On October 22, 2025 Accent Therapeutics, a clinical-stage biopharmaceutical company pioneering a new class of small molecule precision cancer therapies, reported new preclinical data on its two lead programs: the novel KIF18A inhibitor, ATX-295, and the first-in-class DHX9 inhibitor, ATX-559. The company will share the data, which highlight the potential to target key tumor vulnerabilities for selective cancer cell death, 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) (the "Triple Meeting"), being held October 22-26, 2025, in Boston, Massachusetts.

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"The data presented for our KIF18A and DHX9 programs continue to validate the success of our biomarker-driven strategy against challenging, genetically diverse cancers," said Serena Silver, Ph.D., Chief Scientific Officer of Accent Therapeutics. "By precisely targeting the vulnerabilities created by genomic instability, we are excited about the potential of ATX-295 and ATX-559 to address significant unmet needs for patients."

In the presentation entitled "Addressing Novel Oncology Targets for Tumors with Genomic Instability," (Concurrent Session 9, October 25th at 4:45 PM ET) Dr. Silver will discuss the promise of ATX-295 and ATX-559 as precision cancer therapeutics that exploit the genomic instability of cancer cells to effect cancer-selective growth inhibition in vitro and in vivo. She will highlight the potential for KIF18A inhibition by ATX-295 in cancers with high levels of chromosomal instability (CIN) such as ovarian and triple negative breast cancer, and for DHX9 inhibition by ATX-559 in multiple tumor types with high levels of replication stress including dMMR/MSI-H and BRCA alterations.

Additional Poster Presentations
ATX-295 (KIF18A Inhibitor)

Title: Activity of the Novel KIF18A Inhibitor, ATX-295, is Enriched in Whole Genome Doubled Ovarian and TNBC Preclinical Models
Summary: Inhibition of KIF18A by ATX-295 is a compelling strategy for chromosomally unstable cancers, supported by new data identifying whole genome doubling (WGD) as a strong predictive biomarker for tumors such as ovarian cancer and TNBC. This biomarker-driven approach was validated in preclinical models where ATX-295 induced dose-dependent tumor regression in WGD-positive models.
Session Details: October 24th, Session B, 12:30-4:00 PM ET
ATX-559 (DHX9 Inhibitor)

Title: ATX-559, a First-in-Class, Clinical-Stage DHX9 Inhibitor, as a Targeted Therapeutic for Molecularly Defined Tumors with Genomic Instability and Replicative Stress
Summary: Preclinical data show the first-in-class oral DHX9 inhibitor, ATX-559, increases replicative stress and DNA damage, leading to selective cell death in cancers with genomic instability. This activity led to robust, dose-dependent tumor regression in preclinical models with BRCA alterations and microsatellite instability-high (MSI-H).
Session Details: October 24th, Session B, 12:30-4:00 PM ET
About ATX-295
ATX-295 is a potential best-in-class inhibitor for KIF18A, a mitotic kinesin motor protein essential for cell division in select tumors with chromosomal instability. A subset of tumors with an abnormal number of chromosomes (aneuploid), such as those found in ovarian and triple-negative breast cancer (TNBC), are reliant on KIF18A. Treatment with a KIF18A inhibitor leads to rapid cell death in these chromosomally unstable cancer cells while leaving healthy cells with normal numbers of chromosomes unaffected. Accent retains full worldwide rights to the KIF18A program, including ATX-295, which is being evaluated in a Phase 1/2 clinical trial (NCT06799065).

About ATX-559
ATX-559 is a first-in-class potent and selective inhibitor of DHX9, a DNA/RNA helicase that plays a critical role in tumors with high levels of replication stress. Such tumors include those with BRCA loss of function (breast, ovarian), mismatch repair deficient (dMMR) or microsatellite instability-high (MSI-H) cancers (colorectal, endometrial, gastric), and others representing large patient populations with significant unmet medical need. DHX9 is a compelling oncology target as its inhibition exploits key tumor vulnerabilities related to replication, transcription, and the maintenance of genomic stability, resulting in cancer-specific cell death. Accent retains full worldwide rights to ATX-559, currently being evaluated in a Phase 1/2 clinical trial (NCT06625515), and the DHX9 program.

(Press release, Accent Therapeutics, OCT 22, 2025, View Source [SID1234656906])

On October 22, 2025 Myosin Therapeutics, Inc., a clinical-stage biotechnology company developing first-in-class therapies that modulate molecular motor proteins, reported that the U.S. Food and Drug Administration (FDA) has granted Fast Track designation to MT-125 for the treatment of glioblastoma (GBM).

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Fast Track is an FDA program designed to facilitate development and expedite review of drugs that treat serious conditions and address unmet medical needs. This designation benefits patients and drug sponsors by enabling more frequent interactions with the FDA and providing eligibility for rolling review of a marketing application.

"Receiving Fast Track designation validates our conviction that MT-125 has the potential to offer an entirely novel treatment approach to patients with even the most aggressive forms of glioblastoma," said Dr. Courtney Miller, Chief Executive Officer of Myosin Therapeutics. "We are energized by the open communication with the FDA that the Fast Track offers because it will ensure we advance MT-125 as quickly as possible with our patient-centered approach."

MT-125 is a first-in-class dual inhibitor of non-muscle myosin IIA and IIB (NMIIA/IIB). It brings a completely new mechanism of action to a disease where decades of limited progress has built anticipation for genuine therapeutic innovation. By leveraging years of GBM biology research focused on targeting the cellular nanomotor proteins driving tumor cells, MT-125 enables simultaneous tackling of the proliferative and invasive phenotypes of this aggressive primary brain tumor, while improving the efficacy of radiation. A Phase 1/2 trial evaluating safety, pharmacokinetics, and preliminary activity is cleared to proceed (ClinicalTrials.gov: NCT07185880). FDA previously granted Orphan Drug Designation to MT-125 for malignant gliomas, including GBM.

(Press release, Myosin Therapeutics, OCT 22, 2025, View Source [SID1234656905])

On October 22, 2025 Inhibrx Biosciences, Inc. (Nasdaq: INBX) ("Inhibrx" or the "Company"), a clinical-stage biopharmaceutical company focused on developing therapeutics for oncology and rare diseases, reported that it will host a live webcast presentation on Thursday, October 23, 2025 at 1:30 p.m. Pacific Time to provide topline results from the registrational ChonDRAgon study investigating ozekibart (INBRX-109) as a single agent versus placebo in patients with advanced or metastatic, unresectable chondrosarcoma. The Company will also provide an update on the ongoing expansion trials investigating ozekibart in combination with FOLFIRI in late-line colorectal cancer and in combination with irinotecan and temozolomide in refractory Ewing sarcoma.

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Investors may join via the web: View Source or may listen to the call by dialing (1-888-880-3330). Please refer to Inhibrx Biosciences, Inc. or the conference ID 9577647 when calling in. Following the webcast, the presentation may be accessed through a link on the investors section of Inhibrx’s website at View Source The webcast will be available for 60 days following the event. Following the presentation, Inhibrx will update its corporate presentation within the "Investors" section of its website at www.inhibrx.com.

About ozekibart (INBRX-109)
Ozekibart is a precision-engineered, tetravalent death receptor 5 (DR5) agonist antibody designed to exploit the tumor-biased cell death induced by DR5 activation. In January 2021, the FDA granted Fast Track designation to ozekibart for the treatment of patients with metastatic or unresectable conventional chondrosarcoma, and, in November 2021, the FDA granted orphan drug designation to ozekibart for chondrosarcoma.

In June 2021, Inhibrx initiated a randomized, blinded, placebo-controlled, registration-enabling Phase 2 trial of ozekibart in metastatic, unresectable conventional chondrosarcoma.

Additionally, in Phase 1/2 trials, Inhibrx is investigating ozekibart in colorectal cancer in combination with FOLFIRI and Ewing sarcoma in combination with irinotecan/temozolomide, as well as other tumor types.

(Press release, Inhibrx, OCT 22, 2025, View Source [SID1234656904])

On October 22, 2025 Harbour BioMed (HKEX: 02142), a global biopharmaceutical company focused on the discovery and development of novel antibody therapeutics in immunology and oncology, reported positive Phase II clinical data for porustobart (HBM4003), a next-generation, fully human heavy-chain-only anti-CTLA-4 antibody, in combination with tislelizumab, in patients with microsatellite stable (MSS) metastatic colorectal cancer (mCRC).

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The multicenter, open-label Phase II study (NCT05167071) enrolled 24 heavily pretreated patients with non-liver-metastatic (NLM) MSS mCRC. Patients received HBM4003 (0.3 mg/kg) plus tislelizumab (200 mg) every 21 days. The primary efficacy endpoint was objective response rate (ORR) per RECIST 1.1 criteria. The findings showed promising antitumor activity and a manageable safety profile for the combination therapy in this difficult-to-treat population.

Key findings include:

Baseline: All patients (N=24) had received ≥2 prior lines of therapy; 16/24 (66.7%) had lung metastases.
Efficacy: Among the 23 evaluable patients, the combination therapy achieved:
Objective Response Rate (ORR): 34.8% (8 partial responses)
Disease Control Rate (DCR): 60.9% (8 partial responses + 6 stable diseases)
Median Progression-Free Survival (mPFS): 4.2 months
Safety: The regimen was well-tolerated, with no Grade 4 or fatal treatment-emergent adverse events (TEAEs) observed.
TRAEs were reported in 87.5% (21/24) of patients, most commonly (incidence ≥20%) liver function test abnormalities, hematological abnormalities, and pyrexia (mostly Grade 1-2).
Treatment-related serious adverse events (SAEs) occurred in 37.5% (9/24) of patients.
Dr. Jingsong Wang, Founder, Chairman and CEO of Harbour BioMed commented: "The 2025 Nobel Prize in Physiology or Medicine was awarded to three immunologists for their groundbreaking discoveries in regulatory T cells (Treg cells) and their role in controlling the immune system. HBM4003, a next-generation anti-CTLA-4 antibody discovered through our HCAb Harbour Mice platform, is a direct clinical application arising from this foundational research. The positive results from this Phase II clinical study mark an important milestone for Harbour BioMed and underscore the therapeutic potential of HBM4003. We will continue to advance HBM4003 with the goal of delivering transformative immuno-oncology therapies to patients worldwide."

About Porustobart (HBM4003)

Porustobart (HBM4003) is a next-generation, fully human heavy-chain-only anti-CTLA-4 antibody discovered and developed using the HCAb Harbour Mice platform. It is also the first fully human heavy-chain-only antibody which entered clinical development globally. Compared with conventional CTLA-4 antibodies, porustobart has unique, favourable properties, including significant Treg cell depletion and optimized pharmacokinetics for improved safety. Additionally, by enhancing antibody-dependent cellular cytotoxicity (ADCC), porustobart increases the potential to selectively deplete intratumoral Treg cells, helping to overcome the efficacy and toxicity bottleneck of current CTLA-4 therapies. The Company has implemented a global development plan for multiple types of solid tumors with an adaptive treatment design for porustobart. Positive efficacy and safety data have been observed in the monotherapy trial targeting advanced solid tumors, as well as in combination trials with PD-1 inhibitors for melanoma, CRC, NEN and HCC. Final data from the study of HBM4003 in combination with toripalimab for advanced HCC were published in Clinical Cancer Research in August 2025.

(Press release, Harbour BioMed, OCT 22, 2025, View Source [SID1234656903])

On October 22, 2025 Revolution Medicines, Inc. (Nasdaq: RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, reported updated clinical data for elironrasib, a RAS(ON) G12C-selective inhibitor, in previously treated patients with KRAS G12C non-small cell lung cancer (NSCLC) who had received a prior KRAS(OFF) G12C inhibitor. These results will be highlighted in an oral presentation at the AACR (Free AACR Whitepaper)-NCI-EORTC Symposium on Molecular Targets and Cancer Therapeutics in Boston, October 23-25.

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"The compelling clinical activity, durable response and acceptable tolerability profile seen with elironrasib underscore the potential of this differentiated RAS(ON) G12C-selective inhibitor, including in patients who have progressed on G12C(OFF) inhibitors," said Mark A. Goldsmith, M.D., Ph.D., chief executive officer and chairman of Revolution Medicines. "These findings reinforce the promise of our RAS(ON) inhibitor platform to deliver a range of therapies that target the active, GTP-bound state of RAS proteins with the potential to create new global standards of care."

As of the August 4, 2025 data cutoff date, patients with KRAS G12C NSCLC, who had received prior therapy with a KRAS(OFF) G12C inhibitor, were treated with elironrasib at the recommended Phase 2 dose of 200 mg orally twice daily (BID) and were evaluated on key safety and antitumor activity endpoints. These patients (n=24) were heavily pretreated, with a median of three prior lines of therapy (range 2-6), with 92% (22 out of 24 patients) having progressed on a prior KRAS(OFF) G12C inhibitor.​ Elironrasib demonstrated compelling antitumor activity, with a confirmed objective response rate of 42% (95% CI: 22-63) and a disease control rate of 79% (95% CI: 58-93). The median duration of response was 11.2 months (95% CI: 5.9-not estimable), and the median progression-free survival was 6.2 months (95% CI: 4.0-10.3). The median overall survival (OS) was not yet reached and 12-month OS rate was 62% (95% CI: 40-78).

These results are from RMC-6291-001, an ongoing multicenter, Phase 1 trial designed to evaluate elironrasib (RMC‑6291) monotherapy in patients with advanced KRAS G12C solid tumors.

Elironrasib is an innovative, mutant-selective inhibitor that binds selectively and covalently to the oncogenic RAS(ON) form of the RAS G12C variant that drives approximately 12% of cases of NSCLC. Revolution Medicines is exploring elironrasib monotherapy and combinations in various treatment settings and continues work to prioritize among multiple options for advancing its development. In July 2025, elironrasib was granted Breakthrough Therapy Designation for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic NSCLC who have received prior chemotherapy and immunotherapy but have not been previously treated with a KRAS G12C inhibitor.

NSCLC accounts for 80%-85% of all lung cancers, and most patients have advanced or metastatic disease at initial diagnosis.1,2 KRAS mutations are found in nearly 30% of NSCLC cases, among which KRAS G12C is the most common.

Advancing RAS(ON) Inhibitor Platform Across Tumor Types
Jan Smith, Ph. D., chief scientific officer of Revolution Medicines will also highlight encouraging preclinical data supporting the RAS(ON) inhibitor doublet of zoldonrasib and daraxonrasib during a plenary session at the start of the AACR (Free AACR Whitepaper)-NCI-EORTC Symposium.

Several other presentations to be featured at the meeting demonstrate continued progress across Revolution Medicines’ RAS(ON) inhibitor portfolio, including:

"Targeting the Oncogenic State of RAS with Tri-Complex Inhibitors"
"RAS(ON) Inhibitor In-Pathway Combinations Maximize RAS Pathway Suppression in KRAS Mutant CRC Models"
"Resistance Mechanisms to Monotherapy Daraxonrasib (RMC-6236) in RAS Mutant PDAC"
"RASolve 301: A Phase 3 Study of Daraxonrasib (RMC-6236) vs. Docetaxel in RAS-Mutant NSCLC"
Further details and information on presentations can found on the AACR (Free AACR Whitepaper)-NCI-EORTC Symposium website.

About Non-Small Cell Lung Cancer
More than 197,000 people are diagnosed with non-small cell lung cancer (NSCLC) in the U.S. each year.3 Despite treatment advancements, NSCLC remains a leading cause of cancer-related mortality worldwide, primarily due to its late-stage diagnosis and limited response to conventional therapies.

(Press release, Revolution Medicines, OCT 22, 2025, View Source [SID1234656902])