On October 17, 2025 ClearNote Health, a company focused on improving early detection for some of the deadliest cancers, reported a lineup of presentations at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress 2025 in Berlin taking place October 17-21, 2025. Meeting attendees can review the following presentations to learn about ClearNote Health’s innovative early cancer detection technology and latest clinical research success.

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"ClearNote Health looks forward to meeting with the ESMO (Free ESMO Whitepaper) community and presenting the significant advances we’ve achieved in early cancer detection and therapy monitoring through epigenomics." – Samuel Levy, PhD, Chief Scientific Officer, ClearNote Health

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"ClearNote Health looks forward to meeting with the ESMO (Free ESMO Whitepaper) community and presenting the significant advances we’ve achieved in early cancer detection and therapy monitoring through epigenomics," said Samuel Levy, PhD, Chief Scientific Officer at ClearNote Health. "Our highly sensitive, noninvasive Avantect Pancreatic Cancer and Multi-Cancer Tests are designed to detect the biological signals of cancer at its earliest stages, when patients are most likely to benefit from treatment. In addition, our Virtuoso platform empowers clinicians and researchers to quantify therapy response and provide prognostic insights into patient outcomes."

Featured Presentations

Scientific Posters
Validation of an epigenomic-based multicancer detection test
Presenter: Stephen R. Quake, Stanford University
Presentation Number: 1745P

Evaluation of a cell-free DNA-based blood test for early detection of pancreatic cancer in high-risk individuals with family history and genetic predisposition
Presenter: Randall Brand, University of Pittsburgh
Presentation Number: 2245P

SAFE-D trial design: Targeted pancreatic cancer surveillance to evaluate resectability rate and stage shift in patients with new onset diabetes
Presenter: Victoria Goss, Southampton Clinical Trials Unit
Presentation Number: 2255TiP

e-Posters
Epigenomic Multicancer Detection Algorithms Capture Disease Biomarkers through Machine Learning
Presenter: Stephen R. Quake, Stanford University
Presentation Number: 1783eP

Epigenomic cancer detection and the relationship with circulating tumor allele fraction
Presenter: Zaed Hamady, University Hospital Southampton
Presentation Number: 246eP

Epigenomic measurement of tumor fraction contributions to cfDNA in a multicancer test
Presenter: Martin Sjöström, Lund University
Presentation Number: 212eP

Epigenomic liquid biopsy for quantification of platinum and PARP inhibitor response in patients with germ line BRCA-associated PDAC
Presenter: Talia Golan, Sheba Medical Center
Presentation Number: 2270eP

(Press release, ClearNote Health, OCT 17, 2025, View Source [SID1234656759])

On October 17, 2025 Parabilis Medicines, a clinical-stage biopharmaceutical company committed to creating extraordinary medicines for people living with cancer, reported at the ESMO (Free ESMO Whitepaper) Congress 2025 the first-ever clinical data showing that its investigational FOG-001 therapy has successfully drugged β-catenin:TCF – a key cancer-driving node in the Wnt/β-catenin pathway, until now considered "undruggable."

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In the ongoing Phase 1/2 trial of FOG-001 in patients with a range of Wnt/β-catenin-driven tumors, as of mid-August 2025, 12 patients with desmoid tumors had been dosed across three dose levels. Of the 10 patients who had at least one post-baseline scan, tumor reductions were observed at all dose levels with a 100% disease-control rate (DCR). Of the five patients with more than one post-baseline scan, an objective response rate (ORR) of 80% (4/5) was observed, per RECIST 1.1. Responses were seen in both gamma secretase-naive and –treated patients, and FOG-001 demonstrated clinically meaningful anti-tumor activity alongside acceptable safety and tolerability profiles.

FOG-001 achieves its effect by blocking the interaction between β-catenin and the T-cell factor (TCF) family of transcription factors, the key driver of tumorigenesis in Wnt pathway-activated cancer cells. The data support further development of FOG-001 in patients with desmoid tumors, and suggest that FOG-001, unlike other available therapies for this disease, directly addresses the underlying mechanism of disease through inhibition of β-catenin.

"For decades, scientists had said that the Wnt/β-catenin:TCF interaction couldn’t be drugged, but our data prove otherwise," said Mathai Mammen, M.D., Ph.D., Chairman, CEO and President of Parabilis Medicines. "FOG-001 shows what bold science can achieve — taking on one of cancer’s most important drivers and opening the door to an entirely new class of therapies. This milestone validates the power of Parabilis’s distinctive Helicon peptides and marks an important step forward in our mission to create extraordinary medicines for patients."

The Wnt/β-catenin pathway was first identified over 30 years ago as a fundamental driver of cancer and is implicated in millions of cases each year, across both common cancers — including gastrointestinal cancers like colorectal, hepatocellular, and gastric cancers — as well as many rare cancers such as desmoid tumors and adamantinomatous craniopharyngioma (ACP). Attempts to target the β-catenin:TCF interaction, the key downstream node within the Wnt pathway, have repeatedly failed until now with FOG-001.

Parabilis’s Helicon platform has overcome limitations of traditional small molecule therapeutics by designing stabilized α-helical peptides that gently penetrate cells and bind tightly to proteins with relatively flat binding surfaces. With FOG-001, Parabilis has achieved what decades of cancer research could not: directly drugging the "undruggable" β-catenin:TCF interaction.

Beyond ESMO (Free ESMO Whitepaper), additional clinical data on FOG-001 across a range of Wnt/β-catenin-driven tumors will be presented at several additional upcoming scientific meetings, including the AACR (Free AACR Whitepaper)-NCI-EORTC International Conference on Molecular Targets (October 22-26, Boston, MA), the Connective Tissue Oncology Society (CTOS) 2025 Annual Meeting (November 12-15, Boca Raton, FL), and the Society for Neuro-Oncology (SNO) 2025 Annual Meeting (November 19-23, Honolulu, HI). The company will also share new preclinical data on its allosteric active androgen receptor (ARON) and ERG degrader discovery programs for the treatment of prostate cancer at AACR (Free AACR Whitepaper)-NCI-EORTC and the Prostate Cancer Foundation (PCF) Scientific Retreat (October 23-25, Carlsbad, CA).

Details of the presentations are as follows:

ESMO mini oral information:

Presentation Title: "A Phase 1/2 trial of FOG-001, a first-in-class direct β-catenin:TCF4 inhibitor: Safety and preliminary antitumor activity in patients with desmoid tumors"
Date and Time: Friday, October 17, 2025, 4:00 – 5:30 p.m. CEST
Session: Mini oral session: Sarcoma
Location: Essen Auditorium, Hall 7.2A

AACR-NCI-EORTC oral and poster information:

Title: "A Phase 1/2 trial of FOG-001, a first-in-class direct β-catenin inhibitor, preliminary safety and efficacy in patients with solid tumors bearing Wnt pathway-activating mutations (WPAM+)"
Oral Presentation
Date and Time: Friday, October 24, 2025, 10:00 – 11:40 a.m. EDT
Session: Plenary Session 4: Clinical Trials Plenary Session
Location: Level 3, Ballroom AB
Poster Presentation
Date and Time: Friday, October 24, 2025, 12:30 – 4:00 p.m. EDT
Session: Poster Session B
Location: Level 2, Exhibit Hall D

Poster Title: "Distinct aspects of β-catenin biology drive multiple biologically rational FOG-001 combinations for MSS colorectal cancer"
Date and Time: Saturday, October 25, 2025, 12:30 – 4:00 p.m. EDT
Session: Poster Session C
Location: Level 2, Exhibit Hall D

Poster Title: "Degradation of the ETS transcription factor ERG by stabilized helical peptide (Helicon) degraders enable pharmacological validation in ERG-fusion prostate cancer models"
Date and Time: Friday, October 24, 2025, 12:30 – 4:00 p.m. EDT
Session: Poster Session B
Location: Level 2, Exhibit Hall D

Poster Title: "Discovery of Helicon peptides for the selective degradation of the agonist-bound conformation of androgen receptor (ARON) in prostate cancer"
Date and Time: Friday, October 24, 2025, 12:30 – 4:00 p.m. EDT
Session: Poster Session B
Location: Level 2, Exhibit Hall D

PCF presentation and poster information:

Poster Title: "Discovery of Helicon peptides for the selective degradation of the agonist-bound conformation of androgen receptor (ARON) in prostate cancer"
Date and Time: Thursday, October 23, 2025, 7:30 – 10:30 PM PDT
Location: Costa De La Luna Ballroom

Presentation Title: "Discovery and Optimization of ERG Bifunctional, Stapled Peptide Degraders using Generative AI–Driven Multi-Property Modeling"
Date and Time: Saturday, October 25, 2025, 12:45 – 1:00 PM PDT
Location: Costa Del Sol Ballroom

CTOS poster information:

Poster Title: "A Phase 1/2 trial of FOG-001, a first-in-class direct β-catenin inhibitor: Safety and preliminary antitumor activity in patients with desmoid tumors (DT)"
Date and Time: Thursday, November 13, 2025, 5:30 – 6:30 p.m. EST
Session: Poster Reception: Soft Tissue Tumors

SNO mini oral information:

Presentation Title: "A Phase 1/2 trial of FOG-001, a first-in-class direct β-catenin:TCF4 inhibitor: Safety and preliminary antitumor activity in adamantinomatous craniopharyngioma (ACP) patients"
Abstract Number: CTNI-10
Date and Time: Friday, November 21, 2025, 11:30 – 12:30 p.m. HST
Session: Rapid Orals
Location: Hawaii Convention Center, Kamehameha Exhibit Hall II & III

About the Phase 1/2 trial of FOG-001
FOG-001 is being evaluated in a first-in-human Phase 1/2 multicenter, open-label study (NCT05919264) assessing its safety, tolerability, pharmacokinetics, pharmacodynamics, and antitumor activity. The trial includes dose-escalation and dose-expansion phases and is testing FOG-001 both as a monotherapy and in combination with other anticancer agents in patients with advanced or metastatic solid tumors likely or known to harbor a Wnt pathway–activating mutation (WPAM).

About FOG-001
FOG-001 is an investigational first-in-class competitive inhibitor of β-catenin interactions with the T-cell factor (TCF) family of transcription factors and is currently in clinical development. By directly targeting the β-catenin:TCF protein-protein interaction, FOG-001 is intended to block the Wnt signaling pathway irrespective of the various APC and β-catenin mutations that typically drive disease.

FOG-001 combines key features that distinguish it from previously reported Wnt/β-catenin pathway modulators: FOG-001 acts inside the cell where it binds directly to the key oncogenic driver β-catenin; and FOG-001 blocks the Wnt pathway at the key downstream node, disrupting the interaction between β-catenin and the TCF transcription factors, thereby abrogating the signal transmission by which Wnt pathway mutations are believed to drive oncogenesis.

FOG-001 is currently being evaluated in a first-in-human Phase 1/2 clinical trial in patients with locally advanced or metastatic solid tumors.

(Press release, Parabilis Medicines, OCT 17, 2025, View Source [SID1234656758])

On October 17, 2025 Ono Pharmaceutical Co., Ltd. (Headquarters: Osaka, Japan; President and COO: Toichi Takino; "Ono"), reported the two-year efficacy and safety results from its MOTION Phase 3 study of vimseltinib in patients with TGCT in cases where surgical removal of the tumor is not an option will be presented as a poster during the 2025 European Society for Medical Oncology Congress (ESMO) (Free ESMO Whitepaper), taking place October 17-21 in Berlin, Germany.

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"These long-term Phase 3 MOTION results add to the established body of evidence supporting vimseltinib as a best-in-class treatment for TGCT," said Matthew L. Sherman, M.D., Chief Medical Officer of Deciphera. "TGCT often causes debilitating pain, stiffness and impaired mobility and these results demonstrate the durable benefit that vimseltinib can offer patients."

Summary of Data and Findings from the 2-year results of the MOTION Phase 3 Study

Methods

The global Phase 3 MOTION study (NCT05059262) aims to evaluate the efficacy and safety of vimseltinib for the treatment of TGCT in cases where surgical removal of the tumor is not an option.

The study consists of two parts. In Part 1, eligible study participants were assigned to receive either vimseltinib or matching placebo for 24 weeks. Participants assigned to placebo in Part 1 had the option to receive vimseltinib for Part 2. Part 2 was a long-term treatment phase in which all participants received open-label vimseltinib. Patients received vimseltinib 30 mg twice weekly in all periods. Objective response rate (ORR) based on best overall response was assessed by independent radiological review (IRR) per Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v1.1) and per Tumor Volume Score (TVS). Duration of response (DOR) and safety were also evaluated.

Efficacy

In these two-year results from the MOTION Phase 3 trial, vimseltinib continued to demonstrate robust and durable antitumor efficacy with a manageable safety profile that was consistent with prior reports. These long-term results support vimseltinib as a treatment option for patients with TGCT associated with clinically relevant physical function deterioration and in whom surgical options have been exhausted or would induce unacceptable morbidity or disability, where it is approved. These results are reported with two years of follow-up in patients randomized to vimseltinib in Part 1 and crossed over from placebo to vimseltinib in Part 2. The data cutoff for this analysis was February 22, 2025.

In total, 118 patients received vimseltinib. At data cutoff, 51% (60/118) remained on treatment. With at least 2 years of follow-up, results demonstrate robust and durable antitumor activity with vimseltinib per RECIST v1.1 and per TVS, including in patients who crossed over to vimseltinib in Part 2.

Of 83 patients randomized to vimseltinib in Part 1, 73 continued open-label treatment in Part 2. Median (range) treatment duration was 23.6 months (2 to 36).
Of the 40 patients randomized to placebo in Part 1, 35 crossed over to vimseltinib in Part 2. Median treatment duration for this group was 19.1 months (1 to 30).
ORR on study per RECIST v1.1 was 48% (40/83) for patients randomized to vimseltinib and 54% (19/35) for those who crossed over to vimseltinib. ORR on study per TVS was 81% (67/83) for patients randomized to vimseltinib and 71% (25/35) for those who crossed over to vimseltinib.
The corresponding median DOR per RECIST v1.1 and per TVS was still not reached.
Safety

Vimseltinib continued to have a manageable safety profile that was consistent with prior reports with no new safety signals.

Most treatment-emergent adverse events (TEAEs) were grade 1/2, and grade 3/4 TEAEs were similar between randomized vimseltinib and crossover groups.
There were no new TEAEs in ≥15% of patients receiving vimseltinib and no new serious adverse events in more than one patient.
Serum enzyme elevations were consistent with the known mechanism of action of CSF1R inhibition, and there was no evidence of cholestatic hepatotoxicity or drug-induced liver injury.
About Vimseltinib

Vimseltinib is an oral, switch-control tyrosine kinase inhibitor specifically designed to selectively and potently inhibit CSF1R. Vimseltinib has been developed using Deciphera’s proprietary switch-control kinase inhibitor platform. It has been approved in the United States for adult patients with symptomatic TGCT for which surgical resection will potentially cause worsening functional limitation or severe morbidity, and in the European Union for adult patients with TGCT associated with clinically relevant physical function deterioration and in whom surgical options have been exhausted or would induce unacceptable morbidity or disability.

About Tenosynovial Giant Cell Tumor (TGCT)

TGCT is caused by a dysregulation in colony-stimulating factor 1 (CSF1) gene leading to overproduction of CSF1 and recruitment of colony-stimulating factor 1 receptor (CSF1R)-positive inflammatory cells into the lesion.1 TGCT is also known as giant cell tumor of the tendon sheath (GCT-TS) or pigmented villonodular synovitis (PVNS). TGCT is a rare, locally aggressive neoplasm that can grow and cause damage to surrounding tissues and structures inducing pain, swelling, and limitation of movement of the joint. Surgery is the main treatment option; however, these tumors tend to recur, particularly in diffuse-type TGCT. If untreated or if the tumor continually recurs, damage and degeneration may occur in the affected joint and surrounding tissues, which may cause significant disability. For a subset of patients, surgical resection will potentially cause worsening functional limitation or severe morbidity. Systemic treatment options are limited and new therapeutic options are needed.

(Press release, Ono, OCT 17, 2025, View Source [SID1234656755])

On October 17, 2025 Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd. (the "Company") reported that the Company’s human epidermal growth factor receptor 2 (HER2)-directed antibody-drug conjugate (ADC) trastuzumab botidotin (also known as A166) was approved for marketing by the National Medical Products Administration (NMPA) for the treatment of adult patients with unresectable or metastatic HER2-positive breast cancer (BC) who have received one or more prior anti-HER2 therapy.

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The approval is based on a multi-center, randomized, open-label, controlled, Phase 3 KL166-III-06 study that evaluates the efficacy and safety profile of trastuzumab botidotin versus T-DM1 in patients with HER2-positive unresectable or metastatic BC who have received prior trastuzumab and taxane-containing regimens. At a pre-specified interim analysis, trastuzumab botidotin monotherapy demonstrated a statistically significant and clinically meaningful improvement in the primary endpoint of progression-free survival (PFS) as assessed by the blinded independent central review (BICR) compared with T-DM1; the beneficial trend for overall survival (OS) of trastuzumab botidotin was also observed. Results from this study will be presented as an oral report at the 2025 European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress held in Berlin, Germany (Presentation # LBA24, Proffered paper session 1: Breast cancer, metastatic).

The Company has initiated an open, multi-center Phase 2 clinical study of trastuzumab botidotin in the treatment of HER2+ unresectable or metastatic BC that previously received a topoisomerase inhibitor ADC.

Dr. Michael Ge, CEO of Kelun-Biotech said, "We are thrilled to see our first HER2 ADC drug, trastuzumab botidotin, successfully approved for market. This marks a significant advancement in the treatment of HER2-positive breast cancer. As China’s first domestically developed HER2 ADC capable of broadly covering 2L+ HER2 BC patients, trastuzumab botidotin leverages its differentiated structural design to deliver superior efficacy while addressing unmet clinical needs in this population."

About HER2+ BC

Breast cancer, as the most common malignant tumor, poses a serious threat to women’s health. Among its subtypes, HER2-positive breast cancer accounts for approximately 15%–20% of all breast cancer cases[1], and is characterized by its aggressiveness and high malignancy. According to the 2025 CSCO guidelines, first-line treatment for HER2-positive breast cancer primarily consists of trastuzumab and pertuzumab in combination with taxane-based chemotherapeutic agents. Second-line treatment regimens comprise tyrosine kinase inhibitors (TKIs, such as pyrotinib) and antibody-drug conjugates (ADCs, such as T-DM1 and T-DXd). Following disease progression on second-line therapy, subsequent treatment strategies are determined based on prior second-line regimens, the patient’s tolerance to therapy, tumor burden, and other relevant factors. Despite recent advances in anti-HER2 therapeutics, a significant number of patients still experience drug resistance or severe adverse effects, highlighting an urgent need for agents with improved safety profiles to address the treatment requirements of patients with recurrent or drug-resistant HER2-positive breast cancer.

A bout trastuzumab botidotin

Trastuzumab botidotin is a differentiated HER2 ADC to treat advanced HER2+ solid tumors. As an innovative HER2 ADC developed by the Company, it conjugates a novel, monomethyl auristatin F (MMAF) derivative (a highly cytotoxic tubulin inhibitor, Duo-5) via a stable, enzyme-cleavable linker to a HER2 monoclonal antibody with a drug-to-antibody-ratio (DAR) of 2. Trastuzumab botidotin specifically binds to HER2 on the surface of tumor cells and is internalized by tumor cells, releasing the toxin molecule Duo-5 inside the cell. Duo-5 induces tumor cell cycle arrest in the G2/M phase, leading to tumor cell apoptosis. After targeting HER2, trastuzumab botidotin can also inhibit the HER2 signaling pathway; it has antibody-dependent cell-mediated cytotoxicity (ADCC) activity.

(Press release, Kelun, OCT 17, 2025, View Source [SID1234656754])

On October 17, 2025 Marengo Therapeutics, Inc., a clinical-stage biotechnology company pioneering precision immunotherapies for oncology and inflammation & immunology (I&I), reported the first disclosure of interim data from the ongoing Phase 2 trial of its lead program, invikafusp alfa, during a late-breaking oral session at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) 2025 Annual Meeting, taking place October 17-21, 2025, in Berlin, Germany.

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These highly anticipated results continue to validate Marengo’s first-in-class precision T cell activation platform – a novel approach aimed at fully addressing the significant unmet need for both PD-1 resistant and refractory patients, as well as those for whom PD-1 therapy is not currently indicated.

"The compelling single-agent activity and tumor regression we’re observing across multiple tumor types, particularly in PD-1-resistant tumors, underscore the potential of invikafusp alfa as a new pan-tumor backbone immunotherapy," said Zhen Su, M.D., MBA, Chief Executive Officer of Marengo Therapeutics. "By selectively activating Vβ6/Vβ10 T-cell subsets, we are unlocking distinct immune biology that can reprogram the tumor microenvironment and reinvigorate anti-tumor T cell responses in patient populations who have exhausted current immunotherapies."

As of the July 29, 2025 data cutoff, 55 patients with advanced solid tumors harboring high mutational burden (TMB-H or MSI-H/dMMR) were enrolled across 21 histologies; 44 were efficacy-evaluable. Additional outcomes from the Phase 2 study are outlined below.

Tumor shrinkage: 52% of patients experienced target-lesion regression.
In the TMB-H patients, there was a 20.5% overall response rate (ORR) (9/44) and a 79.5% disease control rate (DCR) (35/44) across six tumor types, including colorectal, gastric, lung, breast, GEJ, and head and neck cancers.
In the MSI-H/dMMR patients, there was a 30% ORR (3/10) and 70% DCR (7/10).
Clinical efficacy was observed in PD-1-resistant/refractory tumors and PD-1 naive tumors where PD-1 was not approved as standard of care, confirming PD-1-independent activity.
The safety profile was consistent with selective T cell activation mechanism of action, and treatment-related AEs were transient and manageable with supportive care.
Building on these clinical data, Marengo is advancing a post-PD-1, biomarker-enriched strategy for invikafusp alfa – continuing the Phase 2 monotherapy expansion in TMB-H or MSI-H/dMMR solid tumors to further characterize the depth and durability of responses across priority indications. In parallel, Marengo is pursuing ongoing regulatory interactions, including recently securing U.S. FDA Fast Track designation in TMB-H mCRC.

To reach broader, frontline populations beyond biomarker TMB-H in large indications, the company is also progressing a Phase 2 combination with Trodelvy (TROP2-directed ADC) in TNBC and HR+/HER2– breast cancer to evaluate synergy in ADC and IO settings.

Invikafusp alfa is a first-in-class, bispecific dual T-cell agonist designed to selectively activate and expand Vβ6/Vβ10 T-cell subsets, which represent ~10% of tumor-infiltrating lymphocytes (TILs). Marengo’s lead asset was designed to restore and amplify anti-tumor immunity in patients who have progressed on or are insensitive to prior immune checkpoint blockade, and it has demonstrated rapid progress to date. Phase 1/2 results of the STARt-001 clinical trial evaluating invikafusp alfa in antigen-rich solid tumors were first presented at SITC (Free SITC Whitepaper) 2024, followed by disclosure of the recommended Phase 2 dose (RP2D) selection rationale and early clinical activity at AACR (Free AACR Whitepaper) 2025.

(Press release, Marengo Therapeutics, OCT 17, 2025, View Source;resistant-solid-tumors-as-a-late-breaking-oral-presentation-at-esmo-2025-302587142.html [SID1234656753])