficient mice in CT-26 model, indicating anti-cancer immune activation induced by the treatment. Furthermore, treatment with GNTbm TKI + GNTbm-38 (an immune activator of class ⅠHDACi) combined with ICI significantly improved tumor response rate and boosted survival rate through synergistic effect by normalizing tumor vessels, increasing activated CD8+ T cell infiltration into tumors, inducing memory T cell persistence, and strongly inhibiting mobilization of immunosuppressive cells into tumors. On the other hand, GNTbm-TKI + GNTbm-38 combined with anti-PD-1/VEGF bispecific antibodies in a humanized B-PD-1/PD-L1/VEGFA mouse model also greatly improved anti-cancer with a strong synergistic effect.

GNTbm-TKI is a potent immune-activating multi-tyrosine kinase inhibitor, and it is surprisingly found capable of significantly reshaping the tumor microenvironment when combined with GNTbm-38. When further combined with ICI or anti-PD-1/VEGF bispecific antibodies, it can greatly enhance anti-cancer efficacy, providing a scientific basis for future clinical trials.

About GNTbm-TKI
GNTbm-TKI is a new chemical entity independently developed by GNTbm. It is a drug candidate selected by an immuno-competent tumor-bearing animal testing platform, and has undergone many preclinical research studies to be demonstrated that it has very outstanding anti-cancer activity in tumor microenvironment. GNTbm-TKI is an oral drug with dual effects of strong immune activation and multi-tyrosine kinase, which is unique when compared to the mechanism of other TKI drugs. GNTbm-TKI can remodel the tumor microenvironment (TME) through a unique multiple regulatory mechanism based on its kinase targets which it selectively inhibits. GNTbm-TKI strongly inhibits tumor growth and development, suppresses tumor invasion and metastasis, inhibits tumor angiogenesis, and most importantly, possesses potent tumor immune regulatory activity. When GNTbm-TKI is combined with GNTbm-38, based on their respective unique mechanisms, they have a complementary and powerful tumor microenvironment remodeling function, capable of converting ‘cold tumors’ into ‘hot tumors.’ When further combined with ICI or anti-PD-1/VEGF bispecific antibodies, they exhibit exceptionally superior anti-tumor immuno-oncology activity, which can attract CTL to infiltrate into the TME, and activate CTLs and reduce CTL exhaustion. At the same time, it can also reduce the attraction of immunosuppressive cells (such as: TAM, Treg, and MDSCs) into the TME, so as to achieve the remodeling of the TME, which is more conducive to obtaining the therapeutic benefits of cancer immunotherapy. GNTbm-TKI monotherapy can be used in the treatment of advanced neuroendocrine tumor, and GNTbm-TKI can also be combined with GNTbm-38 or/and ICI/anti-PD-1/VEGF bispecific antibodies for treatment of a variety of solid tumors, mainly through a unique anti-cancer immune-regulating and multiple-tyrosine kinase inhibition mechanism to achieve anti-cancer treatment goals.

(Press release, GNT Biotech & Medicals, OCT 14, 2025, View Source;medicals-corporation-gntbm-presented-preclinical-data-on-gntbm-tki-a-novel-multi-tyrosine-kinase-inhibitor-with-potent-immune-activation-at-the-2025-esmo-annual-meeting-302583015.html [SID1234656657])

On October 14, 2025 NuCana plc (NASDAQ: NCNA) ("NuCana" or the "Company") reported the publication of new data on NUC-3373. The update includes results from the NuTide:303 clinical study, published on medRxiv, the preprint server for health sciences, together with complementary preclinical findings published in the peer-reviewed journal Public Library of Science ONE (PLOS ONE).

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NUC-3373, a potent thymidylate synthase inhibitor that induces DNA damage in cancer cells, has previously shown encouraging activity in combination with the PD-1 inhibitor pembrolizumab in the Phase 1/2b modular study, NuTide:303. In Module 1 of this study, 12 patients with advanced solid tumors who had exhausted all standard treatment options and had previously received PD-1 inhibitors were treated with NUC-3373 plus pembrolizumab.

Encouraging signals of durable activity were observed, including:

A 100% reduction in tumor lesion size (classified as a partial response due to the presence of non-target lesions) in a patient with urothelial carcinoma of the bladder who remained on treatment for over 15 months; and

An 81% reduction in target lesions in a patient with metastatic melanoma resistant to prior pembrolizumab therapy, who continues to remain progression-free at 23 months.

These promising clinical findings are further supported by preclinical data. The published results demonstrate that NUC-3373 in a model in vitro system:

Promotes the release of immunogenic damage-associated molecular patterns (DAMPs);

Enhances activation of first-line defense immune cells, including natural killer (NK) cells; and

In combination with a PD-1 inhibitor, enhances tumor cell death by activating lymphocytes, regardless of the tumor’s genomic stability status.

"It is becoming increasingly clear that the majority of future standards of care for advanced cancers will rely on combination regimens incorporating novel immuno-oncology backbones," said Professor David Harrison, Head of Translational Medicine at NuCana. "The combination of NUC-3373 with pembrolizumab has demonstrated both a favorable safety profile and evidence of efficacy and durable disease control in this patient cohort."

Andrew Kay, NuCana’s Executive Chairman, added: "The complementary mechanisms of action of NUC-3373 and PD-1 inhibition provide a strong rationale for synergy. We are currently evaluating optimal combinations and indications for further clinical studies of NUC-3373, while continuing to maintain our anticipated cash runway into 2029. We are committed to advancing these assets and working toward our vision of delivering significantly improved treatment outcomes for patients with cancer."

(Press release, Nucana, OCT 14, 2025, View Source [SID1234656643])

On October 14, 2025 BostonGene, developer of the leading AI foundational model for cancer and immune system, reported the acceptance of four abstracts at the ESMO (Free ESMO Whitepaper) Congress 2025. This premier global oncology meeting brings together clinicians, researchers, patient advocates and industry experts to advance cancer science and care. The Congress showcases the latest breakthroughs in translational research and clinical practice, featuring practice-changing data across multiple tumor types and serves as a vital platform for the pharmaceutical and biotechnology sectors. The ESMO (Free ESMO Whitepaper) Congress 2025 will take place October 17–21 in Berlin, Germany.

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BostonGene session details are as follows:

Title: Transcriptomic Tumor Microenvironment Subtypes in Cervical Cancer Reveal Prognostic and Therapeutic Opportunities
FPN: 1167P
Date and time: October 18 | 12:00-12:45 CEST
Presenter: Andrey Kravets, Senior Bioinformatician, BostonGene

Leveraging its proprietary multimodal platform, BostonGene developed a tumor microenvironment-based classification system to identify targetable features of cervical cancers. RNA-seq and proteomics data from open-source datasets were evaluated to determine HPV gene expression, associated protein and signaling pathway activity, and correlations with patient survival. This analysis supports the use of precision therapy strategies to improve patient outcomes.

Title: Integrated analysis of KRAS mutations and MTAP loss in pancreatic cancer reveals potential for combined blockade of KRAS and PRMT5
FPN: 2248P
Date and time: October 19 | 12:00-12:45 CEST
Presenter: David Hong, MD, The University of Texas MD Anderson Cancer Center

BostonGene performed genomic and transcriptomic profiling of 437 public and 119 internal pancreatic adenocarcinoma samples using its automated pipelines, identifying frequently co-occurring MTAP mutations in KRAS-mutated tumors. These findings support the strategy of combining PRMT5 and RAS inhibitors in patients harboring both KRAS mutations and MTAP loss. The correlation of MTAP deletion and fibrotic tumor microenvironment also supports treatment strategies that combine PRMT5 inhibitors with immune checkpoint blockade.

Research conducted in collaboration with MD Anderson Cancer Center

Title: ERK/MAPK, RTK, ABL, and WNT Signaling Pathways as Potential Therapeutic Targets in Undifferentiated Pleomorphic Sarcoma
FPN: 2713P
Date and time: October 20 |12:00-12:45 CEST
Presenter: Neal S. Chawla, Associate Director of Clinical Research, Sarcoma Oncology Center

Using RNA-seq data of over 1,000 sarcoma samples and publicly accessible drug response data, BostonGene applied its proprietary analytics platform to derive a gene signature to describe features of undifferentiated pleomorphic sarcoma (UPS). Through this analysis, BostonGene identified that samples with UPS-like features, while associated with worse survival outcomes, also exhibited heightened sensitivity to compounds targeting RTK/RAS/RAF/MEK, ABL, and WNT pathways, highlighting new therapeutic avenues for these aggressive tumors.

Research conducted in collaboration with the Sarcoma Oncology Center

Title: Clinical Benefit Analysis of DNG64-CAR-V Gene Therapy Predicts Successful Efficacy Endpoints for a Planned Phase 2 Basket Study for CCNG1 Expressing Tumors
FPN: 2702P
Date and time: October 20 | 12:00-12:45 CEST
Presenter: Anmol Dia Agarwal, BA, Sarcoma Oncology Center

BostonGene led the clinical testing and data analysis for a study examining the efficacy and safety of DNG64-CAR-V, an RNA vector consisting of a SIG targeting peptide and encoding a CCNG1 inhibitor gene, for treating patients with advanced sarcoma, pancreatic cancer and breast cancer. Using BostonGene’s proprietary multimodal analytics pipeline, it was determined that all patient groups qualified for a Phase 2 basket study to further examine the efficacy and safety of combination regimens of DNG64-CAR-V.

Research done in collaboration with Sarcoma Oncology Center

To learn more or to schedule a meeting with BostonGene during the event, please contact Hannah Oman at [email protected]. For more information, please visit the ESMO (Free ESMO Whitepaper) Congress 2025 website.

(Press release, BostonGene, OCT 14, 2025, View Source [SID1234656658])

On October 14, 2025 Clarity Pharmaceuticals (ASX: CU6) ("Clarity" or "Company"), a clinical-stage radiopharmaceutical company with a mission to develop next-generation products that improve treatment outcomes for patients with cancer, reported that the Co-PSMA (NCT06907641)1 Investigator-Initiated Trial (IIT), led by Prof Louise Emmett at St Vincent’s Hospital Sydney, has achieved its primary endpoint with a statistically significant higher number of prostate-specific membrane antigen (PSMA)-positive prostate cancer lesions detected using 64Cu-SAR-bisPSMA compared to standard-of-care (SOC) 68Ga-PSMA-11 positron emission tomography/computed tomography (PET/CT) in patients with low prostate-specific antigen (PSA) levels.

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Co-PSMA’s official study title is "Comparative performance of 64Copper [64Cu]-SAR-bisPSMA vs. 68Ga-PSMA-11 PET CT for the detection of prostate cancer recurrence in the setting of biochemical failure following radical prostatectomy". This Phase II IIT is evaluating the performance of Clarity’s diagnostic product, 64Cu-SAR-bisPSMA, in comparison to SOC 68Ga-PSMA-11 in 50 patients with low PSA who are candidates for curative salvage therapy. Eligible patients were required to have had radical prostatectomy with no salvage therapy and a PSA level between 0.2 and 0.75 ng/mL.

The Co-PSMA trial has successfully met its primary endpoint, demonstrating that 64Cu-SAR-bisPSMA PET/CT detects significantly more lesions per patient than the SOC, 68Ga-PSMA-11 PET/CT. This result supports the hypothesis that 64Cu-SAR-bisPSMA can improve early detection of recurrence and staging of prostate cancer in patients with low PSA who are candidates for curative salvage therapy. Full analysis of all data generated in the Co-PSMA trial is underway, and results of this study will be presented at an upcoming international conference.

The Co-PSMA topline results corroborate findings from the COBRA trial2, which investigated the diagnostic performance of 64Cu-SAR-bisPSMA in patients with biochemical recurrence (BCR) of prostate cancer who had a negative or equivocal SOC scan at study entry. In the COBRA study, a subset of participants underwent follow-up SOC PSMA PET imaging. Only 60% of these participants had a positive SOC PSMA PET, while 70% of participants had a positive 64Cu-SAR-bisPSMA PET on same-day imaging and 90% on next-day imaging. The number of lesions across all participants (average sum of lesions across all readers) identified by 64Cu-SAR-bisPSMA was also higher (26.3 lesions on same-day imaging, 52.6 on next-day imaging) than that detected by SOC PET agents (20 lesions). The COBRA trial results showed that 64Cu-SAR-bisPSMA was able to identify lesions more than 6 months earlier than SOC PSMA PET agents, with 6 months being the last follow-up visit for that trial.

The Co-PSMA trial further builds on the growing body of evidence of the enhanced diagnostic performance of 64Cu-SAR-bisPSMA compared to SOC PSMA PET agents, which are known to have low sensitivity, especially in patients with low PSA levels3,4. Improvements in sensitivity, as with all diagnostic agents, play a pivotal role in guiding more informed treatment decisions, enabling earlier and more accurate detection of prostate cancer recurrence and ultimately improving patient outcomes.

Dr Alan Taylor, Executive Chairperson of Clarity Pharmaceuticals, commented: "Achieving the primary endpoint in the Co-PSMA trial, which was a head-to-head trial against a SOC competing product, is yet another important step in the development of 64Cu-SAR-bisPSMA as we look to further validate this agent as best-in-class through two registrational trials with two Fast Track Designations (FTDs) under our belt for diagnostic applications and a strong focus on commercialisation.

"We look forward to Prof Emmett releasing the full Co-PSMA trial data at world-leading congresses as we continue to adhere to the highest standards of clinical research in our aspirations to bring a best-in-class diagnostic option to men with prostate cancer with clear evidence of superiority. We have already seen in the first-in-human PROPELLER trial an improved diagnostic performance of 64Cu-SAR-bisPSMA compared to 68Ga-PSMA-11 on same-day imaging, including a higher number of lesions identified and 2-3 times higher tumour uptake and tumour-to-background ratio5. We then showed in the COBRA trial that approximately twice the amount of lesions was identified on 64Cu-SAR-bisPSMA PET on next-day vs. same-day imaging, and vs. SOC PSMA PET2. 64Cu-SAR-bisPSMA also allowed for the identification of lesions in the 2-mm range, something that SOC PSMA PET agents often fail to achieve2, 6-9. This improvement was driven by a substantially increased tumour-to-background ratio and lesion uptake over time with next-day imaging2.

"The current market for PSMA PET imaging in the US alone is around US$2 billion per year, and this is expected to further grow to over US$3 billion by 2029. However, this entire market is currently served by products that have low sensitivity, while the development pipeline of new products, excluding 64Cu-SAR-bisPSMA, offers no differentiation from the existing agents, with some new entrants commercialising the unpatented 68Ga-PSMA-11 agent, which has been capitalised on by three separate groups already. We believe that with the clinical and logistical benefits offered by 64Cu-SAR-bisPSMA we could not only become the new SOC in PSMA PET but grow the market opportunity further by diagnosing prostate cancer earlier, while lesions are still very small.

"We look forward to continuing to work with Prof Emmett, a world-renowned thought leader in the radiopharmaceutical space, in our home city of Sydney on progressing clinical development of the 64Cu-SAR-bisPSMA product, including our CLARIFY and AMPLIFY Phase III trials. This partnership will ensure we continue to generate the highest quality of data supporting our New Drug Applications (NDAs) to the US Food and Drug Administration (FDA) as the next step towards our mutual goal of improving treatment outcomes for men with prostate cancer."

(Press release, Clarity Pharmaceuticals, OCT 14, 2025, View Source [SID1234656623])

On October 14, 2025 Nusano, a physics company transforming the production of radioisotopes, and Ariceum Therapeutics (Ariceum), a targeted radiotherapeutics company dedicated to setting new standards in cancer care, reported the signing of a multi-isotope supply agreement to support Ariceum’s novel radiotherapeutic pipeline.

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The agreement gives Ariceum access to Nusano-produced radioisotopes, including actinium-225 (Ac-225) and lutetium-177 (Lu-177).

"Radiotherapeutics have the potential to redefine the standard of care in oncology," said Manuel Sturzbecher-Höhne, Chief Technology Officer of Ariceum Therapeutics. "This agreement further strengthens our ability to advance 225Ac-SSO110, which is currently being investigated in a Phase 1/2 trial in patients with extensive-stage small cell lung cancer and Merkel cell carcinoma. Reliable access to actinium-225 ensures we can deliver on our commitment to developing transformative therapies for patients facing these aggressive and underserved cancers."

The Nusano radioisotope production platform combines time-proven technology from universities and world-class research centers with the company’s patented particle acceleration technology. The result is the first significant advancement in radioisotope production in decades – a platform that’s smaller and more efficient than existing methods, and capable of the simultaneous manufacturing of up to 12 different radioisotopes.

"Nusano’s production capabilities are designed to stabilize supply chains and enable innovation," said Chris Lowe, CEO of Nusano. "Our scalable production allows us to work with drug developers from the earliest stages through commercial drug availability. We look forward to working with Ariceum on their current and future therapeutic candidates."

(Press release, Nusano, OCT 14, 2025, View Source [SID1234656644])