On October 14, 2025 Pilatus Biosciences Inc., a biopharmaceutical company developing novel metabolic checkpoint immunotherapies for liver and gastrointestinal cancers, reported the granting of its foundational patent in Europe and Australia, entitled "Methods for Modulating Regulatory T Cells and Inhibiting Tumor Growth."

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Pilatus has an exclusive license on the patent from the Ludwig Institute for Cancer Research Ltd and the University of Lausanne, Switzerland, based on work by Dr. Ping-Chih Ho’s laboratory at the Ludwig Lausanne Branch. The patent covers Pilatus’ first-in-class antibody program targeting CD36, a key metabolic checkpoint expressed on regulatory T cells (Tregs) that play a critical role in suppressing anti-tumor immune responses.

This intellectual property milestone provides broad protection for the company’s pioneering work in Treg modulation through metabolic reprogramming, representing a new therapeutic strategy in immuno-oncology.

Tregs are essential for maintaining immune balance but can also enable tumor immune evasion by suppressing effector T cell activity within the tumor microenvironment. CD36, a fatty acid transporter highly expressed on Tregs acts as a metabolic gatekeeper that supports their survival and suppressive function under hypoxic and nutrient-deprived tumor conditions.

Pilatus’ antibody program is designed to disrupt CD36-mediated lipid uptake and signaling in Tregs, thereby reawakening the immune system’s ability to attack tumors without triggering systemic autoimmunity. This approach builds upon discoveries made in the laboratory of Dr. Ping-Chih Ho, Full Member at LICR Lausanne, and forms the scientific foundation for Pilatus’ proprietary pipeline of metabolic checkpoint inhibitors.

Nobel Prize Underscores the Field’s Importance

This announcement comes at a particularly timely moment: the 2025 Nobel Prize in Physiology or Medicine was awarded for groundbreaking discoveries in Regulatory T cell biology, underscoring the growing recognition of immune regulation as a cornerstone of modern medicine.

In fact, one of this year’s Nobel Laureates, Prof. Shimon Sakaguchi, the discoverer of Tregs, was a recent keynote speaker at the Ho Lab anniversary symposium in Lausanne, where he presented on "Targeting Tregs for Cancer Immunotherapy."

"The recognition of Treg biology by the Nobel Committee highlights the importance of immune regulation in health and disease," said Dr. Ping-Chih Ho, Co-Inventor and Full Professor and member at the Ludwig Institute for Cancer Research at University of Lausanne. "Our CD36 discoveries bridge metabolic control and immune suppression, paving the way for transformative treatments in oncology and beyond."

"This patent issuance solidifies Pilatus’ leadership position in metabolic checkpoint immunotherapy," said Raven Lin, Ph.D., Co-Founder and CEO, Pilatus Biosciences. "By targeting the metabolic dependencies of regulatory T cells, we are developing a new class of therapies designed to unlock potent and durable anti-tumor immunity, while demonstrating synergistic potential with PD-1 blockade to benefit patients with difficult to treat cancers."

(Press release, Pilatus Biosciences, OCT 14, 2025, View Source [SID1234656660])

On October 14, 2025 Synnovation Therapeutics, a precision medicine company focused on the discovery and development of best-in-class targeted medicines, reported that it will be presenting the initial results from a Phase 1 Trial of SNV1521, a next-generation, CNS-penetrant PARP1-selective inhibitor, at the 2025 Annual Meeting of the European Society for Medical Oncology in Berlin, Germany.

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"We look forward to sharing the first clinical dataset for our PARP-1 selective inhibitor, SNV1521, with the scientific community in Berlin," said Kevin O’Hayer, M.D., Ph.D., Senior Vice President, Head of Clinical Development at Synnovation. "We have generated encouraging anti-tumor activity and a differentiated safety and PK profile that supports best-in-class potential and further development as a monotherapy and in combination with novel targeted and cytotoxic agents."

Patricia LoRusso, D.O, Ph.D, Associate Center Director for Innovative Medicine at Yale Cancer Center, will present the initial results on Friday, October 17, 2025. The details of the presentation are below:

Oral Presentation:

Title:

First results from a phase 1 trial of SNV1521, a next generation, CNS-penetrant, PARP1-selective inhibitor in patients (pts) with molecularly selected advanced solid tumors (Abstract #923MO)

Presenter:

Patricia LoRusso, DO, PhD

Details:

Developmental Therapeutics Mini Oral Session

Friday, October 17, 2025; Heidelberg Auditorium

10:25 – 10:30 AM EST (4:25 – 4:30 PM CET)

"PARP1 selective agents offer the promise of delivering effective PARP inhibition while mitigating the hematologic and GI toxicity associated with first generation PARP inhibitors," said Patricia LoRusso, D.O., Ph.D., Associated Center Director for Innovative Medicine at Yale Cancer Center. "By optimizing PARP1 selectivity and potency, SNV1521 has the potential to emerge as a best-in-class agent with a differentiated safety profile compared to standard of care and PARP inhibitors in development."

Synnovation also announced a clinical collaboration with DualityBio to evaluate the combination of SNV1521 with Duality’s HER3-directed antibody-drug conjugate (ADC), DB-1310. DB-1310 is a novel ADC targeting HER3 developed using DualityBio’s proprietary DITAC platform. In June 2025, Dr. Aaron E. Lisberg from the University of California, Los Angeles (UCLA) presented the first-in-human Phase I/IIa clinical trial data (NCT05785741) of DB-1310 in an oral session at the 2025 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting. The results demonstrated encouraging efficacy and a manageable safety profile in patients with advanced solid tumors who had failed standard therapies.

"The combination of cytotoxic agents with PARP inhibitors has shown clear preclinical synergy, however, overlapping hematologic toxicity has so far hindered the successful co-development." said Wenqing Yao, Ph.D., CEO and Co-Founder at Synnovation. "This collaboration provides an exciting opportunity to evaluate the combination of two potentially best-in-class therapies—a heme-sparing, PARP1-selective inhibitor, SNV1521, and the HER3-targeting ADC, DB-1310—with the aim of demonstrating synergistic efficacy and improving patient outcomes".

(Press release, Synnovation Therapeutics, OCT 14, 2025, View Source [SID1234656659])

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 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 Mabwell (688062.SH), an innovative biopharmaceutical company with entire industry chain, reported that its self-developed CDH17-targeting ADC (R&D code: 7MW4911) received IND clearance from the National Medical Products Administration (NMPA) in China to initiate clinical study in patients with advanced solid tumors.

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7MW4911 is an investigational CDH17-targeting ADC developed using Mabwell’s proprietary IDDC platform. Its highly optimized structure integrates three key elements:

– Mab0727: A highly specific CDH17 monoclonal antibody with rapid internalization properties, cross-species (human/monkey) moderate affinity, and minimal off-target binding.

– Novel cleavable linker: Ensures precise payload release in tumor tissues.

– MF-6 payload: A proprietary DNA topoisomerase I inhibitor designed to overcome multidrug resistance (MDR), exhibiting superior plasma stability, controlled drug release, and potent bystander effects.

In July 2025, Mabwell published preclinical data in Cell Reports Medicine ("Overcoming multidrug resistance in gastrointestinal cancers with a CDH17-targeted ADC conjugated to a DNA topoisomerase inhibitor"), demonstrating 7MW4911’s tumor-selective cytotoxicity via CDH17-mediated internalization. Key advantages include:

– Optimized molecular design: Homogeneous drug-to-antibody ratio (DAR=4, >95%) and stable linker confer exceptional plasma stability, while membrane-permeable MF-6 drives potent bystander killing.

– Broad Antitumor Efficacy: Demonstrates robust tumor regression in colorectal, gastric, and pancreatic cancer PDX/CDX models, including tumors with RAS/BRAF mutations and diverse Consensus Molecular Subtypes (CMS).

– MDR resistance: Outperforms MMAE/DXd-based ADCs in ABC transporter-mediated MDR models and reverses tumor progression post-ADC treatment.

– Target versatility: Active even in tumors with low-to-moderate CDH17 expression, expanding potential patient eligibility.

– Favorable safety profile: Limited tissue distribution in mice, controllable pharmacokinetics (moderate half-life, no accumulation), and a wide therapeutic window in cynomolgus monkeys, with no significant toxicity signals.

With this profile, 7MW4911 emerges as a promising therapeutic candidate for advanced gastrointestinal cancers. 7MW4911 has also received IND clearance from US FDA to initiate clinical study in patients with advanced colorectal cancer and other advanced gastrointestinal tumors.

About CDH17

CDH17 is a pan-cancer validated target with restricted expression in normal intestinal epithelium but marked overexpression in gastrointestinal cancers (e.g., colorectal, gastric, pancreatic). Its aberrant expression correlates with tumor metastasis and poor prognosis, positioning it as an ideal therapeutic target.

(Press release, Mabwell Biotech, OCT 14, 2025, View Source [SID1234656656])