On October 15, 2025 Amphista Therapeutics ("the Company" or "Amphista"), a leader in the discovery of next generation Targeted Protein Degradation (TPD) medicines, reported the nomination of AMX-883; a potent, selective and orally bioavailable degrader of BRD9, as its first clinical development candidate. Amphista is advancing AMX-883 for the treatment of acute myeloid leukaemia (AML).

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Leveraging Amphista’s Eclipsys platform and proprietary Targeted Glue technology, AMX-883 induces the degradation of BRD9 via induction of the E3 ligase DCAF16, a completely novel mechanism, distinct from CRBN and VHL-based technologies. AMX-883 is a highly potent and rapid degrader, inducing almost complete degradation of BRD9 within just two hours of treatment, whilst retaining exquisite selectivity over all other bromodomain containing proteins, and beyond, as illustrated by global proteomics. This profile translates into robust in vivo efficacy, including in disseminated patient derived xenograft models. Amphista plans to initiate its first clinical trial with AMX-833 in the second half of 2026.

"Nominating AMX-883 as our first clinical candidate, marking the first time a BRD9 degrader has been developed in AML, is a key milestone for Amphista and the TPD field. Our preclinical data package underlines the fundamental role BRD9 plays in the pathogenesis of AML. AMX-883 has the potential to transform the treatment paradigm for this terrible disease, where 5-year survival rates remain at just 33% and is the cause of death for an estimated 130,000 patients globally each year. As a broad-acting, pro-differentiation agent, AMX-883 has the potential to treat AML in a karyotype-independent way, bringing benefit to a larger patient population than current treatments." commented Martin Pass, Chief Development Officer at Amphista.

The nomination of AMX-883 triggers the drawdown of the third tranche of Amphista’s Series B financing, enabling the continued progression of the Company’s portfolio of next generation Targeted Glue therapeutics towards clinical stage development.

Antony Mattessich, Chief Executive Officer at Amphista, said: "We have built a truly unique discovery platform in Eclipsys, which offers the opportunity to deliver advanced protein degraders with performance characteristics beyond what has been achievable with earlier generation approaches. The nomination of AMX-883 as our first development candidate is a testament to our capabilities and we now look forward to filing an IND application in early 2026."

This news follows an announcement in May 2024 when Amphista unveiled its discovery of a new differentiated mechanism of action for BRD9 degradation. This year, the Company also unveiled a new mechanism of action for TEAD degradation via FBXO22, and for SMARCA2 degradation via induction E3 ligase DCAF16.

About BRD9 and Acute Myeloid Leukaemia

Acute myeloid leukaemia (AML) is one of the most aggressive blood cancers and despite the availability of anti-proliferative treatments, patient survival rates remain alarmingly low. The disease is characterized by a differentiation block which prevents myeloid cell maturation and results in an accumulation of immature cells/AML blasts. Therapies which remove the differentiation block and allow maturation of these AML blasts including ATRA, FLT-3 inhibitors, and most recently Menin inhibitors have demonstrated clinical benefit in several sub-sets of AML. However, there is a pressing need for broader-acting treatments that can benefit patients regardless of their genetic profile.

BRD9 is a subunit of the non-canonical BAF complex where it plays a key structural and functional role, being linked to regulation of chromatin structure and maintaining genomic stability in AML. Degradation of BRD9 releases the differentiation block and leads to the differentiation and death of AML blasts

(Press release, Amphista Therapeutics, OCT 15, 2025, View Source [SID1234656671])

On October 15, 2025 Novocure (NASDAQ: NVCR) reported that it will present data at two upcoming oncology congresses, the 2025 European Association of Neuro-Oncology (EANO) Meeting, being held October 16-19 in Prague, Czech Republic, and the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Congress 2025, being held October 17-21 in Berlin, Germany.

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At the EANO 2025 Meeting, Novocure will present pre-clinical data highlighting the potential of Tumor Treating Fields (TTFields) therapy to enhance radiosensitivity of glioblastoma cells by downregulating DNA repair pathways.

At the ESMO (Free ESMO Whitepaper) Congress 2025, Novocure will present a post-hoc analysis of its successful Phase 3 PANOVA-3 trial, which evaluated the use of TTFields therapy concomitantly with gemcitabine and nab-paclitaxel (GnP) as a first-line treatment for adults with unresectable, locally advanced pancreatic adenocarcinoma, compared to GnP alone. The post-hoc analysis assessed the efficacy of TTFields therapy based on daily device usage as well as levels of cancer antigen (CA) 19-9.

Data at the EANO 2025 Meeting

Poster: P18.24.B​: Short exposure to TTFields induces DNA repair pathway downregulation and radiosensitization in glioblastoma cells​

Presenting Author: Anat Klein-Goldberg, Novocure​, Ltd., Haifa, Israel

Date/Time: Saturday, October 18, 5:00-6:30 PM CEST, ​ Forum Hall Foyer 3​

Data at the ESMO (Free ESMO Whitepaper) Congress 2025

Poster: 2235P: Phase 3 study of TTFields in locally advanced pancreatic adenocarcinoma (PANOVA-3): post-hoc subgroup analyses based on device usage and CA 19-9

Presenting Author: Hani Babiker, MD, Mayo Clinic, Jacksonville, FL

Date/Time: Sunday, October 19, 12:00-12:45 PM CEST, Hall 25

About Tumor Treating Fields

Tumor Treating Fields (TTFields) are electric fields that exert physical forces to kill cancer cells via a variety of mechanisms. TTFields do not significantly affect healthy cells because they have different properties (including division rate, morphology, and electrical properties) than cancer cells. These multiple, distinct mechanisms work together to target and kill cancer cells. Due to these multimechanistic actions, TTFields therapy can be added to cancer treatment modalities in approved indications and demonstrates enhanced effects across solid tumor types when used with chemotherapy, radiotherapy, immune checkpoint inhibition, or targeted therapies in preclinical models. TTFields therapy provides clinical versatility that has the potential to help address treatment challenges across a range of solid tumors.

To learn more about TTFields therapy and its multifaceted effect on cancer cells, visit tumortreatingfields.com.

(Press release, NovoCure, OCT 15, 2025, View Source [SID1234656687])

On October 15, 2025 Aprea Therapeutics, Inc. (Nasdaq: APRE) ("Aprea", or the "Company"), a clinical-stage biopharmaceutical company developing innovative treatments that exploit specific cancer cell vulnerabilities while minimizing damage to healthy cells, reported that it has determined the recommended Phase 2 dose (RP2D) of 1,100 mg once daily for ATRN-119, its oral ATR inhibitor in the monotherapy arm of the ongoing ABOYA-119 Phase 1/2a dose-escalation study, in patients with advanced solid tumors.

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ATR program

Building on the completion of dose escalation and supported by new preclinical data suggesting potential synergistic anti-tumor effects, Aprea is considering further ATRN-119 development in combination approaches that could expand its therapeutic potential. The Company believes ATRN-119’s mechanism of action, favorable safety profile, and pharmacologic characteristics make it an ideal candidate for combination with DNA-damaging agents, including radiation therapy, antibody-drug conjugates and immune checkpoint inhibitors.

As part of this strategic focus, Aprea is pausing further enrollment in both once daily and twice daily monotherapy dosing arms of ABOYA-119. Importantly, patients currently being dosed with ATRN-119 as part of this ongoing clinical trial will continue to have access to therapy without interruption.

The Company is currently in discussions with leading academic centers to explore combining ATRN-119 with radiation in patients with HPV+ head and neck cancer, an indication where synergistic anti-tumor effects have been observed in preclinical data. Additional investigator-led studies evaluating ATRN-119 in combination with an I/O agent and antibody-drug conjugates, are also being explored, based on preclinical evidence that ATR inhibition may enhance anti-tumor immune responses.

Phase 1 monotherapy data in the ABOYA-119 dose-escalation study, ATRN-119 demonstrated:

Favorable tolerability profile with manageable adverse events at the RP2D of 1100 mg once daily
Durable disease stabilization in heavily pretreated patients across multiple tumor types
Dose-proportional pharmacokinetics supporting once-daily dosing
Preliminary signs of clinical activity in biomarker-selected populations
"We are very pleased to have identified the recommended monotherapy Phase 2 dose for ATRN-119, which is an important step in our transition to the next stage of development," said Oren Gilad, Ph.D., President and Chief Executive Officer of Aprea. "Based on the growing body of evidence supporting ATR inhibition as a potent sensitizer to DNA-damaging therapies and immunotherapy, we are now considering ATRN-119 in combination approaches that we believe could expand its clinical impact. We believe this candidate’s mechanism, safety profile, and pharmacologic characteristics make it a compelling candidate for pairing with other anti-cancer therapies, including radiation or checkpoint inhibitors, where synergistic anti-tumor effects have been demonstrated preclinically."

A poster titled Updated data from ABOYA-119: A phase 1/2a trial of ATRN-119, a novel macrocyclic ATR inhibitor, in patients with advanced solid tumors harboring DNA damage will be presented at the forthcoming AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) on Friday, October 24, 2025.

WEE1 Program

Aprea continues to advance its lead program, WEE1 kinase inhibitor APR-1051 at full speed. The ongoing Phase 1, first-in-human study (NCT06260514) is actively enrolling patients at three leading clinical sites in the United States. To date, patients with advanced solid tumors harboring specific cancer-associated gene alterations have been treated with APR-1051 at doses up to 150 mg once daily. Early signals of clinical benefit, including disease stabilization in multiple patients, have been observed, supporting continued dose escalation and further clinical evaluation of APR-1051. The Company expects to report clinical data from this study later this month at the AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) and is planning to further explore safety, pharmacokinetics, and signals of antitumor activity.

(Press release, Aprea, OCT 15, 2025, View Source [SID1234656672])

On October 15, 2025 OncoNano Medicine, Inc. ("OncoNano") reported a late-breaking research poster presentation at the EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium on Molecular Targets and Cancer Therapeutics, to take place in Boston, Massachusetts, October 22 – 26, 2025. Details on the posters are below.

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Presentation Details

Title:

Results from part-1 of ON-5001: a multi-center, dose escalation and dose finding Phase 1 trial of ONM-501, a dual-acting STING agonist, alone or in combination with cemiplimab in patients with solid tumors and lymphoma

Session:
Poster Session A

Date & Time:
Thursday, October 23, 12:30-4 pm

About ONM-501

ONM-501 is a dual-activating agonist of the stimulator of interferon gene ("STING") pathway composed of cGAMP (the endogenous activator of STING) linked to a proprietary pH-activated polymer (the OMNI polymer). ONM-501 is presently being studied in a Phase 1 clinical trial (ON-5001). In preclinical models, the dual activation of STING by ONM-501has been shown to lead to direct anti-tumor effect, as well as leading to an anti-tumor immune response over an extended period of time. Development of ONM-501 was funded in part by the Cancer Prevention and Research Institute of Texas.

(Press release, OncoNano Medicine, OCT 15, 2025, View Source [SID1234656688])

On October 15, 2025 OSE Immunotherapeutics reported its consolidated financial results for the first half of 2025.

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(Press release, OSE Immunotherapeutics, OCT 15, 2025, View Source [SID1234661838])