On November 5, 2025 HanchorBio Inc. (TPEx: 7827), a global clinical-stage biotechnology company advancing next-generation immunotherapies for oncology and autoimmune diseases, reported that the preclinical data on HCB301, a novel tri-specific immunotherapeutic fusion protein, has been accepted for presentation at the 40th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper), taking place November 5-9, 2025, in National Harbor, Maryland. Featured in a poster presentation, the data highlight HCB301’s differentiated design and multi-pronged antitumor mechanism, which engages both innate and adaptive immunity.

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HCB301 is designed to simultaneously:

Block SIRPα-CD47 interaction to enable macrophage-mediated phagocytosis
Block PD-1-PD-L1 signaling to restore exhausted T-cell function
Trap TGFβ to overcome stromal and immune exclusion in tumor microenvironment (TME)
This tripartite approach aims to overcome the limitations of existing checkpoint inhibitors by activating both arms of the immune system, especially in tumors with immunologically ‘cold’ or suppressive tumor microenvironments (TMEs) resistant to current treatments.

In addition to the HCB301 preclinical poster presented on November 5, HanchorBio will also present two late-breaking abstracts on November 7 to showcase clinical data on its SIRPα-Fc fusion protein HCB101. Together, the three posters underscore the breadth and translational strength of HanchorBio’s proprietary Fc-Based Designer Biologics (FBDB) platform across innate and adaptive immune pathways.

Scott Liu, Ph.D., Founder, Chairman, and CEO of HanchorBio, commented: "HCB301 builds directly on the foundation of HCB101, our clinical-stage SIRPα-engineered fusion protein. By integrating PD-1 blockade and TGFβ neutralization into a single molecule, HCB301 represents what we believe to be the first-in-class tri-specific fusion protein that simultaneously targets immune checkpoints, immune suppression, and macrophage dysfunction. This design reflects our commitment to building modular, next-generation immunotherapies with global translation potential. With IND clearance and first-patient dosing now achieved in both the US and China, HCB301 demonstrates the scalability of our FBDB platform and the executional readiness of our team across regions. As we advance HCB301 into the clinical stage, this milestone further positions HanchorBio as a long-term innovation partner for global co-development, particularly in cancers with high resistance to conventional immunotherapies."

Preclinical highlights of HCB301 (SITC Poster #P321)
Title: HCB301, a tri-specific fusion protein targeting SIRPα/CD47, PD-1/PD-L1, and TGFβ, promotes anti-tumor macrophage and T cell activity in preclinical models of solid tumors

Strong immune activation: HCB301 induced robust antibody-dependent cellular phagocytosis (ADCP), activated tumor-associated macrophages, and increased CD8+ T cell infiltration.
Synergistic antitumor efficacy: In CT26, MC38, and B16F10 models, HCB301 demonstrated superior tumor growth inhibition compared with single- or dual-arm comparators.
TGFβ suppression: HCB301 potently neutralized active TGFβ, reversing TME immunosuppression, and restoring T cell function.
Fc-effector tuning: Selective Fc engineering optimized immune activation while minimizing off-target toxicity.
"HCB301 was purpose-built to break through the resistance barriers that limit current PD-1 or CD47 monotherapies," remarked Wenwu Zhai, Ph.D., Chief Scientific Officer of HanchorBio. "Each of its three arms addresses a key axis of tumor immune evasion: CD47 for innate immune clearance, PD-1 for adaptive immune reactivation, and TGFβ for TME remodeling. Our preclinical data show that HCB301 delivers synergistic immune activation and tumor control, strongly supporting its advancement into the clinic."

About HCB301
Based on company analysis, HCB301 is the first clinical-stage tri-specific recombinant Fc-fusion protein that simultaneously targets SIRPα/CD47, PD-1/PD-L1, and TGFβ. It was designed using HanchorBio’s FBDB platform, which enables modular multi-arm immunotherapies with tunable Fc regions and enhanced manufacturability.

HCB301 integrates:

A high-affinity SIRPα domain that binds cancer cells’ CD47 to promote macrophage phagocytosis
A PD-1 extracellular domain that blocks PD-L1 and restores T-cell effector function
A TGFβRII domain that traps active TGFβ to alleviate immunosuppressive signals in the tumor microenvironment
The protein shows a favorable safety profile in repeat-dose toxicology studies in cynomolgus monkeys. Its differential tumor vs. RBC binding profile may reduce the risk of anemia, thrombocytopenia, or other cytopenia while maintaining potent anti-tumor activity.

HCB301 achieved IND clearance and first-patient dosing in both the US and China in 2025. The ongoing Phase 1 study (HCB301-101; NCT06487624) is a multi-regional, multi-center, open-label, dose-finding, first-in-human trial evaluating the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary clinical efficacy of HCB301 in patients with advanced solid tumors or relapsed and refractory classical Hodgkin lymphoma.

(Press release, Hanchor Bio, NOV 5, 2025, View Source [SID1234659487])

On November 5, 2025 Alligator Bioscience (Nasdaq Stockholm: ATORX), a clinical-stage biotechnology company developing tumor-directed immuno-oncology antibody drugs, reported the publication of two abstracts accepted for presentation at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 40th Anniversary Annual Meeting, to be held 5–9 November 2025 in National Harbor, MD, USA.

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The mitazalimab abstract presents new data from the OPTIMIZE-1 trial in metastatic pancreatic cancer, further characterizing efficacy, safety, and biomarker responses at two dose levels. These findings strengthen the clinical rationale for selecting the 900 μg/kg dose in the planned Phase 3 study and the exposure-response data further supports mitazalimab contribution to the clinical benefits observed in OPTIMIZE-1. Alligator will also present preclinical data on ATOR-4066, a bispecific antibody targeting CD40 and CEACAM5, demonstrating immune activation and remodeling of the tumor microenvironment.

Mitazalimab presentation details
Title: CD40 agonist mitazalimab + mFOLFIRINOX in patients with metastatic pancreatic ductal adenocarcinoma: dose characterization based on exposure response and biomarker analysis from the OPTIMIZE-1 study
Abstract number: 530
Time: Saturday, 8 November 2025
Presenter: Yago Pico de Coaña, Medical Science Director, Alligator Bioscience

Key findings:

Improved survival outcomes at 6 months:
PFS: 50.8% vs. 38.7%
OS: 89.5% vs. 69.4%
Manageable safety profile: Safety was manageable across both dose levels, with the increased rate of adverse events in the 900 μg/kg group attributed to extended treatment exposure
Biomarker analyses: Greater immune activation at 900 μg/kg, including higher levels of Ki67+ T cells, a marker of actively dividing and proliferating immune cells
Dose selection for Phase 3: Data support 900 μg/kg as the recommended dose for the planned Phase 3 study in metastatic pancreatic cancer
ATOR-4066 presentation details
Title: ATOR-4066, a bispecific antibody targeting CD40 and CEACAM5, induces potent anti-tumor activity that associates with activated intra-tumoral immune cells and disassembly of extracellular tumor matrix
Abstract number: 940
Time: Saturday, 8 November 2025
Presenter: Hampus Andersson, Industrial PhD student, Alligator Bioscience

Key findings:

Localized immune activation: Enhanced dendritic cell and macrophage activation, uptake of tumor antigens, and priming of neoantigen-specific T cells
Potent anti-tumor activity: Superior efficacy compared to CD40 monospecific antibodies in preclinical tumor models
Tumor microenvironment remodeling: Downregulation of extracellular matrix (ECM) organization genes and upregulation of ECM disassembly pathways, correlating with increased immune cell infiltration
"The new OPTIMIZE-1 data provide important validation of mitazalimab’s therapeutic potential in metastatic pancreatic cancer and further strengthen the rationale for the planned Phase 3 study using the 900 μg/kg dose level," said Søren Bregenholt, CEO of Alligator Bioscience. "This is a significant milestone for Alligator as we prepare mitazalimab for late-stage development. In addition, we are pleased to share encouraging preclinical results for ATOR-4066, underscoring the breadth and innovation of our pipeline."

(Press release, Alligator Bioscience, NOV 5, 2025, View Source [SID1234659455])

On November 5, 2025 Nykode Therapeutics ASA (OSE: NYKD), a clinical-stage biopharmaceutical company dedicated to the discovery and development of novel immunotherapies, reported the presentation of new integrated multiomics and biomarker analyses from the phase 1/2 VB N-01 (NCT03548467) and phase 1 VB N-02 (NCT05018273) clinical trials of the individualized cancer vaccine VB10.NEO, designed using Nykode’s AI-powered NeoSELECT platform, at the 40th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) held in National Harbor, Maryland, 5-9 November 2025.

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The poster highlights the capabilities of Nykode’s proprietary AI-powered NeoSELECT platform, which enables individualized cancer vaccine design by integrating multiomics data to select neoantigens with a high potential to trigger clinically relevant tumor-specific immune responses.

In the phase 1/2 VB N-01 and phase 1 VB N-02 trials, VB10.NEO developed using NeoSELECT elicited neoantigen-specific T-cell responses in 94% and 100% of participants, respectively, across multiple solid tumor types. High-quality neoantigens prioritized by NeoSELECT showed enrichment of both overall and stable/amplified immunogenic responses, supporting prolonged and amplified neoantigen-specific immune responses after VB10.NEO vaccination.

"We are very proud of our in-house artificial intelligence and machine learning capabilities. It is great to see the strong performance of our immunogenicity predictions being confirmed across both clinical trials," said Agnete Fredriksen, CSO and Co-founder of Nykode Therapeutics. "While the N-01 cohort was highly heterogeneous and patients received multiple concurrent therapies, we note a favorable association between a higher number of high-quality immunogenic neoantigens and overall survival. This encouraging signal warrants confirmation in controlled studies with more homogeneous patient populations and earlier lines of treatment."

Poster Presentation Details

Abstract #: 117
Title: Integrative analyses of multiomics data and biomarker readout demonstrate clinical and immunological relevance of individualized vaccine design via the NeoSELECT platform
Session Date and Time: Friday, November 7, 2025 | 10:00 AM–7:00 PM ET

The poster will be available on the Nykode website on November 7, at: View Source

(Press release, Nykode Therapeutics, NOV 5, 2025, View Source [SID1234659471])

On November 5, 2025 Precision Biologics, Inc. reported in vitro and in vivo efficacy of its novel tumor-specific ADC (PB-vcMMAE-5) against human carcinomas expressing truncated core 2 O-glycans. Recent data for several human cancer types expressing truncated core 2 O-glycans will be presented in a poster at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting on November 7th, 2025, National Harbor, MD, USA.

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Poster title: In vitro and in vivo efficacy of the antibody-drug-conjugate (ADC) PB-vcMMAE-5 against human carcinoma expressing truncated core 2 O-glycans

Presentation of the poster will be made in person on the following date and location:

Friday, November 7th,  12:15pm – 1:45pm ET; & 5:35pm – 7pm ET

Gaylord National Resort and Convention Center,  National Harbor, MD, USA

Lower Level Atrium – Prince George’s ABC

Primary Category: Immuno-Conjugates and Chimeric Molecules

Abstract Number: 949

BACKGROUND:

Solid tumors remain largely unresponsive to immune checkpoint inhibitors, in part due to their ability to suppress the cytotoxic activity of immune cells infiltrating the tumor microenvironment. One of the disrupted pathways in these cancers is O-glycosylation, a feature particularly associated with cancer progression, metastasis, and poor prognosis.

One strategy to overcome resistance of solid tumor to immunotherapy is the employment of antibody-drug-conjugates (ADCs) selectively targeting cancer cells and not healthy tissues. We developed an ADC, designated PB-vcMMAE-5, composed of the following:

The monoclonal antibody (mAb): We used PB-223, an innovative mAb developed through affinity maturation of clinical stage mAb NEO-102 (Ensituximab), a chimeric human IgG1 mAb that targets truncated core 2 O-glycans, specifically expressed by cancer cells and not by healthy tissues. PB-223 does not bind to normal tissues and it internalizes into human cancer cell lines expressing its target.
The payload: Monomethyl auristatin E (MMAE) was used as payload. MMAE is a potent antimitotic agent that inhibits cell division by blocking the polymerization of tubulin and is the most common ADC payload used to be linked to antibodies in clinical development for oncologic applications.
The linker: mc-vc-PABc was used as a cleavable linker. PB-223 was conjugated to the linker-payload through a cysteine-based conjugation method.
The drug-to-antibody ratio (DAR) of PB-vcMMAE-5 is 3.92.

Study presented at SITC (Free SITC Whitepaper) Annual Meeting 2025 includes the following data:

PB-223 specific binding to human tumor tissues by immunohistochemistry (IHC): PB-223 binds selectively to human tumor tissues and not to human normal tissue. PB-223 strongly reacted with colorectal, pancreatic, lung, prostate, and ovarian tumor tissues.
In vitro  efficacy of PB-vcMMAE-5 against several human cancer cell lines: The in vitro cytotoxicity of PB-vc-MMAE-5 was evaluated in 9 human cancer cell lines, including prostate (PC-3, LnCAP), triple negative breast (HCC1937, MDA-MB-231), ER+,PR+,HER2+ breast (BT-474), squamous cell carcinoma of the lung (NCI-H226), ovarian (OV-90), colorectal (SW403), and pancreatic (CFPAC-1) cancer cell lines. This study shows that PB-vcMMAE-5 effectively killed all cell lines tested, with the highest percentage of killing observed against MDA-MB-231 (triple negative breast), LnCAP (prostate), OV-90 (ovarian), and NCI-H226 (lung) cancer cell lines.
In contrast, naked PB-223 mAb showed no killing in all cell lines tested.

In vivo safety of PB-vcMMAE-5 in mice: NOD-SCID mice bearing OV-90 (ovarian) xenografts were treated with weekly doses of PBS, MMAE alone, or PB-vc-MMAE-5 (1, 3, 6, or 9 mg/kg) for five weeks. Animal body weight was monitored regularly, twice a week, as an indirect measure of toxicity. The ADC PB-vcMMAE-5 was well tolerated in mice. No sign of distress and no loss of body weight were observed.
No significant changes in body weight, blood parameters including hematology and clinical chemistry, nor pathological changes in the liver, spleen, brain, or heart of mice treated with efficacious doses of the ADC were observed compared with control groups.
In vivo  efficacy of PB-vcMMAE-5 in mice: The efficacy of the ADC PB-vcMMAE-5 was assessed in OV-90 (ovarian) subcutaneous xenograft model established in NOD-SCID mice. The ADC PB-vcMMAE-5 was administered intravenously at doses 1, 3, 6 or 9 mg/kg, once per week for five weeks.
On day 31 from the first ADC infusion, most alive mice were sacrificed, and tumors were excised for histological analysis using Ki-67 staining to assess proliferating viable tumor cells. To further assess systemic toxicity and prolonged efficacy, three mice each from the 6 and 9 mg/kg groups were followed to day 45.

Data presented in this study show that PB-vcMMAE-5 induced significant tumor growth inhibition compared to controls in a dose-dependent manner.
The highest tumor growth inhibition was observed at 6 and 9 mg/kg doses.

In addition, analysis of tumors at day 45 showed absence of viable tumor cells and presence of tumor cells in necrosis, in mice treated with PB-vcMMAE-5 at 9 mg/kg.
Findings from this study showed that PB-vcMMAE-5 can kill human cancer cells expressing PB-223’s target, is not toxic in vivo in mice, and is highly effective in vivo at 9 mg/kg in NOD-SCID mice bearing human ovarian cancer. In addition, in a poster presented at AACR (Free AACR Whitepaper) Annual Meeting 2025 we reported that PB-vcMMAE-5 is stable in human plasma.

All these data suggest that PB-vcMMAE-5 has promising potential as a therapeutic option for a range of human malignancies expressing core 2 O-glycans.

The PDF of the poster will be available starting from November 5th, 2025, at the following link:

View Source

(Press release, Precision Biologics, NOV 5, 2025, View Source [SID1234659488])

On November 5, 2025 Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company creating a new class of drugs based on targeted protein degradation, reported financial results for the third quarter ended September 30, 2025, and provided a corporate update.

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"The third quarter was marked by meaningful pipeline progress and strategic decisions aimed at positioning the company for sustained long-term growth and value creation," said John Houston, Ph.D., Chairperson, Chief Executive Officer, and President of Arvinas. "We have entered the beginning of a data-rich period with multiple readouts from our early-stage clinical programs. We also presented the first preclinical data from ARV-027, our promising new clinical candidate that targets the root cause of spinal bulbar muscular atrophy. Looking ahead, our mission is clear: to drive innovation across our PROTAC degrader portfolio and deliver transformative therapies to patients."

3Q 2025 Business Highlights and Recent Developments

ARV-102: Oral PROTAC LRRK2 degrader

Presented positive data from two Phase 1 clinical trials in an oral session at the International Congress of Parkinson’s Disease and Movement Disorders.
In single ascending and multiple ascending doses in healthy volunteers, ARV-102 was generally well tolerated at single doses up to 200 mg and multiple daily doses up to 80 mg, with no discontinuations due to adverse events (AEs) or serious adverse events (SAEs) observed in the study population. ARV-102 showed:
Increased exposure in a dose-dependent manner in plasma and cerebrospinal fluid (CSF), the latter indicating brain penetration.
Greater than 90% reductions of LRRK2 protein in peripheral blood mononuclear cells (PBMCs) and greater than 50% reductions in CSF (repeated daily doses ≥20 mg).
Reduced plasma concentrations of phospho-Rab10T73 and urine concentrations of bis(monoacylglycerol)phosphate (BMP), a sensitive biomarker for modulation of the lysosomal pathway downstream of LRRK2 (repeated daily doses).
Significant decreases in lysosomal pathway markers and neuroinflammatory microglial markers previously shown to be elevated in patients with Parkinson’s disease harboring LRRK2 variants as measured by unbiased proteomic analysis of CSF (ARV-102 80 mg once daily for 14 days).
To the Company’s knowledge, this is the first time an investigational LRRK2 therapy has, at 14 days in healthy volunteers, shown effects on distal pathway biomarkers in CSF that are elevated in patients with Parkinson’s disease.
In the ongoing single ascending dose trial in patients with Parkinson’ disease, single doses of ARV-102 (50 mg or 200 mg) were well tolerated with only mild treatment-related AEs including headache, diarrhea, and nausea; no SAEs occurred. ARV-102 showed:
Dose-dependent increases in exposure in both plasma and CSF, the latter indicating brain penetration.
Median PBMC LRRK2 protein reductions of 86% with the 50 mg dose and 97% with the 200 mg dose.
Initiated the multiple dose cohort of the Phase 1 clinical trial in patients with Parkinson’s disease.
ARV-393: Oral PROTAC BCL6 degrader

Announced there have been multiple responses in early cohorts of both B-and T-cell lymphomas in the first-in-human Phase 1 trial in patients with non-Hodgkin lymphoma (NHL). The anticipated effective exposure level has not been achieved, and dose escalation in the trial is ongoing (ClinicalTrials.gov Identifier: NCT06393738).
ARV-806: Novel PROTAC KRAS G12D degrader

Presented new preclinical data at 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) highlighting its high potency and clear differentiation from both KRAS inhibitors and degraders currently in the clinic while also demonstrating:
Dose-dependent, selective, robust anti-tumor activity, with regressions across preclinical models of KRAS G12D-mutant cancers.
In vitro potency approximately 25 times greater than KRAS inhibitors and 40 times greater than the leading clinical-stage degrader.
Degradation >90% for 7 days after single dose and significant efficacy in models of pancreatic, colorectal, and lung cancer.
Initiated Phase 1 trial evaluating ARV-806 in patients with solid tumors harboring KRAS G12D mutations (ClinicalTrials.gov Identifier: NCT07023731).
ARV-027: Oral PROTAC polyQ-AR degrader

Presented new preclinical data at the International Congress of the World Muscle Society demonstrating induced robust degradation of polyQ-AR in human myotubes derived from spinal bulbar muscular atrophy (SBMA) patient-induced pluripotent stem cells, as well as:
Dose-dependent degradation of polyQ-AR in mouse muscle that was sustained for more than 24 hours (single oral dose).
Reductions in muscle monomeric polyQ-AR levels between 40-60%, improved muscle grip strength, and restored muscle endurance to wild-type levels in an SBMA mouse model.
Vepdegestrant: Oral PROTAC ER degrader
As part of Arvinas’ global collaboration with Pfizer, the companies:

Announced the U.S. Food and Drug Administration (FDA) acceptance of the New Drug Application (NDA) for vepdegestrant for the treatment of estrogen receptor 1 (ESR1) mutated, estrogen receptor-positive (ER+)/human epidermal growth factor receptor 2-negative (HER2-) advanced or metastatic breast cancer previously treated with endocrine-based therapy. The FDA has assigned a Prescription Drug User Fee Act (PDUFA) action date of June 5, 2026.
Announced agreement with Pfizer to jointly select a third party for the commercialization and potential further development of vepdegestrant, with the goal of rapidly bringing it to patients, if approved.
Presented new patient-reported outcomes data from the Phase 3 VERITAC-2 clinical trial and Phase 2 results from the TACTIVE-N clinical trial at the 2025 European Society for Medical Oncology Congress:
Patient-reported outcomes data from the VERITAC-2 clinical trial highlighted that patients with ESR1-mutated disease treated with vepdegestrant reported a statistically significant delay in deterioration of overall quality of life, pain, and multiple functioning domains versus those who received fulvestrant.
The TACTIVE-N clinical trial, which evaluated neoadjuvant vepdegestrant in postmenopausal women with ER+/HER2– localized breast cancer, showed that neoadjuvant vepdegestrant demonstrated biological and clinical activity in this treatment-naïve, predominantly ESR1 wild-type population of postmenopausal women with ER+/HER2- localized breast cancer.
Anticipated Upcoming Milestones and Expectations

ARV-102: Oral PROTAC LRRK2 degrader

Initiate Phase 1b clinical trial in patients with progressive supranuclear palsy (1H 2026).
Present initial data from the multiple dose cohort of the Phase 1 clinical trial in patients with Parkinson’s disease (2026).
ARV-393: Oral PROTAC BCL6 degrader

Share preclinical data in combination with glofitamab in models of aggressive high grade DLBCL at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting (Dec. 6-9, 2025).
Share updated clinical data from the ongoing Phase 1 clinical trial in patients with NHL (ClinicalTrials.gov Identifier: NCT06393738) at a medical congress (2026).
Initiate enrollment in Phase 1 clinical trial in combination with glofitamab in patients with DLBCL (2026).
ARV-806: Novel PROTAC KRAS G12D degrader

Continue enrollment in the Phase 1 trial of ARV-806 in patients with solid tumors harboring KRAS G12D mutations (ClinicalTrials.gov Identifier: NCT07023731).
Share initial clinical data in patients with solid tumors harboring KRAS G12D mutations (2026).
ARV-027: Oral PROTAC polyQ-AR degrader

Initiate a first-in-human Phase 1 clinical trial in healthy volunteers, pending regulatory feedback (2026).
ARV-6723: Oral PROTAC HPK1 degrader

Present preclinical data at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting (Nov. 8, 2025).
Initiate Phase 1 clinical trial in patients with advanced solid tumors, pending regulatory feedback (2026).
Vepdegestrant: Oral PROTAC ER degrader
As part of Arvinas’ global collaboration with Pfizer, the companies plan to:

Identify and select a partner with the capabilities and expertise to maximize the commercial potential of vepdegestrant.
Financial Guidance
Based on its current operating plan, Arvinas believes its cash, cash equivalents, and marketable securities as of September 30, 2025, is sufficient to fund planned operating expenses and capital expenditure requirements into the second half of 2028.

Third Quarter Financial Results
Cash, Cash Equivalents, and Marketable Securities Position: As of September 30, 2025, cash, cash equivalents, and marketable securities were $787.6 million as compared with $1,039.4 million as of December 31, 2024. The decrease in cash, cash equivalents, and marketable securities of $251.8 million for the nine months ended September 30, 2025, was primarily related to cash used in operations of $233.1 million, repurchases of our common shares under our Stock Repurchase Program of $17.8 million, the purchase of lab equipment and leasehold improvements of $1.7 million.

Research and Development Expenses: Generally Accepted Accounting Principles (GAAP) Research and development (R&D) expenses were $64.7 million for the quarter ended September 30, 2025, as compared with $86.9 million for the quarter ended September 30, 2024. The decrease in R&D expenses of $22.2 million for the quarter was primarily due to a decrease in external expenses of $7.4 million and a decrease in compensation and related personnel expenses of $14.2 million, which are not allocated by program. External expenses include program-specific expenses, which decreased by $6.5 million, primarily driven by decreases in our vepdegestrant (ARV-471), luxdegalutamide (ARV-766), and bavdegalutamide (ARV-110) programs of $5.4 million, $4.7 million, and $2.4 million, respectively, partially offset by increases in ARV-806 of $4.3 million.

Non-GAAP R&D expenses were $56.9 million for the quarter ended September 30, 2025, as compared with $73.2 million for the quarter ended September 30, 2024, excluding $0.4 million of restructuring expense for the quarter ended September 30, 2025, and $7.4 million and $13.7 million of non-cash stock-based compensation expense for the quarters ended September 30, 2025, and 2024, respectively. A reconciliation of GAAP to non-GAAP financial measures used in this press release can be found at the end of this press release.

General and Administrative Expenses: GAAP General and administrative (G&A) expenses were $21.0 million for the quarter ended September 30, 2025, as compared with $75.8 million for the quarter ended September 30, 2024. The decrease in G&A expenses of $54.8 million for the quarter was primarily due to a decrease of $43.4 million for the termination of our laboratory and office space lease with 101 College Street LLC in August 2024, a decrease in personnel and infrastructure related costs of $7.3 million, and professional fees of $3.6 million.

Non-GAAP G&A expenses were $14.6 million for the quarter ended September 30, 2025, as compared with $64.8 million for the quarter ended September 30, 2024, excluding $0.6 million of restructuring related reversal of previously recognized expense for the quarter ended September 30, 2025, and $7.0 million and $11.0 million of non-cash stock-based compensation expenses for the quarter ended September 30, 2025, and 2024, respectively. A reconciliation of GAAP to non-GAAP financial measures used in this press release can be found at the end of this press release.

Revenue: Revenue was $41.9 million for the quarter ended September 30, 2025, as compared with $102.4 million for the quarter ended September 30, 2024. Revenue for the quarter is related to the Vepdegestrant (ARV-471) Collaboration Agreement with Pfizer and the collaboration and license agreement with Pfizer. The decrease of $60.5 million was primarily due to $76.7 million of decreased revenue from the Novartis License Agreement and the Novartis Asset Agreement, both of which were entered into during the three months ended June 30, 2024, and were completed by December 31, 2024, as the technology transfer of our ongoing and planned clinical trials of luxdegalutamide (ARV-766) were transitioned to Novartis. Revenue from the Vepdegestrant (ARV-471) Collaboration Agreement with Pfizer decreased by $3.1 million and revenue from the Bayer Collaboration Agreement decreased by $0.5 million as a result of the termination of the Bayer Collaboration Agreement in August 2024. The overall decrease was offset by the recognition of $20.0 million for achievement of a development milestone pursuant to the terms of the Novartis License Agreement.

Investor Call & Webcast Details
Arvinas will host a conference call and webcast today, November 5, 2025, at 8:00 a.m. ET to review its third quarter 2025 financial results and discuss recent corporate updates. Participants are invited to listen by going to the Events and Presentation section under the Investors page on the Arvinas website at www.arvinas.com. A replay of the webcast will be available on the Arvinas website following the completion of the event and will be archived for up to 30 days.

(Press release, Arvinas, NOV 5, 2025, View Source [SID1234659456])