FDA approves Etcamah for advanced breast cancer: Treatment can be adjusted based on blood tests even before imaging progresses

On September 4, 2026, the U.S. Food and Drug Administration granted accelerated approval to camizestrant (trade name Etcamah), a new oral therapy for a certain group of patients with hormone receptor-positive, HER2-negative locally advanced or metastatic breast cancer. The drug is used not alone, but with one of the CDK4/6 inhibitors—abemaciclib, palbociclib, or ribociclib. [1]

The most unusual aspect of this approval isn't even the introduction of another pill. Etcamah is intended for situations where treatment is still apparently working: CT or MRI scans don't yet show progression, but analysis of circulating tumor DNA in the blood already detects an acquired ESR1 mutation. This mutation signals that the tumor has begun to adapt to the aromatase inhibitor and may soon become resistant to current endocrine therapy. [2]

In the randomized phase III SERENA-6 trial, patients with a detected ESR1 mutation either switched early from an aromatase inhibitor to kamisestrant while maintaining the same CDK4/6 inhibitor or continued the previous regimen until usual clinical progression. The median progression-free survival was 16.0 months versus 9.2 months, and the hazard ratio for progression or death was 0.44. In other words, during the follow-up period, an early change in endocrine therapy was associated with an approximately 56% relative reduction in the risk of progression or death. [3]

However, the FDA specifically emphasizes that such early intervention has not yet been proven to ultimately prolong life or provide a definitive clinically significant benefit compared to changing therapy after confirmed progression. This is why the approval was granted under the accelerated approval mechanism, and continued maintenance of the indication will depend on confirmatory studies. Moreover, several months before approval, the FDA's oncology advisory committee voted against recognizing the benefit-risk balance as convincingly proven—6 votes against, 3 in favor. [4]

Key fact	Result
Preparation	camizestrant
Trade name in the USA	Etcamah
FDA approval date	September 4, 2026
Type of approval	accelerated approval
Form	tablet
Dose	75 mg once a day
Together with	abemaciclib, palbociclib, or ribociclib
Disease	HR+/HER2− locally advanced or metastatic breast cancer
Mandatory condition	occurrence of ESR1 mutation during AI + CDK4/6
How is a mutation detected?	circulating tumor DNA in blood
Companion diagnostic	Guardant360 CDx
Main study	SERENA-6, phase III
Randomized	315 patients
PFS	16.0 versus 9.2 months
HR of progression/death	0.44
Overall survival	the data is still immature
DOI of the main article	10.1056/NEJMoa2502929

What is ESR1 and why does cancer become resistant to hormonal therapy?

Most hormone receptor-positive breast tumors rely on estrogen signaling for growth. Therefore, one of the main treatment strategies for advanced HR-positive, HER2-negative cancers is suppression of the estrogen-dependent signaling. Aromatase inhibitors, such as letrozole or anastrozole, dramatically reduce estrogen production, while CDK4/6 inhibitors additionally block the tumor cell cycle. This combination is a common first-line endocrine therapy. [5]

But cancer evolves under the pressure of treatment. One of the most common mechanisms of acquired resistance is a change in ESR1, the gene encoding the estrogen receptor. Some mutations allow the receptor to remain active even when estrogen levels are sharply reduced by an aromatase inhibitor. The tumor cell effectively ceases to be completely dependent on the hormone and regains the ability to maintain its growth program. [6]

At the time of initial diagnosis of HR-positive metastatic disease, ESR1 mutations are relatively rare: the FDA states that they are present in less than 5% of patients. However, after progression on an aromatase inhibitor, such mutations are detected in nearly 40% of patients. This means that in most cases, this is not an innate tumor characteristic, but an evolutionary response to therapeutic pressure. [7]

Before the SERENA-6 concept, doctors typically recognized that first-line therapy had failed when existing metastases expanded, new lesions appeared, or corresponding symptoms arose. The new strategy attempts to identify the molecular mechanism of resistance before anatomical progression. Therefore, ESR1 is becoming not just a prognostic marker, but a signal for immediate change of one treatment component. [8]

How Resilience Develops

Stage	What's happening
Original tumor	depends on the estrogen signal
Aromatase inhibitor	reduces the formation of estrogens
CDK4/6 inhibitor	inhibits the cell cycle
Under pressure of treatment	resistant clones appear
ESR1 mutation	the receptor can be activated by low estrogen levels
On CT/MRI	the tumor may still appear stable
In ctDNA	the mutation can already be detected
New strategy	replace AI with a kamizastrant until radiological progression

Why Etcamah is a new generation of endocrine therapy

Camisetrant is an orally administered, selective estrogen receptor degrader and full estrogen receptor antagonist. Its function is not to reduce estrogen levels, as with aromatase inhibitors, but to directly block the receptor itself and stimulate its degradation. Therefore, the drug may retain activity against tumor cells in which the receptor has acquired certain ESR1 mutations. [9]

This is where the key difference between the old and new regimens lies. An aromatase inhibitor attempts to deprive the receptor of its hormonal ligand, but with an ESR1 mutation, the tumor can partially bypass this mechanism. Kamizestrant directly targets the receptor, which has become the source of resistance. Therefore, instead of enhancing the previous method of estrogen suppression, doctors are changing the level of therapeutic attack.

The FDA-approved regimen requires that kamisestrant be administered at a dose of 75 mg once daily, with or without food. The CDK4/6 inhibitor is unchanged: the patient continues to receive the same abemaciclib, palbociclib, or ribociclib at the same dose they were using when the ESR1 mutation was discovered. [10]

This approach fundamentally differs from a full-fledged switch to second-line treatment. The researchers essentially change only the element of the regimen against which resistance has developed, while retaining the component that likely continues to suppress the cell cycle. Therefore, SERENA-6 can be viewed as an experiment in molecularly controlled first-line correction, rather than simply a comparison of two sequential drugs.

Blood testing becomes part of the decision to change anticancer therapy

Tumor cells constantly die and release small fragments of their DNA into the bloodstream. This portion of genetic material is called circulating tumor DNA, or ctDNA. Modern technologies make it possible to isolate these fragments from a normal blood sample and search for specific tumor genetic changes. [11]

In SERENA-6, patients underwent ctDNA testing approximately every two to three months during the first-line treatment. If an ESR1 mutation was detected but radiological progression had not yet occurred, the patient could proceed to randomization. Thus, the decision to change therapy was made not after tumor growth, but rather upon the emergence of a molecular marker of resistance. [12]

For clinical use, the FDA simultaneously approved Guardant360 CDx as a companion diagnostic—a diagnostic test that identifies ESR1 mutations in patients being considered for treatment with Kamisestrant. This means that the blood test is not an optional addition, but rather part of the approved indication itself. [13]

The FDA calls Etcamah the first approved cancer treatment that uses ctDNA detection of resistance mutations to alter therapy before progression becomes visible on imaging. If this principle proves to be long-term beneficial, its implications could extend far beyond breast cancer: similar approaches could be used to target molecular resistance in other tumors. [14]

The usual strategy	SERENA-6 Strategy
Wait for tumor changes on CT/MRI	regularly test ctDNA
Progression has already occurred	an early mechanism of resistance is discovered
After progression, change the line	change the endocrine component in advance
The decision is based on the anatomy of the tumor	the solution is based on molecular evolution
ESR1 will be discovered later	ESR1 is detected before radiological growth

How the SERENA-6 study was conducted

SERENA-6 was an international, randomized, double-blind, placebo-controlled phase III study. The screening program included 3,256 patients with ER-positive, HER2-negative locally advanced or metastatic breast cancer who received first-line therapy with an aromatase inhibitor and one of three CDK4/6 inhibitors. [15]

To be included in the randomized arm, patients had to have received this first-line regimen for at least six months, have an ESR1 mutation detected in their blood, and still show no progression. Ultimately, 315 patients met the necessary criteria and were allocated 1:1 between the two strategies. [16]

One hundred fifty-seven participants discontinued their aromatase inhibitor and switched to kamisestrant 75 mg daily while continuing their previous CDK4/6 inhibitor. Another 158 continued their aromatase inhibitor—anastrozole or letrozole—along with their previous CDK4/6 inhibitor. Due to the double-blind design, matching placebos were used to minimize the influence of physician and patient expectations on treatment assessment. [17]

The primary endpoint was progression-free survival as assessed by investigators according to RECIST 1.1. This is the time from randomization after detection of an ESR1 mutation to objective disease progression or death. Overall survival was an important secondary endpoint, but data for it were not yet mature at the time of the initial analysis. [18]

Design of SERENA-6

Parameter	Data
Phase	III
Design	randomized, double-blind, placebo-controlled
ClinicalTrials.gov	NCT04964934
Tested on ESR1	3256 patients
Randomized	315
Kamizestrant	157
AI Continuation	158
ctDNA testing	approximately every 2-3 months
Minimum duration of the previous 1st line	6 months
Kamizestrant	75 mg daily
CDK4/6	continued without changing the drug
Primary endpoint	PFS

Switching to a kamizastrant increased the median PFS from 9.2 to 16 months

In the initial analysis, with a median follow-up of 12.6 months, median progression-free survival was 16.0 months in patients who switched to kamisertrant and 9.2 months in those who continued the aromatase inhibitor. The absolute difference in medians was 6.8 months.[19]

The hazard ratio for progression or death was 0.44, 95% confidence interval 0.31–0.60, p<0.0001. This corresponds to an approximately 56% relative reduction in the immediate risk of progression or death during the follow-up period. It is important not to translate this indicator as “each patient gained 56% more life”: the hazard ratio characterizes the comparative dynamics of events in the entire group. [20]

In a later analysis, when the median follow-up was extended to 23.5 months, the result was maintained. The median PFS was now 16.8 months versus 9.2 months, with an HR of 0.45 and a 95% confidence interval of 0.34–0.59. Thus, the early benefit did not disappear as additional events accumulated. [21]

At 24 months, approximately 34.9% of patients in the kamizatrant group remained progression-free, compared with 14.2% in the control group. At 30 months, this figure was 30.4%, compared with only 2.7%. However, at later time points, the number of patients under observation decreases, so these percentages should be interpreted in conjunction with the Kaplan-Meier curves, rather than as a simple proportion of the entire initial sample. [22]

Efficiency	Camisestrant + CDK4/6	AI + CDK4/6
Patients	157	158
Initial median PFS	16.0 months	9.2 months
HR	0.44	reference
95% CI	0.31-0.60	-
p	<0.0001	-
Updated PFS	16.8 months	9.2 months
PFS at 24 months	34.9%	14.2%
PFS at 30 months	30.4%	2.7%

The benefit persisted even after the first progression

One of the main concerns about early switching is the potential "treatment time-shifting" effect. If a drug can still be prescribed after normal disease progression, a longer initial PFS does not necessarily mean the overall disease trajectory is improved. The patient may simply receive an effective drug earlier, without benefiting from an overall longer duration of disease control.

Therefore, SERENA-6 pre-analyzed PFS2—the time to second progression or death—a measure that takes into account not only early experimental therapy but also subsequent treatment after the first progression. In the updated analysis, the median PFS2 was 25.7 months with the kamidine versus 19.1 months with continued aromatase inhibitor therapy. [23]

The hazard ratio for PFS2 was 0.63, 95% CI 0.46–0.86, p=0.00373. At 24 months, 50.8% versus 36.3% remained progression-free, and at 30 months, 41.5% versus 29.7%. This result strengthens the argument that early intervention does not simply “carry forward” the drug, but may maintain benefit beyond the next line of therapy.[24]

Another practically important indicator was the time to the need for chemotherapy or an antibody-drug conjugate. The median time was 22.6 versus 18.7 months, with a HR of 0.64. This suggests that an early change in endocrine therapy allowed, on average, longer treatment with a less intensive systemic strategy. This analysis was secondary and requires appropriate caution, but the trend is consistent with PFS2. [25]

SERENA-6 Long-Term Performance

Indicator	Kamizestrant	AI Continuation
PFS2	25.7 months	19.1 months
HR PFS2	0.63	-
PFS2 at 24 months	50.8%	36.3%
PFS2 after 30 months	41.5%	29.7%
Chemotherapy-free time/ADC	22.6 months	18.7 months
HR	0.64	-

Circulating tumor DNA almost disappeared in half of the patients

At ASCO 2026, the researchers presented additional molecular analysis. Eight weeks after the therapy switch, total circulating tumor DNA in the kamizatrant group decreased by a median of approximately 99%, while in patients who continued the aromatase inhibitor, it increased by approximately 64%. [26]

Even more striking was the rate of complete ctDNA clearance. Among patients with suitable samples, 50 of 98 (51%) had circulating tumor DNA undetectable after switching to kamisestrant. In the control group, this occurred in only 2 of 108 patients—approximately 1.9%. [27]

This result provides a biological explanation for the clinical PFS: the kamisestrant did not simply delay reaching the formal progression threshold on imaging, but rather rapidly suppressed the molecular tumor signal. It was additional data on ctDNA and longer-term outcomes that the FDA requested during the application review process following the controversial advisory committee decision. [28]

However, ctDNA clearance remains a biomarker, not a standalone proof of longer survival. Its appeal lies in its ability to very early reveal the depth of the antitumor response. Further observation is needed to determine the extent to which ctDNA clearance predicts overall survival in this specific setting.

Quality of life deteriorated much later

PFS alone is insufficient for assessing early therapy switching. If the patient is not yet experiencing progression, additional treatment must provide sufficient benefit to justify the new side effects and psychological burden of changing therapy. Therefore, SERENA-6 carefully assessed patient-reported quality of life.

In the initial analysis, the median time to deterioration in overall health and quality of life was 21.0 months on kamizatrant versus 6.4 months with continued aromatase inhibitor therapy. The odds ratio for deterioration was 0.54. [29]

In a later analysis, the direction remained the same. Switching also delayed the deterioration of a number of symptoms and functions—pain, fatigue, shortness of breath, physical, role, and emotional functioning. This is important because it shows that the gain in imaging was not accompanied by an obvious deterioration in the patient's subjective state due to treatment. [30]

However, quality-of-life measures are secondary endpoints and depend on questionnaire completion, censoring, and the statistical model. They enhance the overall efficacy picture but do not replace long-term survival assessment.

Overall survival has not yet been proven.

At the time of the initial analysis of SERENA-6, overall survival data were immature. This was one of the reasons for the FDA's caution: if treatment is started earlier than usual, an increase in PFS alone does not guarantee that the patient will ultimately live longer. [31]

By January 2026, there were 46 deaths in the study group and 49 in the control group. The odds ratio for overall mortality was 0.87, but the 95% confidence interval was wide—0.57–1.30. Therefore, the data are still compatible with either a definite advantage or no significant difference. [32]

This fundamentally distinguishes the statement "kamizestrant prolongs progression-free period" from the statement "kamizestrant prolongs life." The former is well-supported by a randomized trial. The latter has not yet been proven.

This is why the FDA chose accelerated approval rather than full approval. The agency explicitly states that continued approval may be contingent on confirmation of clinical benefit in additional studies. [33]

Indicator	Current status
PFS	significantly improved
PFS2	statistically improved
Quality of life	worsened later
ctDNA	significantly decreased
Time to chemotherapy/ADC	increased
Overall survival	not yet proven
OS HR	0.87
95% CI	0.57-1.30
Supporting data required	Yes

Why the FDA advisory committee initially voted against it

On April 30, 2026, the FDA's Oncologic Drugs Advisory Committee discussed whether SERENA-6 demonstrated a clinically meaningful benefit from early switching to kamisestrant before radiological progression. The result was negative: 6 experts voted against and only 3 voted in favor. [34]

One of the main methodological criticisms was that SERENA-6 compared early switching with continuing an ineffective aromatase inhibitor after ESR1 progression, but did not directly compare current switching with continued switching after normal progression. Therefore, the study cannot fully answer the question of how important it is to intervene at the onset of a ctDNA mutation, rather than several months later. [35]

The second issue is the use of PFS, which is measured from the time of mutation detection. If treatment is started earlier, the patient automatically begins receiving the new therapy earlier, meaning that PFS2, quality of life, time to chemotherapy, and overall survival are particularly important for assessing the true clinical value. At the time of the meeting, some of this data was not yet mature enough. [36]

Following the meeting, the FDA requested additional data. AstraZeneca submitted an updated PFS2, ctDNA analysis, time to more intensive therapy, and additional long-term results. Ultimately, the agency reached a compromise: the drug received accelerated approval, which provides access to patients immediately but maintains the obligation to demonstrate real clinical benefit. [37]

What side effects were observed?

The overall adverse event profile was significantly associated not only with kamizestrant but also with ongoing CDK4/6 therapy. In the FDA data, the most common hematological events included neutropenia, anemia, and leukopenia. Neutropenia of any grade occurred in approximately 55% of patients on kamizestrant versus 45% in the control group; grade 3 or higher events occurred in 45% versus 34%. [38]

The most characteristic non-hematological side effect of the drug was photopsia—brief flashes of light in the visual field. It occurred in 20% of patients versus 7.7% in the control group. An expanded analysis revealed that approximately 90% of such episodes were grade 1; only one patient experienced grade 3 photopsia, and no patients discontinued treatment due to this visual phenomenon. [39]

Overall, visual symptoms of any kind were reported in 31.6% of patients compared to 16.1% of patients. These included photopsia, blurred vision, and, less commonly, visual disturbances, diplopia, and photophobia. The average time to the first visual effect with Kamizastrant was approximately eight days. However, in SERENA-6, these symptoms generally did not require specialized treatment or discontinuation of therapy. [40]

The FDA is also focusing on cardiac effects. The product information includes a boxed warning about the risk of arrhythmia associated with QTc prolongation when combining kamizenestrant with other drugs that prolong QTc. A separate warning is provided about bradycardia and potential harm to the fetus. In SERENA-6, bradycardia was reported in approximately 7.7% of patients taking kamizenestrant versus 0% in the control group. [41]

Main adverse events of SERENA-6

Adverse event	Camisestrant + CDK4/6	AI + CDK4/6
Neutropenia, all degrees	55%	45%
Neutropenia ≥3 degrees	45%	34%
Anemia	17%	17%
Leukopenia	17%	8%
Photopsia	20.0%	7.7%
Arthralgia	16%	17%
Fatigue	16%	14%
Dry eyes	12%	7%
Nausea	10%	14%
Bradycardia	7.7%	0%
Discontinuation due to AE, initial analysis	1.3%	1.9%

Who exactly is the new approval intended for?

Etcamah is not a new, generic "metastatic breast cancer" pill. The FDA has limited its indication to a rather narrow molecular situation: HR-positive, HER2-negative, locally advanced or metastatic breast cancer that is being treated with an aromatase inhibitor in combination with a CDK4/6 inhibitor and in which an ESR1 mutation emerges during this therapy. [42]

The patient must not have radiological progression at the time of treatment change. Therefore, the rationale for the drug lies in early resistance interception. If the disease has already clearly progressed, the clinical situation is different, and the choice of the next line of therapy is determined by other evidence and the molecular characteristics of the tumor.

Prescription requires detection of the ESR1 mutation using an FDA-approved test. Guardant360 CDx was approved concurrently with the drug. Therefore, practical implementation of this new strategy requires periodic molecular blood monitoring during the first line—a potentially significant change to the usual treatment regimen. [43]

Finally, kamizestant does not replace the CDK4/6 inhibitor. After a mutation is detected, the patient continues their previous abemaciclib, palbociclib, or ribociclib regimen, and only the aromatase inhibitor is replaced. This is an important detail that often gets lost in headlines about the "new pill."

Why this solution could change the approach to monitoring metastatic cancer

In most cases, systemic therapy for metastatic cancer is still changed after clinical or imaging evidence of progression. Molecular testing often helps select the next treatment after the previous regimen has officially stopped working.

SERENA-6 reverses this process. Blood testing becomes a kind of early warning system: the tumor hasn't yet grown in size on imaging, but its genome already reveals how it intends to evade treatment. The doctor responds to this evolution before a visible result appears.

If this approach proves to be long-term beneficial, cancer treatment can be envisioned as a continuously adapting system. A patient continues one regimen until a molecular resistance signal appears, then a specific component is switched, without waiting for a large-scale growth of a resistant clone.

But SERENA-6 also highlights the complexity of this approach. The earlier the intervention, the more difficult it is to prove that the patient has truly benefited, and not simply received the next drug sooner. Therefore, future ctDNA-guided trials will focus not only on PFS, but also on PFS2, overall survival, quality of life, toxicity, and time to more intensive treatment.

The approval is already in effect in Europe, but the American decision is particularly significant.

In Europe, Etcamah has also undergone regulatory review. The European Commission granted marketing authorization on July 20, 2026, for the combination of Etcamah with a CDK4/6 inhibitor in adults with ER-positive, HER2-negative advanced breast cancer after detection of an ESR1 mutation without first-line progression. [44]

The US decision is interesting because the FDA granted accelerated approval after a negative vote by its own advisory committee. Such committees make recommendations, but the final decision rests with the agency. After additional data became available, the FDA deemed the PFS a strong enough interim measure to allow access to the drug, subject to further confirmation of benefit. [45]

Thus, the difference between regulatory decisions reflects not so much a debate about whether kamizestrant works on the tumor—the antitumor effect is convincing—but rather the question of when exactly it is best to prescribe it and whether there is sufficient evidence to change therapy before visible progression.

As overall survival data and confirmatory study results mature, this debate will become significantly clearer. If the gains in PFS and PFS2 ultimately translate into longer-term quality of life and/or survival, SERENA-6 could become a model for a whole class of molecular resistance "hijacking" studies.

Major data limitations

The first limitation is the relatively small randomized group. Although ESR1 was routinely screened in over 3,200 patients, the required combination of a novel mutation and lack of progression allowed only 315 patients to be randomized. This was sufficient for primary PFS, but significantly more events and longer follow-up are required for overall survival. [46]

Second, the study does not directly address the question of whether early administration of kamizastrant is superior to administration of this or other effective endocrine therapy after radiological progression. This methodological issue was specifically highlighted by the FDA before the ODAC meeting. [47]

Third, the strategy requires regular ctDNA monitoring. The effectiveness and cost-effectiveness of mass testing every few months in different healthcare systems remains to be assessed. Not all patients consistently excrete sufficient amounts of ctDNA into their blood, and the sensitivity of liquid biopsy may depend on the tumor size and location.

Finally, there is no proven benefit in overall survival. For treatment initiated before the onset of symptoms or radiological progression, this issue is particularly important, as patients are exposed to the new drug and its side effects earlier. Therefore, accelerated approval should be viewed as an interim regulatory decision rather than a final point in the evidence base. [48]

What has already been proven	What else needs to be confirmed?
Kamizestrant is active against emerging ESR1 mutations	improved overall survival
PFS 16.0 vs 9.2 months	optimal switching moment
HR of progression/death 0.44	superiority of early switching over treatment after progression
PFS2 25.7 vs 19.1 months	long-term balance of risk and benefit
ctDNA is significantly reduced	the value of serial testing in general practice
quality of life deteriorates later	economic efficiency of the strategy
the toxicity profile is known	long-term security

What does approval mean for patients in practice?

The most immediate change is that the emergence of an ESR1 mutation now becomes a treatment event, not just a laboratory finding. Previously, a physician could detect such a mutation but continue monitoring the patient until progression was confirmed. Now, in the US, there is an approved option to immediately change the endocrine component of treatment.

However, this does not mean that all patients with HR-positive metastatic cancer should independently seek out any available ESR1 assay. The indication for use is closely related to the specific clinical situation, the type of current therapy, and the FDA-approved companion diagnostic. The decision should be made by an oncologist, taking into account the overall disease process.

The new strategy also doesn't replace conventional imaging. CT, MRI, and other methods are still necessary for assessing tumor burden and clinical response. ctDNA adds a new layer of information—molecular dynamics—that can anticipate anatomical changes.

It is the combination of these two types of monitoring that could be SERENA-6's greatest legacy: the imaging shows what the tumor is doing now, while the liquid biopsy potentially reveals how it is beginning to prepare for the next stage of resistance.

The main conclusion

The FDA approved Etcamah not simply because it offers another active drug against hormone receptor-positive breast cancer. It also approved a fundamentally new treatment strategy: regularly screening for emerging ESR1 mutations in the blood and altering endocrine therapy before radiological progression occurs. [49]

In SERENA-6, this approach increased median progression-free survival from 9.2 to 16.0 months and reduced the relative risk of progression or death by 56%. Longer follow-up confirmed a PFS of approximately 16.8 months and showed a benefit in PFS2 of 25.7 versus 19.1 months. [50]

Additional data appear biologically compelling: after eight weeks, ctDNA was reduced by a median of 99%, and complete disappearance of circulating tumor DNA was observed in approximately 51% of patients versus 1.9% in controls. Concurrently, deterioration in quality of life occurred later. [51]

But a crucial uncertainty remains. It has not yet been proven that early switching prolongs patient survival compared to changing therapy after normal progression. Therefore, the FDA has granted accelerated, conditional approval. If further studies confirm long-term benefit, Etcamah could become not only a new drug but also one of the first examples of oncology shifting from responding to an already growing tumor to actively intercepting its molecular evolution. [52]

News sources

The FDA approval was made on September 4, 2026. The official indication: camizestrant in combination with abemaciclib, palbociclib, or ribociclib in HR-positive, HER2-negative locally advanced or metastatic breast cancer after detection of an ESR1 mutation during therapy with an aromatase inhibitor and CDK4/6 inhibitor. The FDA concurrently approved Guardant360 CDx for patient selection. [53]

The primary peer-reviewed publication SERENA-6, on which the key evidence of efficacy is based:

Bidard FC., Mayer EL, Park YH, Janni W., Ma C., Cristofanilli M., Bianchini G., Kalinsky K., Iwata H., Chia S. et al. First-Line Camizestrant for Emerging ESR1-Mutated Advanced Breast Cancer. The New England Journal of Medicine. 2025;393:569-580. DOI: 10.1056/NEJMoa2502929.

This is the lead publication of a randomized phase III trial describing 315 randomized patients, PFS 16.0 vs 9.2 months, HR 0.44, and time to QOL deterioration 21.0 vs 6.4 months.

In 2026, an extended analysis of SERENA-6 with longer follow-up was published:

Turner NC, Mayer EL, Park YH, Janni W, Ma C, Cristofanilli M et al. Switching to camizestrant at ESR1 mutation emergence before disease progression during first-line treatment of hormone receptor-positive advanced breast cancer (SERENA-6): extended analysis of a double-blind, placebo-controlled, randomized, phase 3 trial. The Lancet Oncology. 2026;27(8):941-958. DOI: 10.1016/S1470-2045(26)00287-1.

In this update, at a median follow-up of 23.5 months, PFS was 16.8 vs 9.2 months, and subsequent data confirmed an increase in PFS2 to 25.7 vs 19.1 months.

The PFS2 supplemental analysis presented at ASCO 2026 has a separate congress abstract DOI: DOI: 10.1200/JCO.2026.44.17_suppl.LBA1007.

Thus, for the main link in the news, it is most correct to use DOI 10.1056/NEJMoa2502929 as the DOI of the pivotal phase III study on which the approval is based, and 10.1016/S1470-2045(26)00287-1 as the DOI of the current extended analysis of SERENA-6.