{"success":true,"data":{"pressRelease":{"id":"136503","rtpr_id":"nBwfqm8Ma-20260904","ticker":"AZN","exchange":"LSE","all_tickers":["AZN"],"title":"ETCAMAH® (camizestrant) in combination with a CDK4/6 inhibitor approved in the US for 1st-line advanced HR-positive breast cancer","author":"Business Wire","published_at":"2026-09-04T23:03:00.092Z","article_body":"ETCAMAH® (camizestrant) in combination with a CDK4/6 inhibitor approved in\nthe US for 1st-line advanced HR-positive breast cancer\n\nApproval based on SERENA-6 Phase III trial results which showed combination\nreduced the risk of disease progression or death by 56% in patients with an\nemergent ESR1 tumor mutation\n\nInnovative treatment strategy has potential to reshape 1st-line treatment\nparadigm for patients in this setting\n\nAstraZeneca’s ETCAMAH(®) (camizestrant) in combination with a\ncyclin-dependent kinase (CDK) 4/6 inhibitor (abemaciclib, palbociclib or\nribociclib) has been approved in the US for the treatment of adult patients\nwith hormone receptor (HR)-positive, HER2-negative, locally advanced or\nmetastatic breast cancer upon detection of ESR1 mutation during aromatase\ninhibitor (AI) and CDK4/6 inhibitor therapy, based on a US Food and Drug\nAdministration (FDA)-authorized test.\n\nThe accelerated approval was based on results from the pivotal SERENA-6\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.astrazeneca-us.com%2Fcontent%2Faz-us%2Fmedia%2Fpress-releases%2F2025%2FCamizestrant-reduced-the-risk-of-disease-progression-or-death-by-56-in-patients-with-advanced-HR-positive-breast-cancer-with-an-emergent-ESR1-tumor-mutation-in-SERENA-6-Phase-III-trial.html&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=SERENA-6&index=1&md5=9d58196d9432a8974eae399930c0d72b)\nPhase III trial presented at the 2025 American Society of Clinical Oncology\n(ASCO) Annual Meeting and simultaneously published in The New England Journal\nof Medicine\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.nejm.org%2F&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=The+New+England+Journal+of+Medicine&index=2&md5=501cfea6ef92819eb01200bffea95318)\n.(1)\n\nKevin Kalinsky, MD, MS, FASCO, Division Director of Medical Oncology, Winship\nCancer Institute of Emory University and investigator for the trial, said:\n“The combination provides an important new option for the one in three\npatients with this form of advanced breast cancer whose tumors develop ESR1\nmutations before clinical or radiographic disease progression. Today’s\napproval will enable clinicians to promptly intervene and change therapeutic\nstrategy at an earlier opportunity ahead of disease progression, rather than\nwaiting until the cancer becomes harder to treat, and patient outcomes and\nquality of life worsen.”\n\nDave Fredrickson, Executive Vice President, Oncology Haematology Business\nUnit, AstraZeneca, said: “Today’s approval is the tenth granted by the FDA\nthis year across AstraZeneca’s portfolio and our fourth in breast cancer\nalone. The ETCAMAH combination reflects AstraZeneca’s leadership in\nredefining breast cancer care by pioneering a new approach using circulating\ntumor DNA and is the first and only medicine of its type in the 1st-line\nsetting.”\n\nIn a planned interim analysis of the SERENA-6 trial, ETCAMAH in combination\nwith a CDK4/6 inhibitor reduced the risk of disease progression or death by\n56% versus standard-of-care treatment with an AI (anastrozole or letrozole) in\ncombination with a CDK4/6 inhibitor (based on a hazard ratio [HR] of 0.44; 95%\nconfidence interval [CI]:0.31-0.60; p<0.00001; median PFS 16.0 versus 9.2\nmonths). While data for the key secondary endpoints of time to second disease\nprogression (PFS2) and overall survival (OS) were immature at the time of the\ninterim analysis, a subsequent pre-planned analysis demonstrated a\nstatistically significant and clinically meaningful PFS2 benefit of 25.7\nmonths versus 19.1 months in favor of the ETCAMAH combination (HR: 0.63; 95%\nCI: 0.46-0.86; p=0.00373) and OS continued to mature in favor of the ETCAMAH\ncombination (HR: 0.87; 95% CI: 0.57-1.30). The trial will continue to assess\nOS as a key secondary endpoint.\n\nThe safety profile of ETCAMAH in combination with palbociclib, ribociclib or\nabemaciclib in the SERENA-6 trial was consistent with the known safety profile\nof each medicine. No new safety concerns were identified, and discontinuations\nwere very low and similar in both arms.(1)\n\nIn the US, breast cancer is the most common cancer in women, with more than\n300,000 new patients diagnosed annually, and more than 42,000 deaths.(2)\nApproximately 37,000 patients with HR-positive metastatic breast cancer in the\nUS are treated with a medicine in the 1st-line setting; most frequently with\nendocrine therapies that target estrogen receptor (ER)-driven disease, which\nare often paired with CDK4/6 inhibitors.(3-5) However, resistance to these\ntherapies frequently develop in many patients.(5 )Once this occurs, treatment\noptions are limited and survival rates are low with just over a third of\npatients anticipated to live beyond five years after diagnosis.(5,6) Mutations\nin the ESR1 gene are a key driver of endocrine resistance and are associated\nwith poor outcomes, emerging during treatment of the disease and becoming more\nprevalent as the disease progresses.(7,8) Approximately 30% of patients with\nendocrine sensitive HR-positive disease develop ESR1 mutations during 1st-line\ntreatment before disease progression.(3)\n\nConcurrently with this approval, the FDA also approved a companion diagnostic\ntest to detect emerging ESR1 resistance mutations in the circulating tumor DNA\n(ctDNA) of patients with HR-positive, HER2-negative advanced or metastatic\nbreast cancer. SERENA-6 is the first global, double-blind, registrational\nPhase III trial to use a ctDNA-guided approach to detect the emergence of\nendocrine resistance and inform a switch in therapy before disease\nprogression. The innovative trial design used ctDNA monitoring via a blood\ntest at the time of routine tumor scans every two to three months to identify\npatients for early signs of endocrine resistance via the emergence of ESR1\nmutations. Following detection of an ESR1 mutation without disease\nprogression, the endocrine therapy of patients was switched to ETCAMAH from\nongoing treatment with an AI, while continuing combination with the same\nCDK4/6 inhibitor.\n\nETCAMAH is also approved in more than 30 countries across the globe, including\nin the EU, Japan, Canada, the UK and several other countries based on the\nSERENA-6 Phase III trial.\n\nIMPORTANT SAFETY INFORMATION\n WARNING: ARRHYTHMIA RISK WITH CONCOMITANT USE OF QTc INTERVAL PROLONGING DRUGS   \n \n                                                                                \n \n                                                                                \n \n                                                                                \n \nETCAMAH in combination with ribociclib, a QTc interval prolonging drug and a    \n strong CYP3A inhibitor, or in combination with other QTc interval prolonging     \n drugs, can increase the risk of Torsades de Pointes (TdP), other ventricular     \n arrhythmias, and sudden death.                                                   \n \n                                                                                \n \n                                                                                \n \n                                                                                \n \nAvoid concomitant use of ETCAMAH with products (other than ribociclib) known    \n to prolong the QTc interval and/or have a known risk of TdP. If concomitant      \n use with other products cannot be avoided, monitor the QTc interval more         \n frequently.                                                                      \n \n                                                                                \n \n                                                                                \n \n                                                                                \n \nObtain electrocardiogram (ECG) prior to initiation and monitor heart rate (HR)  \n and QTc interval during treatment. Assess and correct electrolyte                \n abnormalities prior to initiation and during treatment. Withhold ETCAMAH until   \n resolution of QTc interval prolongation and resume or permanently discontinue    \n ETCAMAH based on severity.                                                       \n\n\nWARNINGS AND PRECAUTIONS\n\nQTc Interval Prolongation: ETCAMAH in combination with a CDK4/6 inhibitor\n(CDK4/6i) is associated with QTc interval prolongation. When ETCAMAH is used\nin combination with ribociclib, a CDK4/6i, there is potential for increased\nrisk of TdP, other ventricular arrhythmias, and sudden death. One Grade 4 case\nof TdP was observed in a dose-finding trial when ETCAMAH was used with\nribociclib. In SERENA-6, QTc interval prolongation occurred in 2.6% of\npatients treated with ETCAMAH in combination with a CDK4/6i. QTc interval\nprolongation led to dose interruption in 0.6% of patients. No patients in\nSERENA-6 discontinued ETCAMAH due to QTc interval prolongation. ETCAMAH also\ncauses bradycardia, which increases the risk of QTc interval prolongation.\n\nPerform an ECG prior to initiating ETCAMAH, then every week for the first 2\nweeks of treatment, and periodically during treatment as clinically indicated.\nObtain serum electrolytes at baseline and during treatment as clinically\nindicated, and correct electrolyte abnormalities. Avoid concomitant use of\nETCAMAH in combination with a CDK4/6i with products that cause QTc interval\nprolongation, are strong CYP3A inhibitors, and/or are drugs known to lower HR.\n\nFor QTc >500 msec or QTc >480 msec and prolongation from baseline >60\nmsec, withhold ETCAMAH. If other contributing causes are identified, then\ntreat or correct the contributing causes.  Resume ETCAMAH when QTc returns to\n<480 msec. Reassess ECGs weekly for the first 2 weeks of treatment, and\nperiodically during treatment as clinically indicated. Permanently discontinue\nETCAMAH if QTc interval prolongation is either >500 msec or >60 msec\nchange from baseline AND associated with any: TdP, polymorphic ventricular\ntachycardia, syncope, or signs/symptoms of serious arrhythmia.\n\nBradycardia: ETCAMAH causes a decrease in HR. Bradycardia increases the risk\nfor life-threatening arrhythmias and sudden death when concomitant QTc\ninterval prolongation is present, such as when ETCAMAH is used in combination\nwith ribociclib, both a QTc interval prolonging product and a strong CYP3A\ninhibitor. In SERENA-6, bradycardia occurred in 8% of patients. The mean HR\ndecrease from baseline was approximately 13 beats per minute (bpm) with the\nmaximum decrease observed on day 15. Median time to onset was 17 days (range\n13 to 283) after starting ETCAMAH. No patients discontinued ETCAMAH due to\nbradycardia. Dose interruption occurred in 3.9% of patients. The safety of\nETCAMAH has not been established in patients with a baseline resting HR <55\nbpm as these patients were excluded from SERENA-6. Monitor HR more frequently\nduring the first 30 days of treatment in patients with bradycardia (HR <60\nbpm) at baseline and those on concomitant medications known to lower HR (eg,\nbeta-blockers).\n\nFor symptomatic (Grade 2 or above) bradycardia, withhold ETCAMAH until\nsymptoms resolve. Obtain ECG to evaluate etiology. If a contributing\nconcomitant medication is identified, modify the dosage or discontinue this\nmedication, as appropriate, until bradycardia symptoms resolve, then resume\nETCAMAH. Consider reassessing the HR after restart. Permanently discontinue\nfor persistent symptomatic bradycardia.\n\nEmbryo-Fetal Toxicity: Based on findings in animals and its mechanism of\naction, ETCAMAH can cause fetal harm when administered to a pregnant woman.\nAdvise pregnant women and females of reproductive potential of the potential\nrisk to a fetus. Advise females of reproductive potential to use effective\nnon-hormonal contraception during treatment with ETCAMAH and for 4 weeks after\nthe last dose. Advise male patients with female partners of reproductive\npotential to use effective contraception during treatment with ETCAMAH and for\n1 week after the last dose.\n\nADVERSE REACTIONS\n\nThe most common (≥20%) adverse reactions, including laboratory\nabnormalities, with ETCAMAH in combination with a CDK4/6i were decreased\nneutrophils (68%), decreased leukocytes (66%), decreased hemoglobin (47%),\ndecreased lymphocytes (39%), decreased platelets (36%), visual disturbances\n(34%), and fatigue (23%).\n\nPermanent discontinuation due to adverse reactions occurred in 1.3% of\npatients. Adverse reactions that resulted in permanent discontinuation of\nETCAMAH included gastroesophageal reflux disease, cholestasis and hepatic\ncytolysis (0.6% each). Dosage interruption of ETCAMAH due to adverse reactions\noccurred in 22% of patients.\n\nVisual disturbances: For visual disturbances limiting instrumental ADLs\n(activities of daily living) (Grade 2) or above, withhold ETCAMAH until\nsymptoms resolve to Grade 1 or below. Refer to an eye professional for an\nophthalmic examination and treatment and reassess at the next visit.\n\nFor other Grade 3 or higher adverse reactions: Withhold ETCAMAH until\nresolution to Grade 2 or below, then resume. Permanently discontinue for\nrecurrence of Grade 3 or higher adverse reactions.\n\nDRUG INTERACTIONS\n\n\n * Strong CYP3A Inhibitors: Monitor for increased adverse reactions to ETCAMAH\nand modify the dosage as recommended\n\n * Strong and Moderate CYP3A Inducers: Avoid the use of strong CYP3A inducers.\nUse caution with the co-administration of a moderate CYP3A inducer.\n\n\n* Avoid concomitant use of moderate CYP3A inducers for patients who are\nreceiving ETCAMAH in combination with abemaciclib or palbociclib. If\nconcomitant use cannot be avoided, increase the ETCAMAH dosage from 75 mg once\ndaily to 150 mg once daily. After the moderate CYP3A inducer has been\ndiscontinued for at least 14 days, resume the ETCAMAH dosage used prior to\ninitiation of the moderate CYP3A inducer\n\n * For patients who are receiving ETCAMAH in combination with ribociclib\nconcomitantly with a moderate CYP3A inducer, no ETCAMAH dosage modification is\nrecommended\n\n\n\n\n * CYP2C9 and/or CYP2C19 Substrates: Avoid concomitant use of ETCAMAH with CYP2C9\nor CYP2C19 substrates during treatment with ETCAMAH and at least 2 weeks after\nthe last dose of ETCAMAH, unless otherwise recommended in the Prescribing\nInformation of the CYP2C9 or CYP2C19 substrate\n\n * Certain CYP3A Substrates: Refer to the Prescribing Information for CYP3A\nsubstrates where minimal increases in the concentration may lead to serious\nadverse reactions\n\n * Drugs that Prolong the QTc Interval: ETCAMAH is indicated in combination with\na CDK4/6i and there is increased risk of QTc interval prolongation with\nribociclib, a strong CYP3A inhibitor that can prolong the QTc interval. Refer\nto the ribociclib Prescribing Information for dosage modifications. Avoid\nconcomitant use of ETCAMAH with products (other than ribociclib) known to\nprolong the QTc interval and/or have a known risk of TdP. If concomitant use\nwith other products cannot be avoided, monitor the QTc interval more\nfrequently. ETCAMAH in combination with a CDK4/6i is associated with QTc\ninterval prolongation\n\n * Drugs that Cause Bradycardia: Avoid concomitant use of ETCAMAH with other\nproducts known to cause bradycardia. Monitor for signs and symptoms of\nbradycardia if concomitant use cannot be avoided. ETCAMAH causes decreases in\nHR that are dose and baseline HR dependent.\n\nRefer to the Prescribing Information for the co-administered CDK4/6i for\ndosage modification guidelines related to adverse reactions, organ impairment,\nand drug-drug interactions.\n\nSPECIAL POPULATIONS\n\nPregnancy: Based on findings in animals and mechanism of action, ETCAMAH can\ncause fetal harm when administered to a pregnant woman. Advise pregnant women\nand females of reproductive potential of the potential risk to a fetus.\n\nLactation: Because of the potential for serious adverse reactions in a\nbreastfed child, advise women not to breastfeed during treatment with ETCAMAH\nand for 1 week after the last dose.\n\nFemales and Males of Reproductive Potential: ETCAMAH can cause fetal harm when\nadministered to pregnant women. Verify pregnancy status of female patients of\nreproductive potential prior to initiating ETCAMAH. Advise female patients of\nreproductive potential to use effective non-hormonal contraception during\ntreatment with ETCAMAH and for 4 weeks after the last dose. Advise male\npatients with female partners of reproductive potential to use effective\ncontraception during treatment with ETCAMAH and for 1 week after the last\ndose. Refer to the Prescribing Information of the CDK4/6i palbociclib, if used\nin combination with ETCAMAH, for contraception information and use for the\nlongest recommended post-treatment duration. ETCAMAH may impair fertility in\nfemale and male patients.\n\nPediatric Use: Safety and effectiveness have not been established in pediatric\npatients.\n\nHepatic Impairment: In patients with severe (Child-Pugh C) hepatic impairment,\nwhen ETCAMAH is combined with ribociclib, reduce the dosing frequency to every\nother day.\n\nNo dosage modifications are required in other patients with hepatic impairment\nof any level, or when ETCAMAH is combined with abemaciclib or palbociclib,\nalthough patients with moderate or severe hepatic impairment (Child-Pugh B or\nC) should be monitored for increased adverse reactions and dosage modified as\nrecommended.\n\nINDICATION\n\nETCAMAH in combination with a CDK4/6 inhibitor (abemaciclib, palbociclib, or\nribociclib) is indicated for the treatment of adult patients with hormone\nreceptor (HR)‑positive, human epidermal growth factor receptor 2\n(HER2)‑negative, locally advanced or metastatic breast cancer upon detection\nof ESR1 mutation during aromatase inhibitor and CDK4/6 inhibitor therapy,\nbased on an FDA-authorized test.\n\nThis indication is approved under accelerated approval based on\nprogression-free survival as measured from detection of ESR1 mutation.\nContinued approval for this indication may be contingent upon verification and\ndescription of clinical benefit in a confirmatory trial(s).\n\nPlease see full Prescribing Information\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.azpicentral.com%2Fpi.html%3Fproduct%3Detcamah&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=Prescribing+Information&index=3&md5=1a572f0cbcd7b88d8269cb4157d9c311)\n, including Boxed WARNING, and Patient Information\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.azpicentral.com%2Fpi.html%3Fproduct%3Detcamah%26medguide%3Dy&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=Patient+Information&index=4&md5=a317358b5c003df489d6887d30877dd1)\nfor ETCAMAH.\n\nNotes\n\nHR-positive breast cancer\n\nBreast cancer is the second most common cancer and one of the leading causes\nof cancer-related deaths worldwide.(9 )More than two million patients were\ndiagnosed with breast cancer in 2024, with more than 690,000 deaths\nglobally.(9) While survival rates are high for those diagnosed with early\nbreast cancer, only about 30% of patients diagnosed with or who progress to\nmetastatic disease are expected to live five years following diagnosis.(6)\n\nHR-positive breast cancer, characterized by the expression of estrogen or\nprogesterone receptors, or both, is the most common subtype of breast cancer\nwith 70% of tumors considered HR-positive and HER2-negative.(6) ERs often\ndrive the growth of HR-positive breast cancer cells.(10)\n\nGlobally, more than 200,000 patients with HR-positive breast cancer are\ntreated with a medicine in the 1st-line setting; most frequently with\nendocrine therapies that target ER-driven disease, which are often paired with\nCDK4/6 inhibitors.(3-5)\n\nThe optimization of endocrine therapy and overcoming resistance to enable\npatients to continue benefiting from these treatments, as well as identifying\nnew therapies for those who are less likely to benefit, are active areas of\nfocus for breast cancer research.\n\nSERENA-6\n\nSERENA-6 is a Phase III, double-blind, randomized trial evaluating the\nefficacy and safety of ETCAMAH in combination with a CDK4/6 inhibitor\n(palbociclib, ribociclib or abemaciclib) versus treatment with an AI\n(anastrozole or letrozole) in combination with a CDK4/6 inhibitor\n(palbociclib, ribociclib or abemaciclib) in patients with HR-positive,\nHER2-negative advanced breast cancer (patients with either locally advanced\ndisease, or metastatic disease) whose tumors have an emergent ESR1 mutation.\n\nThe global trial enrolled 315 adult patients with histologically confirmed\nHR-positive, HER2-negative advanced breast cancer, undergoing treatment with\nan AI in combination with a CDK4/6 inhibitor as 1st-line treatment. The\nprimary endpoint of the SERENA-6 trial is PFS as assessed by investigator,\nwith secondary endpoints including OS, and PFS2 by investigator assessment.\n\nETCAMAH® (camizestrant)\n\nETCAMAH is a potent, next-generation oral selective estrogen receptor degrader\n(SERD) and complete ER antagonist, administered orally, once daily. The\nrecommended dose of ETCAMAH in combination with a CDK4/6 inhibitor is 75 mg.\n\nETCAMAH in combination with a CDK4/6 inhibitor (palbociclib, ribociclib or\nabemaciclib) is approved in the US, EU, Japan and several other countries for\nthe treatment of adult patients with HR-positive (or ER-positive),\nHER2-negative locally advanced or metastatic breast cancer upon detection or\nemergence of ESR1 mutation and without disease progression during 1st-line\nendocrine therapy based on the results from the SERENA-6 Phase III trial.\n\nThe broad, robust and innovative ETCAMAH clinical development program,\nincluding the SERENA-4, CAMBRIA-1 and CAMBRIA-2 Phase III trials, is\nevaluating the safety and efficacy of ETCAMAH when used as a monotherapy or in\ncombination with CDK4/6 inhibitors to address a number of areas of unmet need\nin HR-positive, HER2-negative breast cancer.\n\nAstraZeneca in breast cancer\n\nDriven by a growing understanding of breast cancer biology, AstraZeneca is\nchallenging, and redefining, the current clinical paradigm for how breast\ncancer is classified and treated to deliver even more effective treatments to\npatients in need – with the bold ambition to one day eliminate breast cancer\nas a cause of death.\n\nAstraZeneca has a comprehensive portfolio of approved and promising compounds\nin development that leverage different mechanisms of action to address the\nbiologically diverse breast cancer tumor environment.\n\nWith fam-trastuzumab deruxtecan-nxki, a HER2-directed antibody drug conjugate\n(ADC), AstraZeneca and Daiichi Sankyo are aiming to improve outcomes in\npreviously treated HER2-positive, HER2-low and HER2-ultralow metastatic breast\ncancer and are exploring its potential in earlier lines of treatment and in\nnew breast cancer settings.\n\nIn HR-positive breast cancer, AstraZeneca continues to improve outcomes with\nfoundational medicines fulvestrant and goserelin and aims to reshape the\nHR-positive space with first-in-class AKT inhibitor, capivasertib, the\nTROP-2-directed ADC, datopotamab deruxtecan-dlnk and next-generation oral\nSERD, ETCAMAH.\n\nPARP inhibitor olaparib is a targeted treatment option that has been studied\nin early and metastatic breast cancer patients with an inherited BRCA\nmutation. AstraZeneca with MSD (Merck & Co., Inc. in the US and Canada)\ncontinue to research olaparib in these settings. AstraZeneca is also exploring\nthe potential of saruparib, a potent and selective inhibitor of PARP1, in\ncombination with ETCAMAH in BRCA-mutated, HR-positive, HER2-negative advanced\nbreast cancer.\n\nTo bring much-needed treatment options to patients with triple-negative breast\ncancer, an aggressive form of breast cancer, AstraZeneca is collaborating with\nDaiichi Sankyo to evaluate the potential of datopotamab deruxtecan-dlnk alone\nand in combination with immunotherapy durvalumab.\n\nAstraZeneca in oncology\n\nAstraZeneca is leading a revolution in oncology with the ambition to provide\ncures for cancer in every form, following the science to understand cancer and\nall its complexities to discover, develop and deliver life-changing medicines\nto patients.\n\nThe Company's focus is on some of the most challenging cancers. It is through\npersistent innovation that AstraZeneca has built one of the most diverse\nportfolios and pipelines in the industry, with the potential to catalyze\nchanges in the practice of medicine and transform the patient experience.\n\nAstraZeneca has the vision to redefine cancer care and, one day, eliminate\ncancer as a cause of death.\n\nAbout AstraZeneca \n(https://cts.businesswire.com/ct/CT?id=smartlink&url=http%3A%2F%2Fwww.astrazeneca-us.com%2F&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=About+AstraZeneca&index=5&md5=1f9cfce152d77a4b5cd5fbb628e8c902)\n\nAstraZeneca (LSE/STO/NYSE: AZN) is a global, science-led biopharmaceutical\ncompany that focuses on the discovery, development, and commercialization of\nprescription medicines in Oncology, Rare Diseases, and BioPharmaceuticals,\nincluding Cardiovascular, Renal & Metabolism, and Respiratory &\nImmunology. Based in Cambridge, UK, AstraZeneca’s innovative medicines are\nsold in more than 125 countries and used by millions of patients worldwide.\nPlease visit astrazeneca-us.com\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=http%3A%2F%2Fwww.astrazeneca-us.com%2F&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=astrazeneca-us.com&index=6&md5=21fd5056916178b91f7e43dfcdaf5874)\nand follow the Company on social media @AstraZeneca\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.linkedin.com%2Fcompany%2Fastrazeneca&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=%40AstraZeneca&index=7&md5=b9c2668b5e9a593be7e1297d8519593a)\n.\n\nReferences\n\n\n 1. Bidard FC, et al. First-Line Camizestrant for Emerging ESR1-Mutated Advanced\nBreast Cancer. N Engl J Med 2025; DOI: 10.1056/NEJMoa2502929.\n\n 2. American Cancer Society. Key Statistics for Breast Cancer. Available at: \nhttps://www.cancer.org/cancer/types/breast-cancer/about/how-common-is-breast-cancer.html\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.cancer.org%2Fcancer%2Ftypes%2Fbreast-cancer%2Fabout%2Fhow-common-is-breast-cancer.html&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=https%3A%2F%2Fwww.cancer.org%2Fcancer%2Ftypes%2Fbreast-cancer%2Fabout%2Fhow-common-is-breast-cancer.html&index=8&md5=41405ee8199e08bc39bdd6b900cf514b)\n\n. Accessed September 2026.\n\n 3. Cerner CancerMPact database. Accessed September 2026.\n\n 4. Lin M, et al. Comparative Overall Survival of CDK4/6 Inhibitors Plus Endocrine\nTherapy vs. Endocrine Therapy Alone for Hormone receptor-positive,\nHER2-negative metastatic breast cancer. J Cancer. 2020; 10.7150/jca.48944.\n\n 5. Lloyd M R, et al. Mechanisms of Resistance to CDK4/6 Blockade in Advanced\nHormone Receptor–positive, HER2-negative Breast Cancer and Emerging\nTherapeutic Opportunities. Clin Cancer Res. 2022; 28(5):821-30.\n\n 6. National Cancer Institute. Cancer Stat facts: Female breast cancer subtypes.\nAvailable at: \nhttps://seer.cancer.gov/statfacts/html/breast-subtypes.html\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fseer.cancer.gov%2Fstatfacts%2Fhtml%2Fbreast-subtypes.html&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=https%3A%2F%2Fseer.cancer.gov%2Fstatfacts%2Fhtml%2Fbreast-subtypes.html&index=9&md5=1df4cc0d7ae407da16c8633fa65d3767)\n\n. Accessed September 2026.\n\n 7. Brett O, et al. ESR1 mutation as an emerging clinical biomarker in metastatic\nhormone receptor‑positive breast cancer. Breast Cancer Res. 2021; 23:85.\n\n 8. Zundelevich A, et al. ESR1 mutations are frequent in newly diagnosed\nmetastatic and loco-regional recurrence of endocrine-treated breast cancer and\ncarry worse prognosis. Breast Cancer Res. 2020; 22:16.\n\n 9. Sung H, et al. Global cancer statistics 2024: GLOBOCAN estimates of incidence\nand mortality worldwide for 34 cancers in 186 countries. CA Cancer J Clin.\n2026; DOI: 10.3322/caac.70090.\n\n 10. Scabia V, et al. Estrogen receptor positive breast cancers have patient\nspecific hormone sensitivities and rely on progesterone receptor. Nat Commun.\n2022; 10.1038/s41467-022-30898-0.\n\nUS-66134 Last Updated 07/26\n\n\n\nView source version on businesswire.com:\nhttps://www.businesswire.com/news/home/20260904408121/en/\n(https://www.businesswire.com/news/home/20260904408121/en/)\n\nMedia Inquiries \n\nFiona Cookson +1 212 814 3923\n\n\n\nUS Media Mailbox: usmediateam@astrazeneca.com\n(mailto:usmediateam@astrazeneca.com)\n\n\nCopyright Business Wire 2026","article_body_html":"","raw_payload":{"data":{"id":"nBwfqm8Ma-20260904","title":"ETCAMAH® (camizestrant) in combination with a CDK4/6 inhibitor approved in the US for 1st-line advanced HR-positive breast cancer","author":"Business Wire","ticker":"AZN","created":"2026-09-04T23:03:00.092Z","tickers":["AZN"],"exchange":"LSE","article_body":"ETCAMAH® (camizestrant) in combination with a CDK4/6 inhibitor approved in\nthe US for 1st-line advanced HR-positive breast cancer\n\nApproval based on SERENA-6 Phase III trial results which showed combination\nreduced the risk of disease progression or death by 56% in patients with an\nemergent ESR1 tumor mutation\n\nInnovative treatment strategy has potential to reshape 1st-line treatment\nparadigm for patients in this setting\n\nAstraZeneca’s ETCAMAH(®) (camizestrant) in combination with a\ncyclin-dependent kinase (CDK) 4/6 inhibitor (abemaciclib, palbociclib or\nribociclib) has been approved in the US for the treatment of adult patients\nwith hormone receptor (HR)-positive, HER2-negative, locally advanced or\nmetastatic breast cancer upon detection of ESR1 mutation during aromatase\ninhibitor (AI) and CDK4/6 inhibitor therapy, based on a US Food and Drug\nAdministration (FDA)-authorized test.\n\nThe accelerated approval was based on results from the pivotal SERENA-6\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.astrazeneca-us.com%2Fcontent%2Faz-us%2Fmedia%2Fpress-releases%2F2025%2FCamizestrant-reduced-the-risk-of-disease-progression-or-death-by-56-in-patients-with-advanced-HR-positive-breast-cancer-with-an-emergent-ESR1-tumor-mutation-in-SERENA-6-Phase-III-trial.html&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=SERENA-6&index=1&md5=9d58196d9432a8974eae399930c0d72b)\nPhase III trial presented at the 2025 American Society of Clinical Oncology\n(ASCO) Annual Meeting and simultaneously published in The New England Journal\nof Medicine\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.nejm.org%2F&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=The+New+England+Journal+of+Medicine&index=2&md5=501cfea6ef92819eb01200bffea95318)\n.(1)\n\nKevin Kalinsky, MD, MS, FASCO, Division Director of Medical Oncology, Winship\nCancer Institute of Emory University and investigator for the trial, said:\n“The combination provides an important new option for the one in three\npatients with this form of advanced breast cancer whose tumors develop ESR1\nmutations before clinical or radiographic disease progression. Today’s\napproval will enable clinicians to promptly intervene and change therapeutic\nstrategy at an earlier opportunity ahead of disease progression, rather than\nwaiting until the cancer becomes harder to treat, and patient outcomes and\nquality of life worsen.”\n\nDave Fredrickson, Executive Vice President, Oncology Haematology Business\nUnit, AstraZeneca, said: “Today’s approval is the tenth granted by the FDA\nthis year across AstraZeneca’s portfolio and our fourth in breast cancer\nalone. The ETCAMAH combination reflects AstraZeneca’s leadership in\nredefining breast cancer care by pioneering a new approach using circulating\ntumor DNA and is the first and only medicine of its type in the 1st-line\nsetting.”\n\nIn a planned interim analysis of the SERENA-6 trial, ETCAMAH in combination\nwith a CDK4/6 inhibitor reduced the risk of disease progression or death by\n56% versus standard-of-care treatment with an AI (anastrozole or letrozole) in\ncombination with a CDK4/6 inhibitor (based on a hazard ratio [HR] of 0.44; 95%\nconfidence interval [CI]:0.31-0.60; p<0.00001; median PFS 16.0 versus 9.2\nmonths). While data for the key secondary endpoints of time to second disease\nprogression (PFS2) and overall survival (OS) were immature at the time of the\ninterim analysis, a subsequent pre-planned analysis demonstrated a\nstatistically significant and clinically meaningful PFS2 benefit of 25.7\nmonths versus 19.1 months in favor of the ETCAMAH combination (HR: 0.63; 95%\nCI: 0.46-0.86; p=0.00373) and OS continued to mature in favor of the ETCAMAH\ncombination (HR: 0.87; 95% CI: 0.57-1.30). The trial will continue to assess\nOS as a key secondary endpoint.\n\nThe safety profile of ETCAMAH in combination with palbociclib, ribociclib or\nabemaciclib in the SERENA-6 trial was consistent with the known safety profile\nof each medicine. No new safety concerns were identified, and discontinuations\nwere very low and similar in both arms.(1)\n\nIn the US, breast cancer is the most common cancer in women, with more than\n300,000 new patients diagnosed annually, and more than 42,000 deaths.(2)\nApproximately 37,000 patients with HR-positive metastatic breast cancer in the\nUS are treated with a medicine in the 1st-line setting; most frequently with\nendocrine therapies that target estrogen receptor (ER)-driven disease, which\nare often paired with CDK4/6 inhibitors.(3-5) However, resistance to these\ntherapies frequently develop in many patients.(5 )Once this occurs, treatment\noptions are limited and survival rates are low with just over a third of\npatients anticipated to live beyond five years after diagnosis.(5,6) Mutations\nin the ESR1 gene are a key driver of endocrine resistance and are associated\nwith poor outcomes, emerging during treatment of the disease and becoming more\nprevalent as the disease progresses.(7,8) Approximately 30% of patients with\nendocrine sensitive HR-positive disease develop ESR1 mutations during 1st-line\ntreatment before disease progression.(3)\n\nConcurrently with this approval, the FDA also approved a companion diagnostic\ntest to detect emerging ESR1 resistance mutations in the circulating tumor DNA\n(ctDNA) of patients with HR-positive, HER2-negative advanced or metastatic\nbreast cancer. SERENA-6 is the first global, double-blind, registrational\nPhase III trial to use a ctDNA-guided approach to detect the emergence of\nendocrine resistance and inform a switch in therapy before disease\nprogression. The innovative trial design used ctDNA monitoring via a blood\ntest at the time of routine tumor scans every two to three months to identify\npatients for early signs of endocrine resistance via the emergence of ESR1\nmutations. Following detection of an ESR1 mutation without disease\nprogression, the endocrine therapy of patients was switched to ETCAMAH from\nongoing treatment with an AI, while continuing combination with the same\nCDK4/6 inhibitor.\n\nETCAMAH is also approved in more than 30 countries across the globe, including\nin the EU, Japan, Canada, the UK and several other countries based on the\nSERENA-6 Phase III trial.\n\nIMPORTANT SAFETY INFORMATION\n WARNING: ARRHYTHMIA RISK WITH CONCOMITANT USE OF QTc INTERVAL PROLONGING DRUGS   \n \n                                                                                \n \n                                                                                \n \n                                                                                \n \nETCAMAH in combination with ribociclib, a QTc interval prolonging drug and a    \n strong CYP3A inhibitor, or in combination with other QTc interval prolonging     \n drugs, can increase the risk of Torsades de Pointes (TdP), other ventricular     \n arrhythmias, and sudden death.                                                   \n \n                                                                                \n \n                                                                                \n \n                                                                                \n \nAvoid concomitant use of ETCAMAH with products (other than ribociclib) known    \n to prolong the QTc interval and/or have a known risk of TdP. If concomitant      \n use with other products cannot be avoided, monitor the QTc interval more         \n frequently.                                                                      \n \n                                                                                \n \n                                                                                \n \n                                                                                \n \nObtain electrocardiogram (ECG) prior to initiation and monitor heart rate (HR)  \n and QTc interval during treatment. Assess and correct electrolyte                \n abnormalities prior to initiation and during treatment. Withhold ETCAMAH until   \n resolution of QTc interval prolongation and resume or permanently discontinue    \n ETCAMAH based on severity.                                                       \n\n\nWARNINGS AND PRECAUTIONS\n\nQTc Interval Prolongation: ETCAMAH in combination with a CDK4/6 inhibitor\n(CDK4/6i) is associated with QTc interval prolongation. When ETCAMAH is used\nin combination with ribociclib, a CDK4/6i, there is potential for increased\nrisk of TdP, other ventricular arrhythmias, and sudden death. One Grade 4 case\nof TdP was observed in a dose-finding trial when ETCAMAH was used with\nribociclib. In SERENA-6, QTc interval prolongation occurred in 2.6% of\npatients treated with ETCAMAH in combination with a CDK4/6i. QTc interval\nprolongation led to dose interruption in 0.6% of patients. No patients in\nSERENA-6 discontinued ETCAMAH due to QTc interval prolongation. ETCAMAH also\ncauses bradycardia, which increases the risk of QTc interval prolongation.\n\nPerform an ECG prior to initiating ETCAMAH, then every week for the first 2\nweeks of treatment, and periodically during treatment as clinically indicated.\nObtain serum electrolytes at baseline and during treatment as clinically\nindicated, and correct electrolyte abnormalities. Avoid concomitant use of\nETCAMAH in combination with a CDK4/6i with products that cause QTc interval\nprolongation, are strong CYP3A inhibitors, and/or are drugs known to lower HR.\n\nFor QTc >500 msec or QTc >480 msec and prolongation from baseline >60\nmsec, withhold ETCAMAH. If other contributing causes are identified, then\ntreat or correct the contributing causes.  Resume ETCAMAH when QTc returns to\n<480 msec. Reassess ECGs weekly for the first 2 weeks of treatment, and\nperiodically during treatment as clinically indicated. Permanently discontinue\nETCAMAH if QTc interval prolongation is either >500 msec or >60 msec\nchange from baseline AND associated with any: TdP, polymorphic ventricular\ntachycardia, syncope, or signs/symptoms of serious arrhythmia.\n\nBradycardia: ETCAMAH causes a decrease in HR. Bradycardia increases the risk\nfor life-threatening arrhythmias and sudden death when concomitant QTc\ninterval prolongation is present, such as when ETCAMAH is used in combination\nwith ribociclib, both a QTc interval prolonging product and a strong CYP3A\ninhibitor. In SERENA-6, bradycardia occurred in 8% of patients. The mean HR\ndecrease from baseline was approximately 13 beats per minute (bpm) with the\nmaximum decrease observed on day 15. Median time to onset was 17 days (range\n13 to 283) after starting ETCAMAH. No patients discontinued ETCAMAH due to\nbradycardia. Dose interruption occurred in 3.9% of patients. The safety of\nETCAMAH has not been established in patients with a baseline resting HR <55\nbpm as these patients were excluded from SERENA-6. Monitor HR more frequently\nduring the first 30 days of treatment in patients with bradycardia (HR <60\nbpm) at baseline and those on concomitant medications known to lower HR (eg,\nbeta-blockers).\n\nFor symptomatic (Grade 2 or above) bradycardia, withhold ETCAMAH until\nsymptoms resolve. Obtain ECG to evaluate etiology. If a contributing\nconcomitant medication is identified, modify the dosage or discontinue this\nmedication, as appropriate, until bradycardia symptoms resolve, then resume\nETCAMAH. Consider reassessing the HR after restart. Permanently discontinue\nfor persistent symptomatic bradycardia.\n\nEmbryo-Fetal Toxicity: Based on findings in animals and its mechanism of\naction, ETCAMAH can cause fetal harm when administered to a pregnant woman.\nAdvise pregnant women and females of reproductive potential of the potential\nrisk to a fetus. Advise females of reproductive potential to use effective\nnon-hormonal contraception during treatment with ETCAMAH and for 4 weeks after\nthe last dose. Advise male patients with female partners of reproductive\npotential to use effective contraception during treatment with ETCAMAH and for\n1 week after the last dose.\n\nADVERSE REACTIONS\n\nThe most common (≥20%) adverse reactions, including laboratory\nabnormalities, with ETCAMAH in combination with a CDK4/6i were decreased\nneutrophils (68%), decreased leukocytes (66%), decreased hemoglobin (47%),\ndecreased lymphocytes (39%), decreased platelets (36%), visual disturbances\n(34%), and fatigue (23%).\n\nPermanent discontinuation due to adverse reactions occurred in 1.3% of\npatients. Adverse reactions that resulted in permanent discontinuation of\nETCAMAH included gastroesophageal reflux disease, cholestasis and hepatic\ncytolysis (0.6% each). Dosage interruption of ETCAMAH due to adverse reactions\noccurred in 22% of patients.\n\nVisual disturbances: For visual disturbances limiting instrumental ADLs\n(activities of daily living) (Grade 2) or above, withhold ETCAMAH until\nsymptoms resolve to Grade 1 or below. Refer to an eye professional for an\nophthalmic examination and treatment and reassess at the next visit.\n\nFor other Grade 3 or higher adverse reactions: Withhold ETCAMAH until\nresolution to Grade 2 or below, then resume. Permanently discontinue for\nrecurrence of Grade 3 or higher adverse reactions.\n\nDRUG INTERACTIONS\n\n\n * Strong CYP3A Inhibitors: Monitor for increased adverse reactions to ETCAMAH\nand modify the dosage as recommended\n\n * Strong and Moderate CYP3A Inducers: Avoid the use of strong CYP3A inducers.\nUse caution with the co-administration of a moderate CYP3A inducer.\n\n\n* Avoid concomitant use of moderate CYP3A inducers for patients who are\nreceiving ETCAMAH in combination with abemaciclib or palbociclib. If\nconcomitant use cannot be avoided, increase the ETCAMAH dosage from 75 mg once\ndaily to 150 mg once daily. After the moderate CYP3A inducer has been\ndiscontinued for at least 14 days, resume the ETCAMAH dosage used prior to\ninitiation of the moderate CYP3A inducer\n\n * For patients who are receiving ETCAMAH in combination with ribociclib\nconcomitantly with a moderate CYP3A inducer, no ETCAMAH dosage modification is\nrecommended\n\n\n\n\n * CYP2C9 and/or CYP2C19 Substrates: Avoid concomitant use of ETCAMAH with CYP2C9\nor CYP2C19 substrates during treatment with ETCAMAH and at least 2 weeks after\nthe last dose of ETCAMAH, unless otherwise recommended in the Prescribing\nInformation of the CYP2C9 or CYP2C19 substrate\n\n * Certain CYP3A Substrates: Refer to the Prescribing Information for CYP3A\nsubstrates where minimal increases in the concentration may lead to serious\nadverse reactions\n\n * Drugs that Prolong the QTc Interval: ETCAMAH is indicated in combination with\na CDK4/6i and there is increased risk of QTc interval prolongation with\nribociclib, a strong CYP3A inhibitor that can prolong the QTc interval. Refer\nto the ribociclib Prescribing Information for dosage modifications. Avoid\nconcomitant use of ETCAMAH with products (other than ribociclib) known to\nprolong the QTc interval and/or have a known risk of TdP. If concomitant use\nwith other products cannot be avoided, monitor the QTc interval more\nfrequently. ETCAMAH in combination with a CDK4/6i is associated with QTc\ninterval prolongation\n\n * Drugs that Cause Bradycardia: Avoid concomitant use of ETCAMAH with other\nproducts known to cause bradycardia. Monitor for signs and symptoms of\nbradycardia if concomitant use cannot be avoided. ETCAMAH causes decreases in\nHR that are dose and baseline HR dependent.\n\nRefer to the Prescribing Information for the co-administered CDK4/6i for\ndosage modification guidelines related to adverse reactions, organ impairment,\nand drug-drug interactions.\n\nSPECIAL POPULATIONS\n\nPregnancy: Based on findings in animals and mechanism of action, ETCAMAH can\ncause fetal harm when administered to a pregnant woman. Advise pregnant women\nand females of reproductive potential of the potential risk to a fetus.\n\nLactation: Because of the potential for serious adverse reactions in a\nbreastfed child, advise women not to breastfeed during treatment with ETCAMAH\nand for 1 week after the last dose.\n\nFemales and Males of Reproductive Potential: ETCAMAH can cause fetal harm when\nadministered to pregnant women. Verify pregnancy status of female patients of\nreproductive potential prior to initiating ETCAMAH. Advise female patients of\nreproductive potential to use effective non-hormonal contraception during\ntreatment with ETCAMAH and for 4 weeks after the last dose. Advise male\npatients with female partners of reproductive potential to use effective\ncontraception during treatment with ETCAMAH and for 1 week after the last\ndose. Refer to the Prescribing Information of the CDK4/6i palbociclib, if used\nin combination with ETCAMAH, for contraception information and use for the\nlongest recommended post-treatment duration. ETCAMAH may impair fertility in\nfemale and male patients.\n\nPediatric Use: Safety and effectiveness have not been established in pediatric\npatients.\n\nHepatic Impairment: In patients with severe (Child-Pugh C) hepatic impairment,\nwhen ETCAMAH is combined with ribociclib, reduce the dosing frequency to every\nother day.\n\nNo dosage modifications are required in other patients with hepatic impairment\nof any level, or when ETCAMAH is combined with abemaciclib or palbociclib,\nalthough patients with moderate or severe hepatic impairment (Child-Pugh B or\nC) should be monitored for increased adverse reactions and dosage modified as\nrecommended.\n\nINDICATION\n\nETCAMAH in combination with a CDK4/6 inhibitor (abemaciclib, palbociclib, or\nribociclib) is indicated for the treatment of adult patients with hormone\nreceptor (HR)‑positive, human epidermal growth factor receptor 2\n(HER2)‑negative, locally advanced or metastatic breast cancer upon detection\nof ESR1 mutation during aromatase inhibitor and CDK4/6 inhibitor therapy,\nbased on an FDA-authorized test.\n\nThis indication is approved under accelerated approval based on\nprogression-free survival as measured from detection of ESR1 mutation.\nContinued approval for this indication may be contingent upon verification and\ndescription of clinical benefit in a confirmatory trial(s).\n\nPlease see full Prescribing Information\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.azpicentral.com%2Fpi.html%3Fproduct%3Detcamah&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=Prescribing+Information&index=3&md5=1a572f0cbcd7b88d8269cb4157d9c311)\n, including Boxed WARNING, and Patient Information\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.azpicentral.com%2Fpi.html%3Fproduct%3Detcamah%26medguide%3Dy&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=Patient+Information&index=4&md5=a317358b5c003df489d6887d30877dd1)\nfor ETCAMAH.\n\nNotes\n\nHR-positive breast cancer\n\nBreast cancer is the second most common cancer and one of the leading causes\nof cancer-related deaths worldwide.(9 )More than two million patients were\ndiagnosed with breast cancer in 2024, with more than 690,000 deaths\nglobally.(9) While survival rates are high for those diagnosed with early\nbreast cancer, only about 30% of patients diagnosed with or who progress to\nmetastatic disease are expected to live five years following diagnosis.(6)\n\nHR-positive breast cancer, characterized by the expression of estrogen or\nprogesterone receptors, or both, is the most common subtype of breast cancer\nwith 70% of tumors considered HR-positive and HER2-negative.(6) ERs often\ndrive the growth of HR-positive breast cancer cells.(10)\n\nGlobally, more than 200,000 patients with HR-positive breast cancer are\ntreated with a medicine in the 1st-line setting; most frequently with\nendocrine therapies that target ER-driven disease, which are often paired with\nCDK4/6 inhibitors.(3-5)\n\nThe optimization of endocrine therapy and overcoming resistance to enable\npatients to continue benefiting from these treatments, as well as identifying\nnew therapies for those who are less likely to benefit, are active areas of\nfocus for breast cancer research.\n\nSERENA-6\n\nSERENA-6 is a Phase III, double-blind, randomized trial evaluating the\nefficacy and safety of ETCAMAH in combination with a CDK4/6 inhibitor\n(palbociclib, ribociclib or abemaciclib) versus treatment with an AI\n(anastrozole or letrozole) in combination with a CDK4/6 inhibitor\n(palbociclib, ribociclib or abemaciclib) in patients with HR-positive,\nHER2-negative advanced breast cancer (patients with either locally advanced\ndisease, or metastatic disease) whose tumors have an emergent ESR1 mutation.\n\nThe global trial enrolled 315 adult patients with histologically confirmed\nHR-positive, HER2-negative advanced breast cancer, undergoing treatment with\nan AI in combination with a CDK4/6 inhibitor as 1st-line treatment. The\nprimary endpoint of the SERENA-6 trial is PFS as assessed by investigator,\nwith secondary endpoints including OS, and PFS2 by investigator assessment.\n\nETCAMAH® (camizestrant)\n\nETCAMAH is a potent, next-generation oral selective estrogen receptor degrader\n(SERD) and complete ER antagonist, administered orally, once daily. The\nrecommended dose of ETCAMAH in combination with a CDK4/6 inhibitor is 75 mg.\n\nETCAMAH in combination with a CDK4/6 inhibitor (palbociclib, ribociclib or\nabemaciclib) is approved in the US, EU, Japan and several other countries for\nthe treatment of adult patients with HR-positive (or ER-positive),\nHER2-negative locally advanced or metastatic breast cancer upon detection or\nemergence of ESR1 mutation and without disease progression during 1st-line\nendocrine therapy based on the results from the SERENA-6 Phase III trial.\n\nThe broad, robust and innovative ETCAMAH clinical development program,\nincluding the SERENA-4, CAMBRIA-1 and CAMBRIA-2 Phase III trials, is\nevaluating the safety and efficacy of ETCAMAH when used as a monotherapy or in\ncombination with CDK4/6 inhibitors to address a number of areas of unmet need\nin HR-positive, HER2-negative breast cancer.\n\nAstraZeneca in breast cancer\n\nDriven by a growing understanding of breast cancer biology, AstraZeneca is\nchallenging, and redefining, the current clinical paradigm for how breast\ncancer is classified and treated to deliver even more effective treatments to\npatients in need – with the bold ambition to one day eliminate breast cancer\nas a cause of death.\n\nAstraZeneca has a comprehensive portfolio of approved and promising compounds\nin development that leverage different mechanisms of action to address the\nbiologically diverse breast cancer tumor environment.\n\nWith fam-trastuzumab deruxtecan-nxki, a HER2-directed antibody drug conjugate\n(ADC), AstraZeneca and Daiichi Sankyo are aiming to improve outcomes in\npreviously treated HER2-positive, HER2-low and HER2-ultralow metastatic breast\ncancer and are exploring its potential in earlier lines of treatment and in\nnew breast cancer settings.\n\nIn HR-positive breast cancer, AstraZeneca continues to improve outcomes with\nfoundational medicines fulvestrant and goserelin and aims to reshape the\nHR-positive space with first-in-class AKT inhibitor, capivasertib, the\nTROP-2-directed ADC, datopotamab deruxtecan-dlnk and next-generation oral\nSERD, ETCAMAH.\n\nPARP inhibitor olaparib is a targeted treatment option that has been studied\nin early and metastatic breast cancer patients with an inherited BRCA\nmutation. AstraZeneca with MSD (Merck & Co., Inc. in the US and Canada)\ncontinue to research olaparib in these settings. AstraZeneca is also exploring\nthe potential of saruparib, a potent and selective inhibitor of PARP1, in\ncombination with ETCAMAH in BRCA-mutated, HR-positive, HER2-negative advanced\nbreast cancer.\n\nTo bring much-needed treatment options to patients with triple-negative breast\ncancer, an aggressive form of breast cancer, AstraZeneca is collaborating with\nDaiichi Sankyo to evaluate the potential of datopotamab deruxtecan-dlnk alone\nand in combination with immunotherapy durvalumab.\n\nAstraZeneca in oncology\n\nAstraZeneca is leading a revolution in oncology with the ambition to provide\ncures for cancer in every form, following the science to understand cancer and\nall its complexities to discover, develop and deliver life-changing medicines\nto patients.\n\nThe Company's focus is on some of the most challenging cancers. It is through\npersistent innovation that AstraZeneca has built one of the most diverse\nportfolios and pipelines in the industry, with the potential to catalyze\nchanges in the practice of medicine and transform the patient experience.\n\nAstraZeneca has the vision to redefine cancer care and, one day, eliminate\ncancer as a cause of death.\n\nAbout AstraZeneca \n(https://cts.businesswire.com/ct/CT?id=smartlink&url=http%3A%2F%2Fwww.astrazeneca-us.com%2F&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=About+AstraZeneca&index=5&md5=1f9cfce152d77a4b5cd5fbb628e8c902)\n\nAstraZeneca (LSE/STO/NYSE: AZN) is a global, science-led biopharmaceutical\ncompany that focuses on the discovery, development, and commercialization of\nprescription medicines in Oncology, Rare Diseases, and BioPharmaceuticals,\nincluding Cardiovascular, Renal & Metabolism, and Respiratory &\nImmunology. Based in Cambridge, UK, AstraZeneca’s innovative medicines are\nsold in more than 125 countries and used by millions of patients worldwide.\nPlease visit astrazeneca-us.com\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=http%3A%2F%2Fwww.astrazeneca-us.com%2F&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=astrazeneca-us.com&index=6&md5=21fd5056916178b91f7e43dfcdaf5874)\nand follow the Company on social media @AstraZeneca\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.linkedin.com%2Fcompany%2Fastrazeneca&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=%40AstraZeneca&index=7&md5=b9c2668b5e9a593be7e1297d8519593a)\n.\n\nReferences\n\n\n 1. Bidard FC, et al. First-Line Camizestrant for Emerging ESR1-Mutated Advanced\nBreast Cancer. N Engl J Med 2025; DOI: 10.1056/NEJMoa2502929.\n\n 2. American Cancer Society. Key Statistics for Breast Cancer. Available at: \nhttps://www.cancer.org/cancer/types/breast-cancer/about/how-common-is-breast-cancer.html\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fwww.cancer.org%2Fcancer%2Ftypes%2Fbreast-cancer%2Fabout%2Fhow-common-is-breast-cancer.html&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=https%3A%2F%2Fwww.cancer.org%2Fcancer%2Ftypes%2Fbreast-cancer%2Fabout%2Fhow-common-is-breast-cancer.html&index=8&md5=41405ee8199e08bc39bdd6b900cf514b)\n\n. Accessed September 2026.\n\n 3. Cerner CancerMPact database. Accessed September 2026.\n\n 4. Lin M, et al. Comparative Overall Survival of CDK4/6 Inhibitors Plus Endocrine\nTherapy vs. Endocrine Therapy Alone for Hormone receptor-positive,\nHER2-negative metastatic breast cancer. J Cancer. 2020; 10.7150/jca.48944.\n\n 5. Lloyd M R, et al. Mechanisms of Resistance to CDK4/6 Blockade in Advanced\nHormone Receptor–positive, HER2-negative Breast Cancer and Emerging\nTherapeutic Opportunities. Clin Cancer Res. 2022; 28(5):821-30.\n\n 6. National Cancer Institute. Cancer Stat facts: Female breast cancer subtypes.\nAvailable at: \nhttps://seer.cancer.gov/statfacts/html/breast-subtypes.html\n(https://cts.businesswire.com/ct/CT?id=smartlink&url=https%3A%2F%2Fseer.cancer.gov%2Fstatfacts%2Fhtml%2Fbreast-subtypes.html&esheet=54599144&newsitemid=20260904408121&lan=en-US&anchor=https%3A%2F%2Fseer.cancer.gov%2Fstatfacts%2Fhtml%2Fbreast-subtypes.html&index=9&md5=1df4cc0d7ae407da16c8633fa65d3767)\n\n. Accessed September 2026.\n\n 7. Brett O, et al. ESR1 mutation as an emerging clinical biomarker in metastatic\nhormone receptor‑positive breast cancer. Breast Cancer Res. 2021; 23:85.\n\n 8. Zundelevich A, et al. ESR1 mutations are frequent in newly diagnosed\nmetastatic and loco-regional recurrence of endocrine-treated breast cancer and\ncarry worse prognosis. Breast Cancer Res. 2020; 22:16.\n\n 9. Sung H, et al. Global cancer statistics 2024: GLOBOCAN estimates of incidence\nand mortality worldwide for 34 cancers in 186 countries. CA Cancer J Clin.\n2026; DOI: 10.3322/caac.70090.\n\n 10. Scabia V, et al. Estrogen receptor positive breast cancers have patient\nspecific hormone sensitivities and rely on progesterone receptor. Nat Commun.\n2022; 10.1038/s41467-022-30898-0.\n\nUS-66134 Last Updated 07/26\n\n\n\nView source version on businesswire.com:\nhttps://www.businesswire.com/news/home/20260904408121/en/\n(https://www.businesswire.com/news/home/20260904408121/en/)\n\nMedia Inquiries \n\nFiona Cookson +1 212 814 3923\n\n\n\nUS Media Mailbox: usmediateam@astrazeneca.com\n(mailto:usmediateam@astrazeneca.com)\n\n\nCopyright Business Wire 2026"},"type":"article","timestamp":"2026-09-04T23:03:00.141383713Z","server_sent_at_ms":1788562980141},"received_at":"2026-09-04T23:03:00.321Z","source_url":"https://www.businesswire.com/news/home/20260904408121/en/"},"analysis":{"id":"125380","press_release_id":"136503","analysis_json":{"industry":{"label":"Pharmaceuticals","sector":"Health Care"},"redFlags":["Accelerated approval contingent on verification of clinical benefit in confirmatory trial(s); overall survival data still immature (HR 0.87, 95% CI 0.57-1.30)","Boxed warning for Torsades de Pointes, ventricular arrhythmias and sudden death when combined with QTc-prolonging drugs, notably ribociclib"],"eventType":"fda_approval","narrative":"The FDA granted accelerated approval to AstraZeneca's ETCAMAH (camizestrant) in combination with a CDK4/6 inhibitor (abemaciclib, palbociclib or ribociclib) for adults with HR-positive, HER2-negative locally advanced or metastatic breast cancer upon detection of an ESR1 mutation during aromatase inhibitor and CDK4/6 inhibitor therapy.\n\nApproval was based on the SERENA-6 Phase III trial, which showed a 56% reduction in the risk of disease progression or death versus staying on an aromatase inhibitor (HR 0.44; p<0.00001), with median PFS of 16.0 versus 9.2 months; a subsequent analysis demonstrated a PFS2 benefit of 25.7 versus 19.1 months while overall survival data continue to mature.\n\nThe ctDNA-guided switch strategy is the first and only medicine of its type in the 1st-line setting, targeting roughly 37,000 US first-line HR-positive metastatic breast cancer patients, about 30% of whom develop ESR1 mutations; this is AstraZeneca's tenth FDA approval this year and fourth in breast cancer, and the FDA concurrently approved a companion diagnostic for emerging ESR1 mutations.\n\nThe indication is approved under accelerated approval contingent on confirmatory trial verification of clinical benefit, and the label carries a boxed warning for arrhythmia risk (Torsades de Pointes, sudden death) with concomitant QTc-prolonging drugs such as ribociclib.","sentiment":"bullish","agentHooks":{"shouldPost":true,"suggestedAngle":"First ctDNA-guided 1st-line switch strategy in HR-positive breast cancer extends camizestrant's blockbuster runway for AstraZeneca."},"keyFigures":{"drugName":"ETCAMAH (camizestrant)","phaseOfTrial":"Phase III","customDimensions":{"pfs2_months":[25.7,19.1],"os_hazard_ratio":0.87,"bradycardia_rate":"8%","pfs_hazard_ratio":0.44,"recommended_dose":"75 mg once daily","trial_enrollment":315,"median_pfs_months":[16,9.2],"pfs2_hazard_ratio":0.63,"countries_approved":"more than 30","pfs_hazard_ratio_ci":"0.31-0.60","qtc_prolongation_rate":"2.6%","esr1_mutation_incidence_1l":"~30%","us_breast_cancer_new_cases":"more than 300,000","us_1l_hr_positive_mbc_patients":37000,"risk_reduction_progression_or_death":"56%"}},"quotedText":"Today’s approval is the tenth granted by the FDA this year across AstraZeneca’s portfolio and our fourth in breast cancer alone.","namedEntities":{"people":[{"name":"Kevin Kalinsky","role":"Division Director of Medical Oncology, Winship Cancer Institute of Emory University; SERENA-6 investigator"},{"name":"Dave Fredrickson","role":"Executive Vice President, Oncology Haematology Business Unit, AstraZeneca"}],"products":["ETCAMAH","camizestrant","abemaciclib","palbociclib","ribociclib","anastrozole","letrozole","FDA-authorized ESR1 companion diagnostic test","fam-trastuzumab deruxtecan-nxki","datopotamab deruxtecan-dlnk","olaparib","capivasertib","saruparib","durvalumab"],"companies":[{"name":"AstraZeneca","ticker":"AZN","relationship":"filer"},{"name":"US Food and Drug Administration (FDA)","relationship":"regulatory authority"},{"name":"Daiichi Sankyo","relationship":"collaboration partner (ADC portfolio)"},{"name":"MSD (Merck & Co., Inc. in the US and Canada)","relationship":"research collaboration partner (olaparib)"}],"dollarAmounts":[]},"materialImpact":{"score":4,"reasoning":"FDA accelerated approval of ETCAMAH (camizestrant) plus a CDK4/6 inhibitor for the 1st-line ESR1-mutated HR-positive breast cancer setting opens a substantial new commercial opportunity (~37,000 US 1st-line patients, ~30% of whom develop ESR1 mutations) and is AstraZeneca's tenth US approval this year. Major catalyst for a key oncology franchise, but not a company-defining binary event for a diversified mega-cap."},"tickerRelevance":{"others":[],"primary":"AZN"},"globalImportance":65,"audienceRelevance":62,"eventTypeSecondary":["clinical_trial"],"importanceComponents":{"mitigants":"drug already approved in 30+ countries; indication expansion rather than first-ever approval","tickerTier":"mega-cap","eventGravity":"FDA accelerated approval, new 1st-line indication for key growth asset","sectorWeight":"pharma-oncology","householdBrandBoost":true}},"event_type":"fda_approval","event_type_secondary":["clinical_trial"],"sentiment":"bullish","material_impact_score":4,"narrative":"The FDA granted accelerated approval to AstraZeneca's ETCAMAH (camizestrant) in combination with a CDK4/6 inhibitor (abemaciclib, palbociclib or ribociclib) for adults with HR-positive, HER2-negative locally advanced or metastatic breast cancer upon detection of an ESR1 mutation during aromatase inhibitor and CDK4/6 inhibitor therapy.\n\nApproval was based on the SERENA-6 Phase III trial, which showed a 56% reduction in the risk of disease progression or death versus staying on an aromatase inhibitor (HR 0.44; p<0.00001), with median PFS of 16.0 versus 9.2 months; a subsequent analysis demonstrated a PFS2 benefit of 25.7 versus 19.1 months while overall survival data continue to mature.\n\nThe ctDNA-guided switch strategy is the first and only medicine of its type in the 1st-line setting, targeting roughly 37,000 US first-line HR-positive metastatic breast cancer patients, about 30% of whom develop ESR1 mutations; this is AstraZeneca's tenth FDA approval this year and fourth in breast cancer, and the FDA concurrently approved a companion diagnostic for emerging ESR1 mutations.\n\nThe indication is approved under accelerated approval contingent on confirmatory trial verification of clinical benefit, and the label carries a boxed warning for arrhythmia risk (Torsades de Pointes, sudden death) with concomitant QTc-prolonging drugs such as ribociclib.","key_figures":{"drugName":"ETCAMAH (camizestrant)","phaseOfTrial":"Phase III","customDimensions":{"pfs2_months":[25.7,19.1],"os_hazard_ratio":0.87,"bradycardia_rate":"8%","pfs_hazard_ratio":0.44,"recommended_dose":"75 mg once daily","trial_enrollment":315,"median_pfs_months":[16,9.2],"pfs2_hazard_ratio":0.63,"countries_approved":"more than 30","pfs_hazard_ratio_ci":"0.31-0.60","qtc_prolongation_rate":"2.6%","esr1_mutation_incidence_1l":"~30%","us_breast_cancer_new_cases":"more than 300,000","us_1l_hr_positive_mbc_patients":37000,"risk_reduction_progression_or_death":"56%"}},"named_entities":{"people":[{"name":"Kevin Kalinsky","role":"Division Director of Medical Oncology, Winship Cancer Institute of Emory University; SERENA-6 investigator"},{"name":"Dave Fredrickson","role":"Executive Vice President, Oncology Haematology Business Unit, AstraZeneca"}],"products":["ETCAMAH","camizestrant","abemaciclib","palbociclib","ribociclib","anastrozole","letrozole","FDA-authorized ESR1 companion diagnostic test","fam-trastuzumab deruxtecan-nxki","datopotamab deruxtecan-dlnk","olaparib","capivasertib","saruparib","durvalumab"],"companies":[{"name":"AstraZeneca","ticker":"AZN","relationship":"filer"},{"name":"US Food and Drug Administration (FDA)","relationship":"regulatory authority"},{"name":"Daiichi Sankyo","relationship":"collaboration partner (ADC portfolio)"},{"name":"MSD (Merck & Co., Inc. in the US and Canada)","relationship":"research collaboration partner (olaparib)"}],"dollarAmounts":[]},"model_name":"glm-4.7","prompt_hash":"sha256:727b4b9429a443af","schema_hash":"sha256:05005c02d9cffac9","created_at":"2026-09-04T23:05:10.248Z","global_importance":65,"audience_relevance":62,"importance_components":{"mitigants":"drug already approved in 30+ countries; indication expansion rather than first-ever approval","tickerTier":"mega-cap","eventGravity":"FDA accelerated approval, new 1st-line indication for key growth asset","sectorWeight":"pharma-oncology","householdBrandBoost":true}},"durationMs":129911,"modelName":"glm-4.7"}}