Gilead Provides Update on Phase 3 STAR-221 Study

On December 12, 2025 Gilead Sciences and Arcus Biosciences reported the discontinuation of the Phase 3 STAR-221 study evaluating the anti-TIGIT antibody domvanalimab plus anti-PD-1 antibody zimberelimab and chemotherapy versus nivolumab plus chemotherapy as first-line treatment for HER2-negative advanced gastric and esophageal cancers. The decision is based on the recommendation from the Independent Data Monitoring Committee (IDMC) following their review of data from a pre-specified interim analysis of overall survival (OS).

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In the pre-specified interim analysis, the combination of domvanalimab plus zimberelimab and chemotherapy did not improve OS relative to nivolumab plus chemotherapy, the standard of care, and there was low likelihood of achieving a positive survival benefit with further follow-up. The safety profile for the combination of domvanalimab plus zimberelimab and chemotherapy was consistent with the control arm, nivolumab plus chemotherapy, and there were no new safety findings.

The companies are informing regulators and communicating with investigators for the STAR-221 and the Phase 2 EDGE-Gastric studies to determine appropriate next steps for patients. The companies are conducting a detailed analysis to understand these results, which will be published in the future.

"These results offer valuable insights into the complexity of treating advanced gastroesophageal cancers," said Dietmar Berger, MD, PhD, Chief Medical Officer at Gilead Sciences. "We will collaborate closely to understand the full scope of the data and engage key stakeholders in determining the appropriate next steps. We are deeply grateful to the patients, families, and healthcare professionals who participated in the STAR-221 study and contributed to this important work."

Currently, there are no changes to other ongoing domvanalimab studies beyond the upper gastrointestinal (GI) program. Arcus and Gilead will share further guidance as it becomes available.

Domvanalimab and zimberelimab are investigational molecules, and neither Gilead nor Arcus has received approval from any regulatory authority for any use globally, and their safety and efficacy have not been established.

(Press release, Gilead Sciences, DEC 12, 2025, View Source [SID1234661411])

Natera and MEDSIR to Collaborate on the MiRaDoR Trial in Breast Cancer

On December 12, 2025 Natera, Inc. (NASDAQ: NTRA), a global leader in cell-free DNA and precision medicine, and MEDSIR (Medica Scientia Innovation Research), a global leader in oncology research, reported their collaboration on the MiRaDoR (NCT05708235) study, which is a multicenter, phase II clinical trial in hormone receptor-positive, HER2-negative (HR+/HER2-) breast cancer.

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Breast cancer is the most common cancer in women worldwide, with approximately 2.3 million new cases diagnosed in 2022.1 Despite advances in treatment, recurrence remains a key concern for patients with HR+/HER2- disease, which represents roughly 70% of all breast cancer cases.2

Funded by F. Hoffman-La Roche Ltd., and sponsored by MEDSIR, MiRaDoR will use Signatera Genome to evaluate the efficacy of different therapeutic approaches in early-stage HR+/HER2- breast cancer. Up to 60 patients who are Signatera-positive without clinical nor radiological evidence of disease recurrence will be sequentially enrolled into one of four treatment arms:

Arm A: Standard of care endocrine therapy given during the first 90-day period, then patients switch to Arms B, C or D
Arm B: Giredestrant (oral selective estrogen receptor degrader)
Arm C: Giredestrant plus Abemaciclib (CDK4/6 inhibitor)
Arm D: Giredestrant plus Inavolisib (PIK3CA inhibitor; for patients with PIK3CA mutations)
The trial will enable investigators to evaluate serial circulating-tumor DNA (ctDNA) levels in each treatment arm as a predictive marker of treatment response. The study’s primary endpoint is the proportion of patients who have achieved a 90% decrease or clearance in baseline ctDNA after three months of treatment. Participants will have additional Signatera testing at 6, 9 and 12 months, and every six months thereafter until study treatment discontinuation. Results may help determine if specific therapy combinations are more effective in terms of ctDNA decrease than standard of care endocrine treatment.

"Uniting Signatera Genome’s ability to detect molecular residual disease with genomic profiling creates a new standard for precision oncology clinical trials," said Angel Rodriguez, M.D., senior medical director of oncology at Natera. "In the MiRaDoR trial, investigators are moving beyond surveillance; they are also characterizing the specific genomic driver, PIK3CA, and no longer just asking ‘is the cancer back?’ but also answering ‘how do we treat it?’"

Enrollment for MiRaDoR is underway, with several U.K. sites already active and additional site activations expected in Europe in 2026.

(Press release, MedSIR, DEC 12, 2025, View Source [SID1234661410])

Arcus Provides Update on Phase 3 STAR-221 Study and Concentrates Its R&D Investment on Casdatifan and Emerging Inflammation and Immunology Portfolio

On December 12, 2025 Arcus Biosciences, Inc. (NYSE:RCUS), a clinical-stage, global biopharmaceutical company focused on developing differentiated molecules and combination therapies for patients with cancer, inflammatory and autoimmune diseases, reported the discontinuation of the Phase 3 STAR-221 study, being conducted in partnership with Gilead Sciences, Inc., due to futility. The decision is based on the recommendation from the Independent Data Monitoring Committee (IDMC) following its review of data from an event-driven, pre-specified interim analysis of overall survival (OS).

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STAR-221 evaluated the anti-TIGIT antibody domvanalimab plus anti-PD-1 antibody zimberelimab and chemotherapy versus nivolumab plus chemotherapy as a first-line treatment for advanced gastric and esophageal cancers. At the interim analysis, the domvanalimab-based combination did not improve OS relative to that of nivolumab plus chemotherapy. The safety profile for the domvanalimab-based combination was similar to that of nivolumab plus chemotherapy, and there were no new safety findings identified.

"Patients in the domvanalimab-containing arm derived the same benefit as patients treated in the control arm, and there were no new safety concerns," said Richard Markus, MD, chief medical officer at Arcus. "We are disappointed with this outcome and sincerely thank all those who participated in the study and made this research possible. We remain committed to advancing research for people living with cancer and immune-related diseases."

The STAR-221 and the Phase 2 EDGE-Gastric studies will be discontinued, and Arcus and Gilead are communicating with investigators to determine appropriate next steps for patients in the study in addition to conducting a detailed analysis to better understand these results.

Future Direction

Arcus’s R&D investment and resources will focus on casdatifan, a potential best-in-class HIF-2a inhibitor, and its emerging small molecule I&I programs.

"The results from STAR-221 are not what we had hoped for, and we have important work ahead to meet the needs of patients on our domvanalimab studies and also accelerate the casdatifan and I&I programs," said Terry Rosen, chief executive officer of Arcus. "We are fortunate to be well capitalized and plan to focus our resources on casdatifan, including studying new early-line combinations in kidney cancer, broadening its development into new tumor types, and extending our capabilities beyond oncology."

Casdatifan targets a validated mechanism of action and has shown robust single-agent activity based on data reported from more than 120 patients with late-line clear cell renal cell carcinoma (ccRCC) in the ARC-20 Phase 1/1b clinical study. Those data have shown improvement on every efficacy measure evaluated, including overall response rate and progression-free survival (PFS), relative to reported data for the only marketed HIF-2a inhibitor. Arcus owns all of the rights to casdatifan outside of Japan and certain other Asian territories, which were optioned by Taiho Pharmaceutical Co., Ltd. in October 2025.

Arcus is focused on rapidly developing casdatifan in both immunotherapy (IO)-experienced and first-line metastatic ccRCC, and its clinical investment in 2026 and 2027 will be primarily focused on maximizing the potential of casdatifan. The casdatifan program is expected to have multiple data readouts and cohort and study initiations in 2026 including:

Early 2026: Additional analyses from the ARC-20 cohorts evaluating casdatifan monotherapy in late-line ccRCC, including updated PFS data for the 100mg once-daily (QD) cohort, which utilizes the selected Phase 3 dose and formulation.
Mid-2026: More mature data from the ARC-20 cohort evaluating casdatifan plus cabozantinib in the IO-experienced setting. This is the same setting and combination being evaluated in the ongoing Phase 3 PEAK-1 study.
2H 2026: Initial data from one or more ARC-20 cohorts evaluating casdatifan in early-line settings, as well as a go-no-go decision on the Phase 3 portion of eVOLVE-RCC02.
Late 2026: Potential initiation of a Phase 3 registrational study in an early-line or first-line ccRCC setting.
Arcus’s oncology portfolio also includes quemliclustat, a small-molecule CD73 inhibitor that completed enrollment of PRISM-1, the Phase 3 study in pancreatic cancer, earlier this year. Results are expected in 2027 for the registrational study, which is evaluating quemliclustat plus gemcitabine/nab-paclitaxel versus gemcitabine/nab-paclitaxel in first-line metastatic pancreatic ductal adenocarcinoma.

Arcus’s I&I portfolio includes several oral, small molecules being developed in indications currently dominated by injectable drugs. The portfolio includes the following programs: MRGPRX2, TNF, CCR6, CD89 and CD40L. Arcus expects to advance two potentially best-in-class small molecule inhibitors into the clinic in the timeframes noted below:

2026: MRGPRX2, a potential treatment for atopic dermatitis and chronic spontaneous urticaria; and
Late 2026 – early 2027: TNF, a potential treatment for rheumatoid arthritis, psoriasis and inflammatory bowel disease (such as ulcerative colitis).
Domvanalimab, zimberelimab and quemliclustat are investigational molecules, and neither Arcus nor Gilead has received approval from any regulatory authority for any use globally, and their safety and efficacy have not been established. Casdatifan is also an investigational molecule, and Arcus has not received approval from any regulatory authority for any use globally, and its safety and efficacy have not been established.

About RCC

According to the American Cancer Society, kidney cancer is among the top 10 most commonly diagnosed forms of cancer among both men and women in the U.S., and an estimated 80,980 Americans will be diagnosed with kidney cancer in 2025. Clear cell RCC is the most common type of kidney cancer in adults. If detected in its early stages, the five-year survival rate for RCC is high; for patients with advanced or late-stage metastatic RCC, however, the five-year survival rate is only 18%. In 2022, approximately 32,200 patients with advanced kidney cancer required systemic therapy in the U.S., with over 20,000 patients receiving first-line treatment.

About Casdatifan (AB521)

Casdatifan is a small-molecule inhibitor of HIF-2a, a master switch that turns on hundreds of genes in response to low oxygen levels. In a majority of people with the most common form of kidney cancer (clear cell renal cell carcinoma), genetic anomalies result in the misregulation of this master switch and transformation of normal kidney cells into cancerous ones. Casdatifan was designed to provide deep and durable inhibition of the HIF-2a pathway. Early clinical studies have shown high response rates and a low primary progression rate relative to clinical benchmarks, warranting further investigation in late-stage studies. Casdatifan, which is administered in pill form once daily, has a safety profile that allows it to be investigated in combination with other treatments.

About Gastric and Esophageal Cancer

According to the World Health Organization, gastric cancer and esophageal cancer are the fifth and seventh leading causes of cancer deaths globally, accounting for more than 1.1 million cancer deaths each year. More than one-third of patients are diagnosed at an advanced stage, when five-year survival rates are only 5-7%.

About the STAR-221 Study

The STAR-221 study is a global, randomized, open-label, Phase 3 trial evaluating domvanalimab plus zimberelimab and chemotherapy versus nivolumab plus chemotherapy as a first-line treatment in locally advanced, unresectable or metastatic HER-2 negative gastric, gastroesophageal junction and esophageal adenocarcinomas. The study enrolled 1,040 patients from nearly 30 countries and participants were randomized 1:1 between two arms:

1600mg of domvanalimab intravenously (IV) every four weeks plus 480mg of zimberelimab IV every four weeks plus FOLFOX (oxaliplatin, leucovorin, fluorouracil) every two weeks or 1200mg of domvanalimab plus 360mg of zimberelimab every three weeks plus CAPOX (capecitabine and oxaliplatin) every three weeks.
240mg of nivolumab IV every two weeks plus FOLFOX every two weeks or 360mg of nivolumab plus CAPOX every three weeks.
The primary endpoints of the study are overall survival in PD-L1-high tumors (TAP ≥5%), PD-L1-positive tumors (TAP ≥1%) and in the intent-to-treat population (all PD-L1 levels), as assessed by central PD-L1 testing based on Tumor Area Positivity (TAP) score. Key secondary endpoints include progression-free survival (PFS) and patient-reported outcomes (PROs). Secondary endpoints include objective response rate (ORR), duration of response (DOR) and safety.

Taiho Pharmaceutical has development and commercial rights in Japan and other countries in Asia, excluding China, for domvanalimab and zimberelimab, and is conducting the ongoing STAR-221 Phase 3 registrational study in Japan.

More information about STAR-221 is available at ClinicalTrials.gov: NCT05568095.

About Domvanalimab

Domvanalimab is the first and most clinically advanced Fc-silent investigational monoclonal antibody that is specifically designed with Fc-silent properties to bind and block to the T-cell immunoreceptor with Ig and ITIM domains (TIGIT), a checkpoint receptor on immune cells that acts as a brake on the anticancer immune response. By binding to TIGIT with Fc-silent properties, domvanalimab is believed to work by freeing up immune-activating pathways and activating immune cells to attack and kill cancer cells without depleting the peripheral regulatory T cells important in avoiding immune-related toxicity. Combined inhibition of both TIGIT and programmed cell death protein-1 (PD-1) is believed to significantly enhance immune cell activation, as these checkpoint receptors play distinct, complementary roles in anti-tumor activity.

About Zimberelimab

Zimberelimab is an anti-programmed cell death protein-1 (PD-1) monoclonal antibody that binds PD-1, with the goal of restoring the antitumor activity of T cells. Zimberelimab has demonstrated high affinity, selectivity and potency in various tumor types. Zimberelimab is being evaluated in the U.S. and globally as a foundational anti-PD-1 treatment option in multiple ongoing clinical studies in combination with other immunotherapies. Guangzhou Gloria Biosciences Co. Ltd., which holds commercialization rights for zimberelimab in greater China, has obtained approval for zimberelimab for the treatment of recurrent or metastatic cervical cancer and for relapsed or refractory classical Hodgkin’s lymphoma. Zimberelimab is not approved for any use in the U.S. or other regions outside of China. Gloria conducts its development and commercialization activities independent of Arcus and Gilead.

(Press release, Arcus Biosciences, DEC 12, 2025, View Source [SID1234661409])

Marengo to Present Initial Results from Invikafusp Alfa and TRODELVY® Combination Study, STARt-002, at the 2025 San Antonio Breast Cancer Symposium

On December 12, 2025 Marengo Therapeutics, Inc., a clinical-stage biotechnology company pioneering precision immunotherapy for oncology and inflammation & immunology (I&I), reported initial clinical results from its ongoing STARt-002 phase 1b/2 trial during a late breaking presentation at the 2025 San Antonio Breast Cancer Symposium (SABCS) taking place December 9-12.

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Early findings from the combination study of Invikafusp alfa (Invika) and TRODELVY (sacituzumab govitecan-hziy; SG) suggest that this novel regimen, which leverages two key modalities (immunotherapy and ADCs), is well tolerated and biologically active across all dose levels evaluated. The safety profile of the combination was consistent with the known profiles of each agent.

"The early safety and pharmacodynamic data from STARt-002 are highly encouraging," said Steven Isakoff, M.D., Ph.D., Director of Breast Cancer Clinical Research at the Massachusetts General Hospital Cancer Center. "The combination of Invika with TRODELVY is scientifically compelling — pairing targeted T cell activation with ADC-mediated tumor killing. Seeing consistent Vβ6/10 expansion alongside early tumor responses reinforces the potential of this regimen to meaningfully benefit patients with metastatic breast cancer, and I look forward to the results from the ongoing phase 2 cohorts."

Pharmacodynamic analyses confirmed that Invika maintains its mechanism of action in combination with Trodelvy, inducing robust and selective expansion of Vβ6/10 T cells in patients with previously treated metastatic triple-negative breast cancer (TNBC) and HR+/HER2– metastatic breast cancer. Evidence of early anti-tumor activity was observed in almost all patients treated with this combination, including two confirmed partial responses.

A recommended phase 2 dose (RP2D) has now been established, and enrollment is ongoing in two phase 2 expansion cohorts for people with metastatic triple-negative breast cancer (TNBC) and HR+/HER2– metastatic breast cancer at select cancer centers across North America.

"Invikafusp has already demonstrated promising single-agent activity in PD-1-resistant tumors, including breast cancer," said Kevin Chin, M.D., Chief Medical Officer of Marengo Therapeutics. "These initial findings further support Invika as a potential immunotherapy backbone, particularly when paired with ADCs to treat immunologically ‘cold’ tumors such as breast cancer. We are encouraged by the safety, pharmacology, and early signs of clinical activity observed with the Invika and SG regimen and look forward to understanding the full clinical potential of this treatment regimen as STARt-002 advances through Phase 2."

Additional presentation details are as follows:

Presentation: Initial clinical and pharmacology results from START-002
Abstract Number: LBA 3714
Presentation Number: PS4-06-28
Poster Presentation Date/Time: Thursday, December 11, 2025, 5:00 PM – 6:30 PM
Presentation: Trial-in-progress: START-002
Abstract Number: 2124
Presentation Number: PS5-09-16
Poster Presentation Date/Time: Friday, December 12, 2025, 12:30 PM – 2:00 PM
The combination of invikafusp alfa and sacituzumab govitecan-hziy is investigational and not approved by any health authority globally. The safety and efficacy of this combination has not been established.

(Press release, Marengo Therapeutics, DEC 12, 2025, View Source [SID1234661407])

U.S. FDA approves AKEEGA® as the first precision therapy for BRCA2-mutated metastatic castration-sensitive prostate cancer with 54% reduction in disease progression vs standard of care*

On December 12, 2025 Johnson & Johnson (NYSE:JNJ) reported the U.S. Food and Drug Administration (FDA) approved the supplemental New Drug Application (sNDA) for AKEEGA (niraparib and abiraterone acetate dual-action tablet) plus prednisone for the treatment of patients with BRCA2-mutated metastatic castration-sensitive prostate cancer (mCSPC).1 Patients with BRCA mutations often have more aggressive forms of prostate cancer leading to poor prognosis, representing a significant unmet need not addressed by previously available therapies.2

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"There remains an urgent need for novel therapies for patients with BRCA2-mutated mCSPC, who face significantly faster disease progression and often shorter survival compared to those without the mutation," said Bradley McGregor, M.D., Director of Clinical Research for the Lank Center of Genitourinary Oncology at Dana-Farber Cancer Institute. "AMPLITUDE is the first study to show that this precision medicine combination of a PARP inhibitor with an androgen receptor pathway inhibitor delays both radiographic and symptomatic disease progression."

The approval is based on positive results from AMPLITUDE (NCT04497844), a randomized, double-blind, placebo-controlled, international Phase 3 clinical study. In patients with BRCA2-mutated mCSPC, treatment with AKEEGA plus prednisone and androgen deprivation therapy (ADT) significantly reduced the risk of radiographic progression or death by 54 percent (hazard ratio [HR] 0.46; 95 percent confidence interval [CI], 0.32–0.66) compared to placebo/abiraterone acetate plus prednisone and ADT, which is the current standard of care.1 AKEEGA plus prednisone and ADT also significantly prolonged the time to symptomatic progression by 59 percent (HR 0.41; 95 percent CI, 0.29–0.65).1

The observed safety profile of the combination of AKEEGA plus prednisone was consistent with the known safety profile of each FDA-approved monotherapy. In the AMPLITUDE clinical study, the most common adverse reactions (≥20%) including laboratory abnormalities, were decreased hemoglobin, decreased lymphocytes, musculoskeletal pain, fatigue, decreased platelets, increased alkaline phosphatase, constipation, hypertension, nausea, decreased neutrophils, increased creatinine, increased potassium, decreased potassium, decreased aspartate aminotransferase, fluid retention/edema, increased bilirubin, respiratory tract infection and arrhythmia.1

"This expanded indication for AKEEGA reflects our commitment to push the boundaries of science and deliver more personalized, effective treatment options across the prostate cancer continuum," said Mahadi Baig, M.D., M.H.C.M., Vice President, Head of Solid Tumors, U.S. Medical Affairs, Johnson & Johnson Innovative Medicine. "Supported by strong clinical data, AKEEGA is now the first and only PARP-based precision medicine combination treatment in BRCA2-mutated mCSPC, offering patients hope for more time with a new way to potentially delay their cancer from progressing."

Johnson & Johnson is committed to helping patients access our treatments. Once a patient and their doctor have decided that AKEEGA is right for the patient, J&J withMe provides a simple, comprehensive patient support program offering cost support and educational resources, at no cost to the patient.

*The hazard ratio [HR] 0.46; 95 percent confidence interval [CI], 0.32–0.66) compared to standard of care, AKEEGA plus prednisone and ADT also significantly prolonged the time to symptomatic progression by 59 percent (HR 0.41; 95 percent CI, 0.29–0.65).1

About AMPLITUDE
AMPLITUDE (NCT04497844) is an ongoing, Phase 3, randomized, double-blind, placebo-controlled, multicenter, global study evaluating the efficacy and safety of niraparib and abiraterone acetate in a dual-action tablet (DAT) formulation with prednisone plus androgen deprivation therapy (ADT) compared to matching oral placebo/abiraterone acetate with prednisone plus ADT in patients with deleterious germline or somatic homologous recombination repair (HRR) gene-altered metastatic castration-sensitive prostate cancer (mCSPC). The primary endpoint is radiographic progression-free survival (rPFS). The study enrolled 696 participants from 32 countries.

About Metastatic Castration-Sensitive Prostate Cancer
Metastatic castration-sensitive prostate cancer (mCSPC), also known as metastatic hormone-sensitive prostate cancer (mHSPC), refers to prostate cancer that has spread to other parts of the body but still responds to hormone therapy (androgen deprivation therapy).3 While the treatment landscape has advanced in recent years, almost all patients eventually develop resistance to therapy, and the disease progresses to metastatic castration-resistant prostate cancer (mCRPC) – an aggressive and currently incurable disease stage.4 Approximately 25 percent of patients with mCSPC have HRR gene alterations, including BRCA, which have been shown to negatively impact outcomes.2,5 Patients with BRCA mutations experience approximately 50 percent faster disease progression and shorter survival, representing a significant unmet medical need not addressed by previously available therapies.2

About AKEEGA (niraparib and abiraterone acetate)
AKEEGA is a dual-action tablet (DAT), combining niraparib, a highly selective poly (ADP-ribose) polymerase (PARP) inhibitor, and abiraterone acetate, a CYP17 inhibitor. AKEEGA together with prednisone or prednisolone was approved in April 2023 by the European Medicines Agency, and in August 2023 by the U.S. FDA following Priority Review, for the treatment of patients with BRCA-mutated metastatic castration-resistant prostate cancer (mCRPC). AKEEGA plus prednisone was approved by the U.S. FDA in December 2025 under Priority Review for the treatment of patients with BRCA2-mutated metastatic castration-sensitive prostate cancer (mCSPC). Patients are selected for therapy based on an FDA-approved test for genetic alterations. Additional marketing authorization applications are under review across a number of countries globally.

In April 2016, Janssen Biotech, Inc. entered a worldwide (except Japan) collaboration and license agreement with TESARO, Inc. (acquired by GlaxoSmithKline [GSK] in 2019) for exclusive rights to niraparib in prostate cancer.

For more information visit www.akeegahcp.com.

AKEEGA INDICATIONS AND IMPORTANT SAFETY INFORMATION

INDICATIONS

AKEEGA is a combination of niraparib, a poly (ADP-ribose) polymerase (PARP) inhibitor, and abiraterone acetate, a CYP17 inhibitor indicated with prednisone for the treatment of adult patients with:

deleterious or suspected deleterious BRCA2-mutated (BRCA2m) metastatic castration-sensitive prostate cancer (mCSPC).
deleterious or suspected deleterious BRCA-mutated (BRCAm) metastatic castration-resistant prostate cancer (mCRPC).
Select patients for therapy based on an FDA approved test for AKEEGA
IMPORTANT SAFETY INFORMATION

WARNINGS AND PRECAUTIONS

Myelodysplastic Syndrome/Acute Myeloid Leukemia
AKEEGA may cause myelodysplastic syndrome/acute myeloid leukemia (MDS/AML).

In the individual AMPLITUDE and MAGNITUDE studies, MDS or AML, including cases with fatal outcomes, were reported in 0.6% (2/347) and 0.5% (1/212) of patients treated with AKEEGA plus prednisone, respectively.

All patients in other tumor types treated with niraparib, a component of AKEEGA, who developed secondary MDS/cancer-therapy-related AML had received previous chemotherapy with platinum agents and/or other DNA-damaging agents, including radiotherapy.

For suspected MDS/AML or prolonged hematological toxicities, refer the patient to a hematologist for further evaluation. Discontinue AKEEGA if MDS/AML is confirmed.

Myelosuppression
AKEEGA may cause myelosuppression (anemia, thrombocytopenia, or neutropenia).

In AMPLITUDE, Grade 3-4 anemia, neutropenia, and thrombocytopenia were reported, respectively in 29 %, 10 %, and 4.9% of patients receiving AKEEGA. Overall, 25% of patients with anemia required a red blood cell transfusion, including 15% who required more than one transfusion. Discontinuation due to anemia occurred in 1.2% of patients.

In MAGNITUDE Cohort 1, Grade 3-4 anemia, thrombocytopenia, and neutropenia were reported, respectively in 28%, 8%, and 7% of patients receiving AKEEGA. Overall, 27% of patients with anemia required a red blood cell transfusion, including 19.5% who required more than one transfusion. Discontinuation due to anemia occurred in 3% of patients.

Monitor complete blood counts weekly during the first month of AKEEGA treatment, every two weeks for the next two months, monthly for the remainder of the first year and then every other month, and as clinically indicated. Do not start AKEEGA until patients have adequately recovered from hematologic toxicity caused by previous therapy. If hematologic toxicities do not resolve within 28 days following interruption, discontinue AKEEGA and refer the patient to a hematologist for further investigations, including bone marrow analysis and blood sample for cytogenetics.

Hypokalemia, Fluid Retention, and Cardiovascular Adverse Reactions
AKEEGA may cause hypokalemia and fluid retention as a consequence of increased mineralocorticoid levels resulting from CYP17 inhibition. In post-marketing experience, QT prolongation and Torsades de Pointes have been observed in patients who develop hypokalemia while taking abiraterone acetate, a component of AKEEGA. Hypertension and hypertensive crisis have also been reported in patients treated with niraparib, a component of AKEEGA.

In AMPLITUDE, which used prednisone 5 mg daily in combination with AKEEGA, Grades 3-4 hypokalemia was detected in 9% of patients on the AKEEGA arm, and Grades 3-4 hypertension was observed in 30% of patients on the AKEEGA arm.

In MAGNITUDE Cohort 1, which used prednisone 10 mg daily in combination with AKEEGA, Grades 3-4 hypokalemia was detected in 2.7% of patients on the AKEEGA arm and Grades 3-4 hypertension was observed in 14% of patients on the AKEEGA arm.

Monitor patients for hypertension, hypokalemia, and fluid retention at least weekly for the first two months, then once a month. Closely monitor patients whose underlying medical conditions might be compromised by increases in blood pressure, hypokalemia, or fluid retention, such as those with heart failure, recent myocardial infarction, cardiovascular disease, or ventricular arrhythmia. Control hypertension and correct hypokalemia before and during treatment with AKEEGA. Discontinue AKEEGA in patients who develop hypertensive crisis or other severe cardiovascular adverse reactions.

The safety of AKEEGA in patients with New York Heart Association (NYHA) Class II to IV heart failure has not been established because these patients were excluded from AMPLITUDE and MAGNITUDE.

Hepatotoxicity
AKEEGA may cause hepatotoxicity.

Hepatotoxicity in patients receiving abiraterone acetate, a component of AKEEGA, has been reported in clinical trials. In post-marketing experience, there have been abiraterone acetate-associated severe hepatic toxicity, including fulminant hepatitis, acute liver failure, and deaths.

In AMPLITUDE, Grade 3-4 ALT or AST increases (at least 5x ULN) were reported in 1.9% and 1.3% of patients, respectively.

In MAGNITUDE Cohort 1, Grade 3-4 ALT or AST increases (at least 5x ULN) were reported in 1.8% and 0.9% of patients respectively.

The safety of AKEEGA in patients with moderate or severe hepatic impairment has not been established as these patients were excluded from AMPLITUDE and MAGNITUDE.

Measure serum transaminases (ALT and AST) and bilirubin levels prior to starting treatment with AKEEGA, every two weeks for the first three months of treatment and monthly thereafter. Promptly measure serum total bilirubin, AST, and ALT if clinical symptoms or signs suggestive of hepatotoxicity develop. Elevations of AST, ALT, or bilirubin from the patient’s baseline should prompt more frequent monitoring and may require dosage modifications.

Permanently discontinue AKEEGA for patients who develop a concurrent elevation of ALT greater than 3 x ULN and total bilirubin greater than 2 x ULN in the absence of biliary obstruction or other causes responsible for the concurrent elevation, or in patients who develop ALT or AST ≥20 x ULN at any time after receiving AKEEGA.

Adrenocortical Insufficiency
AKEEGA may cause adrenal insufficiency.

Adrenocortical insufficiency has been reported in clinical trials in patients receiving abiraterone acetate, a component of AKEEGA, in combination with prednisone, following interruption of daily steroids and/or with concurrent infection or stress. Monitor patients for symptoms and signs of adrenocortical insufficiency, particularly if patients are withdrawn from prednisone, have prednisone dose reductions, or experience unusual stress. Symptoms and signs of adrenocortical insufficiency may be masked by adverse reactions associated with mineralocorticoid excess seen in patients treated with abiraterone acetate. If clinically indicated, perform appropriate tests to confirm the diagnosis of adrenocortical insufficiency. Increased doses of corticosteroids may be indicated before, during, and after stressful situations.

Hypoglycemia
AKEEGA may cause hypoglycemia in patients being treated with other medications for diabetes.

Severe hypoglycemia has been reported when abiraterone acetate, a component of AKEEGA, was administered to patients receiving medications containing thiazolidinediones (including pioglitazone) or repaglinide.

Monitor blood glucose in patients with diabetes during and after discontinuation of treatment with AKEEGA. Assess if antidiabetic drug dosage needs to be adjusted to minimize the risk of hypoglycemia.

Increased Fractures and Mortality in Combination with Radium 223 Dichloride
AKEEGA with prednisone is not recommended for use in combination with Ra-223 dichloride outside of clinical trials.

The clinical efficacy and safety of concurrent initiation of abiraterone acetate plus prednisone/prednisolone and radium Ra 223 dichloride was assessed in a randomized, placebo-controlled multicenter study (ERA-223 trial) in 806 patients with asymptomatic or mildly symptomatic castration-resistant prostate cancer with bone metastases. The study was unblinded early based on an Independent Data Monitoring Committee recommendation.

At the primary analysis, increased incidences of fractures (29% vs 11%) and deaths (39% vs 36%) have been observed in patients who received abiraterone acetate plus prednisone/prednisolone in combination with radium Ra 223 dichloride compared to patients who received placebo in combination with abiraterone acetate plus prednisone.

It is recommended that subsequent treatment with Ra-223 not be initiated for at least five days after the last administration of AKEEGA, in combination with prednisone.

Posterior Reversible Encephalopathy Syndrome
AKEEGA may cause Posterior Reversible Encephalopathy Syndrome (PRES).
PRES has been observed in patients treated with niraparib as a single agent at higher than the recommended dose of niraparib included in AKEEGA.

Monitor all patients treated with AKEEGA for signs and symptoms of PRES. If PRES is suspected, promptly discontinue AKEEGA and administer appropriate treatment. The safety of reinitiating AKEEGA in patients previously experiencing PRES is not known.

Embryo-Fetal Toxicity
The safety and efficacy of AKEEGA have not been established in females. Based on animal reproductive studies and mechanism of action, AKEEGA can cause fetal harm and loss of pregnancy when administered to a pregnant female.

Niraparib has the potential to cause teratogenicity and/or embryo-fetal death since niraparib is genotoxic and targets actively dividing cells in animals and patients (e.g., bone marrow).

In animal reproduction studies, oral administration of abiraterone acetate to pregnant rats during organogenesis caused adverse developmental effects at maternal exposures approximately ≥ 0.03 times the human exposure (AUC) at the recommended dose.

Advise males with female partners of reproductive potential to use effective contraception during treatment and for 4 months after the last dose of AKEEGA. Females who are or may become pregnant should handle AKEEGA with protection, e.g., gloves.

ADVERSE REACTIONS
BRCA2-mutated Metastatic Castration-Sensitive Prostate Cancer (mCSPC)
Serious adverse reactions occurred in 36% of patients who received AKEEGA. Serious adverse reactions reported in >2% of patients included anemia (4.9%), and pneumonia (3.7%). Fatal adverse reactions occurred in 4.9% of patients who received AKEEGA, including sudden death (1. 9%), COVID-19 pneumonia (1.2%), pneumocystis jirovecii pneumonia (0.6%), pneumonia (0.6%), and cardio-respiratory arrest (0.6%).

The most common adverse reactions (>20%), including laboratory abnormalities, in patients who received AKEEGA were decreased hemoglobin, decreased lymphocyte count, hypertension, decreased neutrophil count, musculoskeletal pain, decreased platelet count, constipation, fatigue, decreased potassium, increase creatinine, nausea, increased alkaline phosphate, increased aspartate aminotransferase, respiratory tract infection, arrhythmia, increased blood bilirubin, and fluid retention/edema.

BRCA-mutated Metastatic Castration-Resistant Prostate Cancer (mCRPC)

Serious adverse reactions occurred in 41% of patients who received AKEEGA. Serious adverse reactions reported in >2% of patients included COVID-19 (7%), anemia (4.4%), pneumonia (3.5%), and hemorrhage (3.5%). Fatal adverse reactions occurred in 9% of patients who received AKEEGA, including COVID-19 (5%), cardiopulmonary arrest (1%), dyspnea (1%), pneumonia (1%), and septic shock (1%).

The most common adverse reactions (>20%), including laboratory abnormalities, in patients who received AKEEGA were hemoglobin decreased, lymphocyte decreased, musculoskeletal pain, fatigue, platelets decreased, constipation, alkaline phosphatase increased, hypertension, nausea, neutrophils decreased, creatinine increased, potassium increased, potassium decreased, and aspartate aminotransferase increased.

DRUG INTERACTIONS

Effect of Other Drugs on AKEEGA
Avoid coadministration with strong CYP3A4 inducers.
Abiraterone is a substrate of CYP3A4. Strong CYP3A4 inducers may decrease abiraterone concentrations, which may reduce the effectiveness of abiraterone.

Effects of AKEEGA on Other Drugs
CYP2D6 Substrates
Avoid coadministration unless otherwise recommended in the Prescribing Information for CYP2D6 substrates for which minimal changes in concentration may lead to serious toxicities. If alternative treatments cannot be used, consider a dose reduction of the concomitant CYP2D6 substrate drug.

Abiraterone is a CYP2D6 moderate inhibitor. AKEEGA increases the concentration of CYP2D6 substrates, which may increase the risk of adverse reactions related to these substrates.

CYP2C8 Substrates
Monitor patients for signs of toxicity related to a CYP2C8 substrate for which a minimal change in plasma concentration may lead to serious or life-threatening adverse reactions.

Abiraterone is a CYP2C8 inhibitor. AKEEGA increases the concentration of CYP2C8 substrates, which may increase the risk of adverse reactions related to these substrates.

USE IN SPECIFIC POPULATIONS

Geriatric Use

Of the 162 patients with BRCA2 gene alteration(s) who received AKEEGA in AMPLITUDE, 40% of patients were less than 65 years, 36% of patients were 65 years to 74 years, and 23% were 75 years and over.

Of the 113 patients with BRCA gene alteration(s) who received AKEEGA in MAGNITUDE, 34.5% of patients were less than 65 years, 38.9% of patients were 65 years to 74 years, and 26.5% were 75 years and over.

No overall differences in effectiveness were observed between patients 65 years of age or older and younger patients in AMPLITUDE or MAGNITUDE. Patients 75 years of age or older who received AKEEGA experienced a higher incidence of fatal adverse reactions than younger patients. The incidence of fatal adverse reactions was 4.3% in patients younger than 75 and 13% in patients 75 or older.

Hepatic Impairment

Avoid use in patients with moderate or severe hepatic impairment. No dosage modification is necessary for patients with mild hepatic impairment.

Renal Impairment

Monitor patients with severe renal impairment for increased adverse reactions and modify dosage as recommended for adverse reactions. No dosage modification is recommended for patients with mild to moderate renal impairment.

Please see the full Prescribing Information for AKEEGA.

(Press release, Johnson & Johnson, DEC 12, 2025, View Source [SID1234661406])