On October 24, 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 an update on the ongoing Phase 1 ACESOT-1051 (A Multi-Center Evaluation of WEE1 Inhibitor in Patients with Advanced Solid Tumors, APR-1051) study. The latest results show that, at the 100 mg APR-1051 dose level, 3 out of 4 patients achieved stable disease, as measured using RECIST v1.1 criteria.

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A poster titled Early safety and efficacy of APR-1051, a novel WEE1 inhibitor, in patients with cancer-associated gene alterations: Updated data from ACESOT-1051 Phase 1 trial will be presented today 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 poster, to be presented by Drs. Timothy Yap MBBS, PhD, FRCP, University of Texas MD Anderson Cancer Center and lead investigator of the study, and Philippe Pultar, MD, Senior Medical Advisor at Aprea, summarizes preliminary results from the trial with a cutoff date of September 17, 2025. A copy of the poster will be available on Investors page of the Aprea corporate website under "Investor Presentations & Resources."

"We continue to be encouraged by these early clinical findings, which demonstrate signals of anti-tumor activity with APR-1051 in a heavily pre-treated patient population," said Dr. Pultar. "We believe the observation of disease control in tumors harboring FBXW7, CCNE1, and KRAS mutations align with our mechanistic understanding of WEE1 inhibition and reinforces the scientific rationale for APR-1051 development. We believe these promising data provide an important foundation as we continue with dose escalation in the ongoing study and we look forward to providing further updates as we advance to higher dose level in the ongoing study."

ACESOT-1051 Clinical Update (data cutoff October 19, 2025)

The primary objective of the trial is to characterize the safety profile, dose-limiting toxicity, maximum tolerated dose or maximum administered dose, and recommended Phase 2 dose of APR-1051. Secondary objectives are to 1) to characterize the pharmacokinetics of APR-1051 and the major metabolites and active metabolites of APR-1051, and 2) to assess preliminary efficacy of APR-1051
Results from Dose Level 6 (100 mg), show 3 out of 4 patients achieved stable disease, per RECIST v1.1 in heavily pretreated gastrointestinal and gynecologic malignancies
Disease stabilization was observed in patients with FBXW7, CCNE1, and KRASG12V + TP53 alterations
Favorable tolerability: No dose limiting toxicities (DLTs) or unexpected safety issues reported to date.
Following successful clearance of the 100 mg cohort, dose escalation has progressed to Dose Level 7 (150 mg)
For more information on ACESOT-1051, refer to ClinicalTrials.gov NCT06260514.

Individual Patient Results

86-year-old female with rectal cancer: Treated at a 100 mg dose after five prior lines, the patient achieved stable disease (-13% reduction). Tumor harbored FBXW7 mutation which is a mechanistically relevant biomarker for WEE1 inhibition. 145 days on treatment and ongoing
55-year-old male with rectal cancer: Treated at a 100 mg dose after four prior lines, the patient achieved stable disease (+1%). Tumor harbored KRASG12V + TP53-mutant patient supports mechanistic activity in this genotype. 63 days on treatment and ongoing
73-year-old female with endometrial cancer: Treated at a 100mg after five prior lines, patient achieved stable disease by RECIST v1.1 criteria (+15%) at the first evaluation before voluntarily withdrawing consent after approximately two months of treatment. Tumor harbored CCNE1 and TP53 mutations supports mechanistic activity in this genotype.
50-year-old female with colon cancer: Treated at 100mg after two prior lines. This patient had disease progression at first assessment (8 weeks).

(Press release, Aprea, OCT 24, 2025, View Source [SID1234656973])

On October 24, 2025 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of differentiated targeted radiotherapies, reported new preclinical data for ATNM-400, its novel, first-in-class antibody radioconjugate armed with the potent alpha-emitter Actinium-225 (Ac-225) at the 32nd Annual Prostate Cancer Foundation (PCF) Scientific Retreat being held October 23 – 25, 2025 in Carlsbad, CA.

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ATNM-400, which targets a non-PSMA antigen associated with prostate cancer progression and treatment resistance, demonstrated superior tumor control and improved overall survival compared with the active agents in key standard-of-care therapies including enzalutamide (the active agent in Xtandi, Astellas/Pfizer) and 177Lu-PSMA-617 (the active agent in Pluvicto, Novartis), as well as 225Ac-PSMA-617 across multiple preclinical prostate cancer models.

These data further reinforce ATNM-400’s potential as a paradigm changing, PSMA-independent Ac-225 alpha radiotherapy, offering opportunities for use as a monotherapy, in combination regimens, and in patients relapsing after ARPI or PSMA-directed treatments. ATNM-400 data has now been presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper), Society for Nuclear Medicine and Molecular Imaging (SNMMI) and PCF annual conferences in 2025 demonstrating its growing potential in various treatment settings in prostate cancer. In addition, data highlighting its potential in non-small cell lung cancer will be presented 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) on Saturday, October 25, 2025.

Key Findings in Prostate Cancer Treatment Settings:

Potent and Durable Tumor Control, Increased Overall Survival and Synergistic Activity in Enzalutamide Resistant Prostate Cancer

Studies were performed in 22Rv1 prostate cancer models, which are known to be resistant to enzalutamide

ATNM-400 demonstrated superior and 5-times more durable anti-tumor efficacy extending to 100 days compared to approximately 20 days with enzalutamide alone

Given that ARPI therapies like enzalutamide are known to increase the ATNM-400 target antigen expression, combination treatment with ATNM-400 and enzalutamide was synergistic, resulting in complete tumor eradication in 40% of treated animals and significantly prolonged survival, whereas enzalutamide alone provided no durable disease control
Potent and Durable Tumor Control, Increased Overall Survival and Synergistic Activity in Enzalutamide Resistant Prostate Cancer

In models that progressed on enzalutamide, subsequent treatment with ATNM-400 achieved robust tumor control and extended survival, highlighting its potential in post-enzalutamide settings
Subsequent treatment with ATNM-400 achieved robust tumor control and extended survival, highlighting its potential in post-enzalutamide settings

Highly Effective and Increased Overall Survival in 177Lu-PSMA-617 Resistant Prostate Cancer

22Rv1 prostate cancer models are also resistant to 177Lu-PSMA-617

ATNM-400 overcame 177Lu-PSMA-617 resistance with approximately 5-times long tumor control and 2-times longer overall survival in tumor bearing animals
Highly Effective and Increased Overall Survival in 177Lu-PSMA-617 Resistant Prostate Cancer

Potent Therapeutic Activity Independent of PSMA Expression Levels

ATNM-400 targets a highly differentiated, non-PSMA antigen associated with the development and progression of prostate cancer, exhibiting potent therapeutic activity independent of PSMA expression levels

The expression of the ATNM-400 antigen target was not altered post-177Lu-PSMA-617
Potent Therapeutic Activity Independent of PSMA Expression Levels

22Rv1 cell lines are low-PSMA expressing and LNCaP cell lines are high-PSMA expressing
Addressing Critical Unmet Needs in mCRPC

Prostate cancer patients who progress to mCRPC face limited treatment options. While ARPI therapies like enzalutamide and PSMA-targeted radiotherapies like Pluvicto have extended survival, resistance and disease progression remain major challenges. In addition, a significant number of patients do not respond to PSMA-targeted radiotherapy as approximately 25%-30% of patients with mCRPC have low or no detectable PSMA and approximately 60% of patients have at least one PSMA-negative prostate cancer lesion.

By targeting a distinct, non-PSMA antigen associated with treatment resistance and poor outcomes, ATNM-400 represents a mechanistically differentiated alpha-radiotherapy approach that has potential in various treatment settings in prostate cancer. Its combination of a high-affinity antibody and potent alpha-emitting Ac-225 payload provides a path to overcome therapeutic resistance and extend patient survival beyond current standards of care.

Differentiation and Potential Clinical Impact

Sandesh Seth, Chairman and Chief Executive Officer, Actinium Pharmaceuticals, Inc., stated, "Since unveiling ATNM-400 earlier this year at AACR (Free AACR Whitepaper), our enthusiasm for this program only continues to grow commensurate with the promising results generated supporting its potential in various treatment settings in prostate cancer. ATNM-400 combines the precision of antibody targeting with the unparalleled potency of Ac-225 alpha particles, and importantly, it does so through a biologically distinct, PSMA-independent mechanism. These new preclinical data presented at PCF provide further validation for ATNM-400 and positions it as a candidate capable of transforming the treatment paradigm for patients with mCRPC. We are thrilled by the positive reactions to our ATNM-400 data and its differentiated non-PSMA approach."

Mr. Seth added, "As we have recently announced, beyond prostate cancer, we are also advancing ATNM-400 into non-small cell lung cancer (NSCLC), where it has shown the ability to overcome resistance to osimertinib (TAGRISSO, AstraZeneca) an EGFR-TKI therapy in preclinical models. Together, these data highlight Actinium’s innovate approach to R&D that leverages our radiochemistry expertise and strong translational biology capabilities to create first-in-class, multi-indication radiotherapeutics."

Actinium Pharmaceuticals envisions multiple clinical applications for ATNM-400 in prostate cancer, including:

Monotherapy in earlier disease settings prior to PSMA-directed radiotherapy.

Combination therapy with ARPI’s to enhance and prolong treatment responses.

Sequential therapy for patients relapsing after ARPI or PSMA-targeted radioligand treatments.
Summary of Preclinical Highlights of ATNM-400

Novel Mechanism: First-in-class Ac-225-based antibody radioconjugate against a non-PSMA target, overexpressed in advanced and resistant prostate cancer.

Superior Efficacy: Outperformed 177Lu-PSMA-617, Ac225-PSMA-617 and enzalutamide in direct head-to-head preclinical comparisons.

Durable Responses: A single 40 µCi/kg dose produced strong tumor inhibition; multi-dose regimens yielded long-term tumor control exceeding both enzalutamide and 177Lu-PSMA-617.

Overcomes Resistance: ATNM-400 maintained potent anti-tumor activity in models resistant to both enzalutamide and 177Lu-PSMA-617.

Combination Synergy: Synergized with enzalutamide, achieving complete tumor regressions in 40% of treated animals and markedly extending survival.

Favorable Biodistribution: Demonstrated selective and durable tumor uptake and rapid clearance from normal tissues, supporting a strong therapeutic index.
About ATNM-400

ATNM-400 is a highly innovative, first-in-class, and multi-indication Actinium-225 (Ac-225) targeted radiotherapy candidate in development for prostate cancer and non-small cell lung cancer (NSCLC). ATNM-400 is highly differentiated in prostate cancer as it targets a distinct non-PSMA antigen strongly implicated in prostate cancer progression and treatment resistance. Unlike 177Lu-PSMA-617, the active agent in Pluvicto and the majority of radiotherapies under development, which rely on PSMA targeting, ATNM-400 is designed to maintain efficacy in low-PSMA or PSMA-resistant disease, a major unmet clinical need. Ac-225 delivers high-linear-energy-transfer alpha particles that induce irreparable double-strand DNA breaks, offering superior potency over beta emitters like Lutetium-177 (177Lu), and has a shorter tissue path length that may reduce off-target toxicity. The receptor specifically targeted by ATNM-400 continues to be expressed at a high level even after androgen receptor inhibitor (ARPI) and ATNM-400 has shown to overcome resistance to the ARPI therapy enzalutamide and work synergistically in combination with enhanced tumor control including complete tumor regression. In NSCLC, ATNM-400 has shown to overcome resistance to osimertinib, an EGFR tyrosine kinase inhibitor (TKI) that is a standard of care therapy.

Prostate cancer is the most commonly diagnosed cancer in men, with ~1.5 million new cases globally and over 313,000 cases expected in the U.S. in 2025. While early-stage disease is typically managed with surgery, radiation, and ARPI therapy, up to 20% of cases progress to mCRPC – a lethal stage with limited treatment options. Targeted radiotherapy is a growing field in prostate cancer, dominated by PSMA-targeting agents like Pluvicto, which had sales of over $1.3 billion in 2024, yet many patients either lack PSMA expression or develop resistance to Pluvicto. In the U.S., 40,000 to 60,000 mCRPC patients annually progress after ARPI therapy that as a class generated sales of over $10.0 billion in 2024 including enzalutamide (Xtandi), which led the ARPI class with sales of over $5.9 billion in 2024, highlighting a significant unmet need. Lung cancer is the leading cause of cancer deaths and there are there are over 200,000 new cases expected in the U.S. in 2025. NSCLC accounts for approximately 85% of all lung cancer cases. The EGFR TKI Osimertinib (TAGRISSO, AstraZeneca) generated sales of $6.6 billion in 2024. Across prostate cancer and NSCLC, there are approximately 500,000 new cases in the U.S. alone.

(Press release, Actinium Pharmaceuticals, OCT 24, 2025, View Source [SID1234656990])

On October 24, 2025 Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company creating a new class of drugs based on targeted protein degradation, reported preclinical data for ARV-806, a PROTAC KRAS G12D degrader, at the 2025 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) in Boston, Massachusetts. The ARV-806 data presented show a differentiated profile based on degradation potency, antiproliferative activity, and induction of cancer cell death. ARV-806 is designed to target both the ON and OFF forms of KRAS G12D, which is the most common mutation of the KRAS protein. ARV-806 has the potential to address high unmet need in solid tumors, such as pancreatic, colorectal and non-small cell lung cancer.

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"These data suggest the potential of targeted protein degradation to overcome historical limitations in addressing undruggable KRAS mutations," said Angela Cacace, Ph.D., Chief Scientific Officer of Arvinas. "ARV-806’s ability to eliminate both ON and OFF forms of KRAS G12D, combined with its potency and durability shown in preclinical models, supports our confidence in its clinical potential to deliver meaningful benefit for patients with KRAS G12D-mutated cancers."

Key highlights from the presentation include:

In vitro, ARV-806 degraded KRAS G12D with picomolar potency across pancreatic, colorectal, and lung cancer cell lines but did not induce degradation of wild-type and other mutant RAS isoforms.
ARV-806 is differentiated from other KRAS G12D targeting agents in development and has potential to be a best-in-class therapy for KRAS G12D mutated cancers due to:
Catalytic activity, which allows it to overcome upregulation, a common mechanism of resistance to inhibitor treatment
Compared with clinical-stage KRAS G12D ON and OFF inhibitors and another clinical-stage G12D degrader, ARV-806 demonstrated:
>25-fold greater potency in reducing cancer cell proliferation,
>40-fold higher potency in degrading KRAS G12D protein (versus the comparable clinical-stage G12D degrader), and
>10-fold lower concentrations required to induce pro-apoptotic BIM expression.
Following a single intravenous dose in a colorectal tumor xenograft model, ARV-806 degraded >90% of KRAS G12D for seven days, with parallel suppression of c-MYC (a key driver of cancer cell proliferation) and induction of BIM (Bcl-2-interacting mediator of cell death, a pro-apoptotic factor) for ≥5 days.
ARV-806 demonstrated robust efficacy responses at low doses in tumor models including: ≥30% tumor volume reductions in pancreatic and colorectal cell line-derived xenograft (CDX) models and a patient-derived xenograft (PDX) model of lung cancer.

These data demonstrate sustained pharmacodynamic activity consistent with long-lasting target degradation, which we believe supports intermittent clinical dosing. Arvinas is currently evaluating ARV-806 in a Phase 1 clinical trial in patients with KRAS G12D–mutated advanced solid tumors (NCT07023731).

Also shown in the poster, orally bioavailable pan-KRAS degraders have been identified that potently degrade multiple variants of KRAS and spare other RAS isoforms. A tool pan-KRAS PROTAC demonstrated robust single-agent activity and superior combination efficacy with immune checkpoint blockade compared with a pan-RAS ON inhibitor (7 complete responses compared with 2 complete responses).

About ARV-806
ARV‑806 is a novel, investigational PROTAC degrader designed to selectively target and degrade mutant Kirsten rat sarcoma (KRAS) G12D which is the most common mutation of the KRAS protein. Therefore, ARV-806 has the potential to address high unmet need in solid tumors, such as pancreatic, colorectal and lung cancer. ARV‑806 is currently being evaluated in a Phase 1 clinical trial in patients with advanced solid tumors harboring KRAS G12D mutations.

(Press release, Arvinas, OCT 24, 2025, View Source [SID1234656974])

On October 24, 2025 Merus N.V. (Nasdaq: MRUS) (Merus, the Company, we, or our), an oncology company developing innovative, full-length multispecific antibodies and antibody drug conjugates (Biclonics, Triclonics and ADClonics), reported interim clinical data as of a July 29, 2025 data cutoff from the ongoing phase 2 trial of the bispecific antibody petosemtamab in combination with standard of care FOLFOX/FOLFIRI in 1L and 2L metastatic colorectal cancer (mCRC), and petosemtamab monotherapy in 3L+ mCRC. These data will be presented in a plenary session oral presentation by Dr. Moh’d Khushman M.D., Washington University School of Medicine, St. Louis, MO, 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) on Friday, October 24 at 10:20 a.m. ET.

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"Petosemtamab’s unique mechanism of action, including targeting both EGFR and LGR5, and potential to safely combine with FOLFOX/FOLFIRI, represents an important finding for patients with EGFR inhibitor-naïve metastatic colorectal cancer," said Fabian Zohren, M.D., Ph.D., Chief Medical Officer of Merus. "These data demonstrate petosemtamab’s clinical activity beyond head and neck squamous cell carcinoma. We are encouraged that petosemtamab has the potential to become a transformational treatment and new standard of care for patients across a range of solid tumors."

"Metastatic colorectal cancer remains a formidable challenge with limited effective therapies. The promising early results with petosemtamab offer hope for advancing care and bringing new treatment possibilities to patients facing this difficult disease," added Dr. Khushman.

Petosemtamab (MCLA-158: EGFR x LGR5 Biclonics)

Presentation title: Petosemtamab (MCLA-158) monotherapy or with chemotherapy in metastatic colorectal cancer: Preliminary antitumor activity and safety data from a phase 2 trial
Observations in the presentation include:
As of a July 29, 2025 data cutoff date:

54 patients (pts) with left- and/or right-sided, KRAS, NRAS, and BRAF wildtype microsatellite stable mCRC received petosemtamab 1500 mg every two weeks, in combination with FOLFOX/FOLFIRI or as monotherapy
Pts treated in 1L or 2L had no prior anti-EGFR therapy
Pts treated in 2L received 1 prior chemotherapy regimen in the metastatic setting
Pts treated in 3L+ received at least 2 prior regimens in the metastatic setting, including a prior anti-EGFR therapy
Efficacy evaluable population consisted of patients with ≥1 dose of petosemtamab who had opportunity for ≥8 weeks follow up and ≥1 post baseline tumor assessment or discontinued petosemtamab early due to disease progression, symptomatic deterioration and/or death
1L petosemtamab with FOLFOX/FOLFIRI
14 pts were treated in 1L (10 FOLFOX and 4 FOLFIRI)
10 pts were efficacy evaluable, 8 left-sided; 10 (100%) remained on treatment
80% (8 of 10) response rate: 1 confirmed complete response, 7 partial responses (PRs) (4 unconfirmed of which 1 confirmed post data cutoff); 2 stable diseases (SDs)
88% (7 of 8) response rate in left-sided: 1 confirmed complete response, 6 PRs (3 unconfirmed, 1 unconfirmed response confirmed post data cutoff); 1 SD
One SD observed to be an unconfirmed PR post data cutoff leading to 100% (8/8) response rate left-sided and 90% (9/10) response rate overall in 1L
All unconfirmed PRs remained on treatment without disease progression
2L petosemtamab with FOLFOX/FOLFIRI
14 pts were treated in 2L (2 FOLFOX and 12 FOLFIRI)
13 were efficacy evaluable; 10 (77%) remained on treatment
62% response rate: 8 PRs (3 unconfirmed of which 1 confirmed post data cutoff); 4 SDs and 1 clinical deterioration prior to first scan
All unconfirmed PRs and SDs remained on treatment without disease progression
3L+ petosemtamab monotherapy:
26 pts were treated
20 were efficacy evaluable, 6 (30%) remained on treatment
10% confirmed response rate: 2 PRs; 9 SDs (5 remained on treatment)
Safety:
Petosemtamab safety profile in mCRC observed thus far, appears consistent with its established safety profile in recurrent/metastatic head and neck squamous cell carcinoma
No significant overlapping toxicities identified in combination with FOLFOX/FOLFIRI
No new safety signals identified
Infusion related reactions (IRRs) were managed with premedication and prolonged infusion on cycle 1 day 1; no discontinuations due to IRRs
Presentation:
Title: Petosemtamab (MCLA-158) monotherapy or with chemotherapy in metastatic colorectal cancer: Preliminary antitumor activity and safety data from a phase 2 trial
Session Title: Plenary Session 4: Clinical Trials Plenary Session
Date and Time: Friday, October 24, 10:20 a.m. ET
The same data will also be available in a poster:
Session Title: Poster Session B
Session Date and Time: Friday, October 24, 12:30-4:00 p.m. ET

As full presentations become available at the conference, they will contemporaneously be available on the Merus website.

(Press release, Merus, OCT 24, 2025, View Source [SID1234656991])

On October 24, 2025 Chugai Pharmaceutical Co., Ltd. (TOKYO: 4519) reported its financial results for the third quarter of fiscal year 2025.

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Chugai reported increased revenue and operating profit year-on-year for the third quarter (Core-basis).

Regarding revenue, domestic sales increased by 3.6%. In the oncology field, sales increased by 0.2%. While our mainstay product Avastin was affected by NHI drug price revisions and generics, this was offset by steady growth of new products Phesgo, Lunsumio, and our mainstay product Polivy. In the specialty field, sales increased by 7.7%, driven by steady performance of mainstay products Vabysmo, Hemlibra, and Enspryng, along with successful market penetration of the new product PiaSky. Overseas sales increased by 7.7%, driven by a substantial increase in exports of Actemra to Roche. Other revenue decreased by 0.9%, despite the increase in income related to Hemlibra, mainly due to a decrease in one-time income.

Cost to sales ratio increased by 0.6 percentage points year-on-year to 33.1%, mainly due to changes in the product mix. Research and development expenses increased by 0.7% due to investments into drug discovery and early development, and increases associated with the progress of development projects, while selling, general and administrative expenses decreased by 4.3% mainly driven by various expenses. Other operating income (expense) resulted in income of ¥0.4 billion. As a result, Core operating profit was ¥450.5 billion (+5.6%) with a Core operating profit margin (to revenue) of 49.4%.

Chugai made good progress in both in-house products and products in-licensed from Roche.

For in-house products, PiaSky was launched in Taiwan as the first subcutaneous formulation for paroxysmal nocturnal hemoglobinuria. Enspryng has obtained results from Phase III clinical trials for thyroid eye disease, and will be discussed with health authorities. For Chugai originated project, Orforglipron, an oral GLP-1 receptor agonist out-licensed to Eli Lilly, met primary endpoints in multiple Phase III clinical trials for obesity and type 2 diabetes.

For products in-licensed from Roche, Tecentriq has obtained approval for an expanded indication for relapsed or refractory extranodal NK/T-cell lymphoma, nasal type. Avastin has been filed for an expanded indication for neurofibromatosis type II. Glofitamab has initiated Phase II clinical trials in Japan for both relapsed or refractory diffuse large B-cell lymphoma and relapsed or refractory mantle cell lymphoma. Additionally, afimkibart has initiated Phase III clinical trial for Crohn’s disease, and divarasib initiated Phase Ib/II clinical trial for non-small cell lung cancer (first-line treatment). Furthermore, Chugai has in-licensed CT-388, a long-acting GLP-1/GIP receptor agonist, from Roche.

[2025 third quarter results]

Billion JPY 2025
Jan – Sep 2024
Jan – Sep % change
Core results
Revenue 911.6 868.5 +5.0%
　Sales 794.6 750.3 +5.9%
　Other revenue 117.1 118.2 -0.9%
Operating profit 450.5 426.6 +5.6%
Net income 320.0 301.3 +6.2%
IFRS results
Revenue 911.6 868.5 +5.0%
Operating profit 429.8 418.6 +2.7%
Net income 305.6 295.8 +3.3%
[Sales breakdown]

Billion JPY 2025
Jan – Sep 2024
Jan – Sep % change
Sales 794.6 750.3 +5.9%
Domestic sales 343.7 331.7 +3.6%
　Oncology 180.7 180.3 +0.2%
　Specialty 163.0 151.3 +7.7%
Overseas sales 450.9 418.7 +7.7%
[Oncology field (Domestic) Top5-selling medicines]

Billion JPY 2025
Jan – Sep 2024
Jan – Sep % change
Tecentriq 46.0 47.4 -3.0%
Polivy 27.0 24.5 +10.2%
Phesgo 24.5 15.0 +63.3%
Alecensa 24.3 22.4 +8.5%
Avastin 19.6 25.6 -23.4%
[Specialty field (Domestic) Top5-selling medicines]

Billion JPY 2025
Jan – Sep 2024
Jan – Sep % change
Hemlibra 44.7 41.5 +7.7%
Actemra 36.7 34.8 +5.5%
Enspryng 20.9 17.8 +17.4%
Vabysmo 18.5 14.7 +25.9%
Evrysdi 12.0 11.3 +6.2%
[Progress in R&D activities from Jul 25th, 2025 to Oct 24th, 2025]

About Core results

Chugai discloses its results on a Core basis from 2013 in conjunction with its decision to apply IFRS. Core results are the results after adjusting Non-Core items to IFRS results. Chugai’s recognition of non-recurring items may differ from that of Roche due to the difference in the scale of operations, the scope of business and other factors. Core results are used by Chugai as an internal performance indicator, for explaining the underlying business performance both internally and externally, and as the basis for payment-by-results such as a return to shareholders.

Trademarks used or mentioned in this release are protected by law.

(Press release, Chugai, OCT 24, 2025, View Source [SID1234656975])