Only 1L therapy delivers the longest window of PFS benefit in HR+/HER2- mBC1-10

For patients with HR+/HER2- mBC, the 1L treatment phase is a unique window of opportunity to maximize time on endocrine therapy, where patients reported being able to maintain quality of life, as well as fewer impairments in daily activities, for longer. As a frontline advocate on the care team, you may have the power to help patients stay on their 1L CDK4/6i regimen longer.1-10

When an ESR1 mutation is first detected, it can quietly begin to limit the effectiveness of 1L ET, even before symptoms worsen.10-12

About ETCAMAH

About ETCAMAH + CDK4/6i

ETCAMAH in combination with a CDK4/6i (ribociclib, abemaciclib, or palbociclib) for the treatment of adult patients with HR+/HER2− aBC or mBC upon detection of ESR1m during first-line endocrine-based therapy based on an FDA-approved test. Under accelerated approval in combination with a CDK4/6i for HR+/HER2- mBC upon ESR1m detection during AI + CDK4/6i. Clinical benefit to be verified in confirmatory trials.13

By proactively identifying ESR1 mutations with ctDNA and switching to ETCAMAH + CDK4/6i at the earliest sign, you may be able to help your patients12:

1

1L + CDK4/6i exposure

  • Unaddressed endocrine resistance increases tumor genomic complexity, which may be harder to treat in 2L11,12,14,16,17

2

ESR1m detection

  • Up to 40% of patients develop ESR1m, tripling the risk of disease progression 6 months after detection11,12

3

Early intervention with ETCAMAH

  • Designed to proactively address endocrine resistance to extend time on 1L12,16-18,*
Treatment Timeline Showing ESR1 Mutation Emergence And Disease Progression With ETCAMAH Plus CDK4/6 InhibitorTreatment Timeline Showing ESR1 Mutation Emergence And Disease Progression With ETCAMAH Plus CDK4/6 Inhibitor

For illustrative purposes

Stay proactive against progression: Intervene at ESR1m detection for the opportunity to extend time on 1L CDK4/6i12

*After 23.1 months median time on AI + CDK4/6i, the median progression-free survival from time of ctDNA-guided switch: HR=0.44 (95% CI: 0.31-0.60; (P<0.0001) 16 months for patients on ETCAMAH + CDK4/6i (95% CI: 12.7-18.2) vs 9.2 months for patients on AI + CDK4/6i (95% CI: 7.2-9.5).12,13

Your essential role in early intervention and ETCAMAH + CDK4/6i treatment

How your role helpsWhy it matters for patients
Explain the potential benefit
of early intervention		Patients may wonder why treatment is changing before disease progression and the impact this may have on 1L outcomes.13
Discuss ctDNA monitoringctDNA testing (liquid biopsy) can detect ESR1 mutations before disease progression.12
Support medication adherenceETCAMAH is a once-daily pill taken by mouth at the same time each day, in combination with any FDA-approved CDK4/6i. Patients should take ETCAMAH exactly as instructed by their doctor.13
Monitor for adverse reactionsPatients will work with you and the healthcare team to help manage any potential adverse reactions and dosing modifications.13
Empower active participationPatients may feel anxious about ctDNA testing and switching therapy before disease progression. You can discuss with them that ETCAMAH may help delay disease progression and may extend their time without progression on 1L CDK4/6i.13,19

For more information about ETCAMAH, download our ETCAMAH Advanced Practice Provider and Nurse Brochure

ETCAMAH mechanism of action

Dual-action effect on estrogen receptors12,20

ETCAMAH, a potent, next-generation oral SERD, blocks and degrades both ESR1wt and ESR1m receptors

ER Antagonism

Complete ER antagonism

effectively blocks estrogen from binding to the receptor20

  • Prevents ER-dependent changes in gene expression, reducing tumor growth
ER Degradation

Potent ER degradation

reduces the pool of ERs available for downstream signaling20

Mechanism of action based on preclinical research.

The dual-action mechanism of ETCAMAH can potentially address endocrine resistance20,21

ESR1m Monitoring for HR+/HER2- Breast Cancer

What to know about ESR1m monitoring

Liquid biopsy (blood test) to detect ESR1m can identify early signs of potential treatment resistance and help healthcare providers intervene before breast cancer progresses.12,13,22

WhoPatients with HR+/HER2- mBC on 1L Al + CDK4/6i for ≥6 months12

WhenAdd ESR1m testing to routine bloodwork every 3 months13

HowDetect ESR1m with ctDNA via liquid biopsy, using an FDA-authorized test13,22

Monitor your existing patients for ESR1m.
Intervene during 1L to stay ahead of disease progression12

Guide to ESR1m Monitoring During 1L Therapy

For more information about monitoring, download our ETCAMAH ESR1m Monitoring Guide for HCPs

ETCAMAH Cardiac Monitoring and Dosing

Upon ESR1m detection,

Switch to ETCAMAH–a convenient, once-daily tablet taken in combination with any FDA-approved CDK4/6i13

*For patients with severe hepatic impairment receiving ETCAMAH in combination with ribociclib, dose 75 mg once every other day.13

Avoid concomitant use of strong CYP3A inducers, and moderate CYP3A inducers when combining ETCAMAH with abemaciclib or palbociclib. If concomitant use of a moderate CYP3A inducer cannot be avoided, dose modifications will differ based on the CDK4/6i used.13

Advise patients when taking ETCAMAH13,†:

Clock Icon

Take once daily at the same time each day

If a dose of ETCAMAH is missed, instruct the patient to take the missed dose within 6 hours or skip the missed dose if more than 6 hours have passed. The next dose should be taken at the usual time the following day. If the patient vomits a dose of ETCAMAH, instruct the patient not to take an additional dose and to take the next dose at the usual time.

Swallow the tablet whole

Do not crush, chew, or split tablets prior to swallowing. Do not take any ETCAMAH tablets that are broken, cracked, or otherwise not intact.

Please see full Prescribing Information for drug interactions, dosing, and administration. Refer to the full Prescribing Information of the CDK4/6i or other concomitant medications for dosing.

The recommended dose of a CDK4/6 inhibitor is continued at the same dose at the time of initiation of ETCAMAH as when the ESR1m was detected.13

†Until disease progression or unacceptable toxicity.13

For specific populations,

Cardiac assessments for ETCAMAH should be completed within the first month of therapy13

Cardiac Assessments Table Cardiac Assessments Table
  • Perform an electrocardiogram (ECG) prior to initiating ETCAMAH, then every week for the first 2 weeks of treatment, and periodically during treatment as clinically indicated
  • Obtain serum electrolytes at baseline and during treatment as clinically indicated, and correct electrolyte abnormalities
  • Monitor heart rate more frequently during the first 30 days of treatment with ETCAMAH in patients with bradycardia (resting heart rate less than 60 bpm) at baseline and those on concomitant medications known to lower heart rate (eg, beta‑blockers) if concomitant use cannot be avoided

ETCAMAH AR Management Strategies

ETCAMAH adverse reactions and management

In SERENA-6,

Adverse reactions were mostly grade 1 or 213

1.3%

discontinued due to ARs
with ETCAMAH + CDK4/6i13,*

~90%

of patients did not
report diarrhea
9% had grade 1 or 2 diarrhea
with
ETCAMAH + CDK4/6i12

  • Dose interruption of ETCAMAH due to adverse reactions occurred in 22% of patients13,†

Adverse Reaction in
≥10% of patients14,‡

ETCAMAH + CDK4/6

 

AI + CDK4/6
All grades
%		Grade 3/4
%

 

All grades
%		Grade 3/4
%
Eye disorders

 

 

 

 

 

Eye disorders

 

 

 

 

 

Visual disturbances§340.6

 

160
Dry eye120

 

70
General disorders and administration site conditions

 

 

 

 

 

General disorders
and administration
site conditions

 

 

 

 

 

Fatigue230

 

190.6
Musculoskeletal and connective
tissue disorders

 

 

 

 

 

Musculoskeletal and
connective
tissue disorders

 

 

 

 

 

Arthralgia160

 

170.6
Back pain100.6

 

100
Gastrointestinal disorders

 

 

 

 

 

Gastrointestinal
disorders

 

 

 

 

 

Nausea100

 

140.6

*Adverse reactions that occurred in at least one patient leading to permanent discontinuation were gastroesophageal reflux disease (0.6%), and one patient experienced both cholestasis and hepatic cytolysis (0.6% each).13

†The adverse reactions (≥2%) leading to dose interruptions were bradycardia (3.9%) and visual disturbances (2.6%).

‡Graded according to NCI CTCAE version 5.0.

§Visual disturbances include: photopsia, vision blurred, visual impairment, diplopia, and photophobia of eye disorders MedDRA SOC and visual perseveration of nervous system disorders MedDRA SOC.

Fatigue includes: fatigue and asthenia.

In SERENA-6,

Additional safety and tolerability data13

  • The median duration of exposure was 10.1 months in the ETCAMAH + CDK4/6i arm13
  • Serious adverse reactions occurred in 10% of patients in the ETCAMAH + CDK4/6i arm. Serious adverse reactions in >1% of patients included urinary tract infection, pneumonia, and osteonecrosis of jaw (1.3% each). Fatal adverse reactions occurred in 1.3% of patients who received ETCAMAH + CDK4/6i including acute respiratory distress syndrome and sudden death (0.6% each)13

Laboratory abnormalities

(≥10% of patients)1,*,†

ETCAMAH
+ CDK4/6i (n=155)

 

AI +
CDK4/6i (n=155)

All grades,

%

Grade ≥3,

%

 

All grades,

%

Grade ≥3,

%

Hematology

 

 

 

 

 

Neutrophils decreased6842

 

6639
Leukocytes decreased6623

 

5817
Hemoglobin decreased473.9

 

385
Lymphocytes decreased399

 

378
Platelets decreased362.6

 

301.3
Chemistry

 

 

 

 

 

Aspartate aminotransferase
increased		172.6

 

291.3
Corrected calcium decreased170

 

120.7
Creatinine increased160.6

 

201.3
Gamma glutamyl transferase increased122.7

 

238
Alanine aminotransferase increased121.3

 

200
Creatine kinase increased120

 

60
Alkaline phosphatase increased100.7

 

220.7

*Graded according to NCI CTCAE version 5.0.13

†Includes patients with at least one on‑treatment postbaseline result.13

<1% of patients had a dose modification due to liver toxicity13,‡

‡0.6% permanently discontinued due to hepatic cytolysis.13

In SERENA-6,

Cardiac events associated with ETCAMAH were generally low grade and reversible13

Bradycardia

Heartbeat IconHeartbeat Icon

Low incidence - 8%13

Heart Rate Monitor IconHeart Rate Monitor Icon

No grade 3 or above
events reported12
(Grade 1–5.2%; Grade 2–2.6%)

Prohibited IconProhibited Icon

No medical
interventions
were
required beyond
dose interruption13

Calendar IconCalendar Icon

Median time to onset was
17
days (range: 13-283)
Maximum decrease
in heart rate observed
on day 1513

Patients with bpm <55 were excluded in SERENA-6.

QTc interval prolongation when combined with ribociclib or other known QTc interval prolonging drugs

Heartbeat IconHeartbeat Icon

Low incidence - 2.6%13

Heart Rate Monitor IconHeart Rate Monitor Icon

Generally low grade23,24
(Grade 1–1.3%; Grade 2–0.6%; Grade 3–0.6%)

In a dose-finding trial, a Grade 4
Torsades de Pointes was observed in one
patient with confounding factors receiving ETCAMAH + ribociclib

Heartbeat IconHeartbeat Icon

No clinically meaningful arrhythmia reported28

Reversible IconReversible Icon

Reversible with
dose interruption23

Please see full Prescribing Information for additional information on cardiac monitoring, dose modifications, and drug interactions.

Dose interruptions13

  • Dose interruptions of ETCAMAH due to bradycardia occurred in 3.9% of patients

How to grade bradycardia (CTCAE criteria)13,*:

Grade 1

  • Asymptomatic

Grade 2

  • Symptomatic

Management of bradycardia13,†

Management of bradycardia13,†

Grade 1

No intervention needed.

Grade ≥2*

Withhold ETCAMAH until symptoms resolve.

Obtain ECG to evaluate etiology of symptomatic bradycardia.

If a contributing concomitant medication is identified, modify the dosage or discontinue this medication as appropriate until bradycardia symptoms resolve and then resume ETCAMAH.

Consider reassessing the heart rate after restart of ETCAMAH dosing.

Permanently discontinue ETCAMAH for persistent symptomatic bradycardia.

*Grading according to NCI CTCAE version 5.0. Grade 1: Asymptomatic, intervention not indicated; Grade 2: Symptomatic, intervention not indicated; change in medication.13

†Bradycardia includes bradycardia and sinus bradycardia.13

In SERENA-6,

Visual disturbances were reported to have no or generally minimal effect on patients' daily activities12,13

In patients who reported visual disturbances12,13,25,*:

The vast majority were grade 1

and not impacting activities of daily living

  • Rates: ~90% grade 1, ~8% grade 2, and ~2% grade 3 or higher†
  • Median time to onset: 8 days
  • Duration: <1 minute/episode
  • Frequency: ≤3 days a week

*34% of patients in the ETCAMAH + CDK4/6i arm (n=155) and 16% of patients in the AI + CDK4/6i arm (n=155).25

vission-icon

No increased risk of clinically meaningful changes in visual acuity12,13,25

  • No or negligible impact on ability to drive or use machines
vission-icon

No baseline eye exam required13

  • Nonstructural and reversible effect on the eye25,26,‡
  • No increased severity over time25,§

No patients discontinued ETCAMAH due to visual disturbances13

2.6% of patients had a dose interruption due to visual disturbances13

Visual disturbances in SERENA-612,25

The most common visual disturbances was photopsia, which is the perception of flashing or flickering lights without an external stimulus.12

  • Photopsia was typically observed in the periphery and was not associated with structural eye abnormalities12

 ETCAMAH + CDK4/6i (n=155) All grades, %AI + CDK4/6i (n=155) All grades, %
Visual 
disturbances

34

16

Photopsia207.7
Vision blurred7.17.1
Visual impairment3.91.9
Diplopia1.91.3
Photophobia1.90
Visual perseveration1.30

How to grade photopsia (CTCAE criteria)13,27,II:

Grade 1

  • Symptomatic but not limiting activities of daily living

Grade 2

  • Limiting instrumental activities of daily living

Grade 3

  • Limiting self-care activities of daily living

Management of visual disturbances13,¶

Management of visual disturbances

Grade 1

No intervention needed.

Grade ≥2II

Withhold ETCAMAH until symptoms resolve to Grade 1 or below.

Refer the patient to an eye care professional if visual symptoms are progressive, persistent, or interfere with instrumental ADLs. Reassess visual disturbances at the next visit.

†Grade 2: Limiting instrumental ADL; Grade 3: Limiting self-care ADL.13

‡The NEI-VFQ-25 assesses how visual function affects daily activities and overall vision-related QoL. This questionnaire comprises 11 subscales. Adherence was calculated for each timepoint and was defined as the number of patients with an evaluable questionnaire (≥1 subscale completed) divided by the total number of patients expected to complete the questionnaire at that timepoint. At baseline, 69% of patients in the ETCAMAH + CDK4/6i arm and 59% of patients in the AI + CDK4/6i arm completed ≥1 subscale of the NEI-VFQ-25.25

§Based on ophthalmological review of patients reporting visual disturbances.12

Findings from the VSAQ and NEI-VFQ-25 are exploratory and descriptive, intended to characterize patient-reported visual symptoms and function and may be subject to inherent limitations of PRO measures. Clinicians should apply their own judgment. These questionnaires were not designed to evaluate early visual disability; results may underrepresent such impairments.

IISeverity as defined by NCI CTCAE version 5.0.13

Visual disturbances include: photopsia, blurred vision, visual field defect, decreased visual acuity, visual impairment, diplopia, photophobia and visual preservation.13

Additional safety information

Management of adverse reactions13

Management of other adverse reactions13

Grade ≤2

No intervention needed.

Grade ≥3*

Withhold ETCAMAH until resolution to Grade 2 or below, then resume ETCAMAH.

Permanently discontinue ETCAMAH for recurrence of Grade 3 or higher adverse reactions.

*Severity as defined by NCI CTCAE version 5.0.13

Refer to the full Prescribing Information for the coadministered CDK4/6i inhibitor or dose modification guidelines in the event of toxicity and other relevant safety information.13

ETCAMAH Drug Interactions

Drug interactions with ETCAMAH1

Advise your patients to inform their healthcare team of all the medications that will be taken with ETCAMAH, including prescription medicines, over-the-counter medicines, vitamins, and herbal medicines.

Clinical impact

Prevention/management

CYP3A4/5 inducers

  • Based on Physiological Based Pharmacokinetic (PBPK) modelling, CYP3A4/5 inducers may reduce the exposure levels of ETCAMAH
  • Avoid the use of strong CYP3A4/5 inducers (e.g. carbamazepine and St. John’s wort) when co-administered
  • Consider an alternative drug product with no or weak potential to induce CYP3A4/5 enzymes
  • Co-administration of ETCAMAH and a moderate CYP3A4/5 inducer (eg, phenobarbital) is allowed with caution

CYP2C9 and/or CYP2C19 substrates

  • Based on PBPK modelling, co-administration of ETCAMAH may increase the exposure levels of drug products that are sensitive substrates or substrates with a narrow therapeutic index of CYP2C9 and/or CP2C19 substrates
  • Avoid use of drug products that are sensitive substrates or substrates with narrow therapeutic index of CYP2C9 and/or CYP2C19 (eg, warfarin, phenytoin) at least 2 weeks before the first dose and at least 2 weeks after the last dose
  • Coadministration of ETCAMAH and moderately sensitive CYP2C9 and/or CYP2C19 substrates (eg, lansoprazole) allowed with caution; consider alternative if possible

CYP3A4/5 substrates

  • Co-administration of ETCAMAH may affect exposure levels of products that are sensitive CYP3A4/5 substrates
  • Coadministration of ETCAMAH and CYP3A4/5 substrates with a narrow therapeutic index (eg, alfentanil and fentanyl) may require dose adjustment and are to be monitored closely
  • Coadministration of ETCAMAH and sensitive CYP3A4/5 substrates (eg, midazolam and simvastatin) are to be used with caution

Drug Products Known to Prolong the QT Interval

  • QT interval prolongation can occur when coadministered with products known to prolong QT interval
  • ETCAMAH in combination with ribociclib has been studied clinically. Clinical monitoring and dose modifications with reference to approved ribociclib label is recommended
  • Avoid the use of drug products known to prolong the QT interval and/or have a known risk of Torsades de Pointes (eg, ciprofloxacin, ondansetron). Monitor ECGs as clinically indicated if concomitant use cannot be avoided

For additional information on drug interactions with ETCAMAH, please see Full Prescribing Information.

APP/Nurse Resources

Find Support and Resources for You and Your Patients

ETCAMAH Dosing and Treatment Management Guide

DOWNLOAD
Guide to ESR1m Monitoring During 1L Therapy

ETCAMAH ESR1m Monitoring Guide for HCPs

DOWNLOAD

ETCAMAH Advanced Practice Provider and Nurse Brochure

DOWNLOAD

1L=first line; 2L=second line; aBC=inoperable locally advanced or metastatic breast cancer; ADL=activities of daily living; AI=aromatase inhibitor; AR=adverse reaction; CDK4/6i=cyclin-dependent kinase 4/6 inhibitor; CTCAE=Common Terminology Criteria for Adverse Events; ctDNA=circulating tumor DNA; ER=estrogen receptor; ESR1=estrogen receptor 1; ESR1m=estrogen receptor 1 gene mutation; ESR1wt=estrogen receptor 1 wild-type; ET=endocrine therapy; FDA=Food and Drug Administration; HER2−=human epidermal growth factor receptor 2–negative; HR+=hormone receptor–positive; mBC=metastatic breast cancer; NCI=National Cancer Institute; NEI-VFQ-25=National Eye Institute Visual Function Questionnaire-25; PRO=patient-reported outcome; SERD=selective estrogen receptor degrader; VSAQ=Visual Symptom Assessment Questionnaire.

References:

  1. Finn RS, Martin M, Rugo HS, et al. Palbociclib and letrozole in advanced breast cancer. N Engl J Med. 2016;375(20):1925-1936. doi:10.1056/NEJMoa1607303
  2. Hortobagyi GN, Stemmer SM, Burris HA, et al. Updated results from MONALEESA-2, a phase III trial of first-line ribociclib plus letrozole versus placebo plus letrozole in hormone receptor-positive, HER2-negative advanced breast cancer. Ann Oncol. 2018;29(7):1541-1547. doi:10.1093/annonc/mdy155
  3. Johnston S, Martin M, Di Leo A, et al. MONARCH 3 final PFS: a randomized study of abemaciclib as initial therapy for advanced breast cancer. NPJ Breast Cancer. 2019;5:5. doi:10.1038/s41523-018-0097-z
  4. Kalinsky K, Bianchini G, Hamilton E, et al. Abemaciclib plus fulvestrant in advanced breast cancer after progression on CDK4/6 inhibition: results from the phase III postMONARCH trial. J Clin Oncol. 2025;43(9):1101-1112. doi:10.1200/JCO-24-02086
  5. Turner NC, Oliveira M, Howell SJ, et al; CAPItello-291 Study Group. Capivasertib in hormone receptor-positive advanced breast cancer. N Engl J Med. 2023;388(22):2058-2070. doi:10.1056/NEJMoa2214131
  6. Bidard FC, Kaklamani VG, Neven P, et al. Elacestrant (oral selective estrogen receptor degrader) versus standard endocrine therapy for estrogen receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer: results from the randomized phase III EMERALD trial. J Clin Oncol. 2022;40(28):3246-3256. doi:10.1200/JCO.22.00338
  7. Rugo HS, Bardia A, Marmé F, et al. Sacituzumab govitecan in hormone receptor-positive/human epidermal growth factor receptor 2-negative metastatic breast cancer. J Clin Oncol. 2022;40(29):3365-3376. doi:10.1200/JCO.22.01002
  8. O'Shaughnessy J, Schwartzberg L, Piccart M, et al. Results from CONTESSA: a phase 3 study of tesetaxel plus a reduced dose of capecitabine versus capecitabine alone in patients with HER2-, hormone receptor + (HR+) metastatic breast cancer (MBC) who have previously received a taxane. Presented at: San Antonio Breast Cancer Symposium; December 8-11, 2020; San Antonio, TX. Presentation GS4-01.
  9. Marschner N, Zacharias S, Lordick F, et al. Association of disease progression with health-related quality of life among adults with breast, lung, pancreatic, and colorectal cancer. JAMA Netw Open. 2020;3(3):e200643. doi:10.1001/jamanetworkopen.2020.0643
  10. Jhaveri KL, Neven P, Casaluovo ML, et al; EMBER-3 Study Group. Imlunestrant with or without abemaciclib in advanced breast cancer. N Engl J Med. 2025;392(12):1189-1202. doi:10.1056/NEJMoa2410858
  11. Clatot F, Perdrix A, Beaussire L, et al. Risk of early progression according to circulating ESR1 mutation, CA-15.3 and cfDNA increases under first-line anti-aromatase treatment in metastatic breast cancer. Breast Cancer Res. 2020;22(1):56. doi:10.1186/s13058-020-01290-x
  12. Bidard FC, Mayer EL, Park YH, et al; SERENA-6 Study Group. First-line camizestrant for emerging ESR1-mutated advanced breast cancer. N Engl J Med. 2025;393(6):569-580. doi:10.1056/NEJMoa2502929
  13. ETCAMAH® (camizestrant) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2026.
  14. Grinshpun A, Chen V, Sandusky ZM, Fanning SW, Jeselsohn R. ESR1 activating mutations: from structure to clinical application. Biochim Biophys Acta Rev Cancer. 2023;1878(1):188830. doi:10.1016/j.bbcan.2022.188830
  15. Oliveira M, Hamilton EP, Kulybaya Y, et al. Dynamics of ESR1 mutation (ESR1m) circulating tumour DNA (ctDNA) in patients (pts) with estrogen receptor (ER+), HER2- metastatic breast cancer (mBC) receiving camizestrant or fulvestrant: exploratory analyses from the SERENA-2 trial. Abstract presented at: ESMO Congress; September 13-17, 2024; Barcelona, Spain.
  16. Cabel L, Bachelot T, Hardy-Bessard AC, et al. 1O Kinetics and determinants of blood ESR1 mutation under AI and palbociclib in HR+/HER2- metastatic breast cancer patients in the PADA-1 trial. Presented at: ESMO Breast Cancer Annual Congress; May 14-17, 2025; Munich, Germany.
  17. Pejerrey SM, Dustin D, Kim JA, Gu G, Rechoum Y, Fuqua SAW. The impact of ESR1 mutations on the treatment of metastatic breast cancer. Horm Cancer. 2018;9(4):215-228. doi:10.1007/s12672-017-0306-5
  18. Data on File. US-112875. AstraZeneca Pharmaceuticals LP, 2026.
  19. Wong K, Kameoka A, Fukui JA. Exploring the utility of ctDNA testing in high-risk breast cancer patients in a community setting: case series. Ther Adv Med Oncol. 2025;17:1-13. doi:10.1177/17588359251351121
  20. Lawson M, Cureton N, Ros S, et al. The next-generation oral selective estrogen receptor degrader camizestrant (AZD9833) suppresses ER+ breast cancer growth and overcomes endocrine and CDK4/6 inhibitor resistance. Cancer Res. 2023;83(23):3989-4004. doi:10.1158/0008-5472.CAN-23-0694
  21. Scott JS, Moss TA, Balazs A, et al. Discovery of AZD9833, a potent and orally bioavailable selective estrogen receptor degrader and antagonist. J Med Chem. 2020;63(23):14530-14559. doi:10.1021/acs.jmedchem.0c01163
  22. Bidard FC, Mayer EL, Park YH, et al; SERENA-6 Study Group. First-line camizestrant for emerging ESR1-mutated advanced breast cancer. N Engl J Med. 2025;393(6)(suppl):1-18.
  23. Data on File. REF-343615. AstraZeneca Pharmaceuticals LP, 2026.
  24. Hamilton E, Oliveira M, Turner N, et al. A phase I dose escalation and expansion trial of the next-generation oral SERD camizestrant in women with ER-positive, HER2-negative advanced breast cancer: SERENA-1 monotherapy results. Ann Oncol. 2024;35(8):707-717. doi:10.1016/j.annonc.2024.04.012 
  25. Brufsky A, Park YH, Bidard FC, et al. SERENA-6 visual patient-reported outcomes and safety: camizestrant for emerging ESR1m advanced breast cancer during first-line endocrine-based therapy. Oncologist. 2026;31(9):oyag278. doi:10.1093/oncolo/oyag278
  26. Hamm G, Maglennon G, Purbrick S, et al. Camizestrant causes reversible pharmacological effects on retinal responses in rats. Transl Oncol.
    2025;62:102539. doi:10.1016/j.tranon.2025.102539
  27. National Cancer Institute (NCI). Common terminology criteria for adverse events (CTCAE), Version 5.0. November 27, 2017. Accessed January 14, 2026. https://dctd.cancer.gov/research/ctep-trials/for-sites/adverse-events/ctcae-v5-5x7.pdf
  28. Data on File. REF-347237. AstraZeneca Pharmaceuticals LP, 2026.

Photopsia is the perception of flashing or flickering lights without an external stimulus. In the SERENA-6 trial, this symptom was typically observed in the periphery and was not associated with structural eye abnormalities.2

fpo popup fpo popup

Reference: Dorland's Illustrated Medical Dictionary.