艾拉司群(Elacestrant hydrochloride) - 药物靶点：ERα_在研适应症：局部晚期乳腺癌，晚期乳腺癌，转移性乳腺癌_专利_临床

A Phase II Study of Elacestrant, an Oral Selective Estrogen Receptor Degrader (SERD) Combined With Everolimus in Patients With Recurrent or Metastatic ER-Positive (ER+) Endometrial Cancer (ELAVERA)

This phase II trial tests how well elacestrant with everolimus works for the treatment of estrogen receptor (ER) positive endometrial cancer that has come back after a period of improvement (recurrent), that may have spread from where it first started to nearby tissue, lymph nodes, or distant parts of the body (advanced) or that has spread from where it first started (primary site) to other places in the body (metastatic). Estrogen can cause the growth of cancer cells. Elacestrant lowers the amount of estrogen made by the body. This may help stop the growth of cancer cells that need estrogen to grow. Everolimus is in a class of medications called kinase inhibitors. It is also a type of angiogenesis inhibitor. Everolimus works by stopping cancer cells from reproducing and by decreasing blood supply to the cancer cells. Giving elacestrant with everolimus may be effective for treating patients with recurrent, advanced or metastatic ER positive endometrial cancer.

开始日期2026-12-18

申办/合作机构

Jonsson Comprehensive Cancer Center

[+1]

NCT07753954

/ Not yet recruiting临床2期IIT

Imaging to Re-evaluate Elacestrant Clinical Application

The goal of this clinical trial is to evaluate whether elacestrant, an oral selective oestrogen receptor degrader, can improve outcomes in patients with oestrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced or metastatic breast cancer without detectable ESR1 mutation after progression on endocrine therapy plus a CDK4/6 inhibitor.
The study aims to answer two key questions:
* Does [18F]-fluor-oestradiol positron emission tomography/computed tomography (18F-FES-PET/CT) result (homogeneous vs. heterogeneous) determine the efficacy of elacestrant in participants with advanced/metastatic ER-positive breast cancer and ESR1-mut-nd?
* Does 18F-FES-PET/CT imaging predict patient outcomes, including progression-free survival, overall survival, or tumor response?
There is no comparison group in this study. All participants receive elacestrant. Researchers will compare outcomes in people who have different levels of estrogen-receptor heterogeneity on FES-PET/CT imaging.
Participants in the study will:
* Take elacestrant 345 mg orally once a day, in 28-day treatment cycles (the dose may be lowered to 258 mg if needed due to side effects).
* Undergo 18F-FES-PET/CT and 18F-FDG-PET/CT imaging both at the beginning of the study and as part of routine clinical evaluation every 8 weeks
* Undergo blood sample collection every 8 weeks
* If selected for a sub-study, undergo an additional FES-PET/CT scan 4 weeks after starting treatment

开始日期2026-09-13

申办/合作机构

Jules Bordet Institute

[+2]

NCT07766018

/ Recruiting临床2期

A Phase 2 Open-Label, Single-Arm, Multicenter Trial to Evaluate the Efficacy and Safety of Elacestrant Monotherapy for the Treatment of Japanese Participants With ER+/HER2- Advanced or Metastatic Breast Cancer With ESR1-mutation Following CDK4/6 Inhibitor Therapy

This is a multicenter, open-label, Phase 2 bridging study to evaluate the efficacy and safety of elacestrant in Japanese post-menopausal women and men with estrogen receptor positive (ER+)/human epidermal growth factor receptor 2 negative (HER2-) advanced or metastatic breast cancer with estrogen receptor 1 gene mutation (ESR1-mut) whose disease has relapsed or progressed on at least 1 and no more than 2 prior lines of endocrine therapy for metastatic breast cancer, which must have included cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) therapy in combination with fulvestrant or an aromatase inhibitor.

开始日期2026-08-18

申办/合作机构

Stemline Therapeutics, Inc.

100 项与艾拉司群相关的临床结果

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100 项与艾拉司群相关的转化医学

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100 项与艾拉司群相关的专利（医药）

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115

项与艾拉司群相关的文献（医药）

2026-08-01·Advanced Healthcare Materials

A 3D‐Printed Vascular‐Like Perfusion Tumor‐on‐a‐Chip Recapitulates High‐Grade Breast Cancer With in Vivo‐Relevant Drug Resistance

Article

作者: Fang, Nicholas X. ; Lee, Geonhui ; Sun, Bingjie ; Xia, Chunguang

ABSTRACT:

Tumor progression and drug resistance in breast cancer are fundamentally governed by a complex microenvironment, characterized by extreme cell densities and associated nutrient/oxygen gradients. Conventional in vitro models often fail to replicate these features due to mass transport limitations in non‐perfused systems. Here, we present a next‐generation tumor‐on‐a‐chip platform engineered via high‐resolution projection micro‐stereolithography (PµSL) to sustain exceptionally high‐density breast cancer tissues (up to 400 million cells/mL) under continuous perfusion. By integrating a vascular‐inspired perfusion architecture with precision‐engineered micropores (∼7 µm), our system enhances nutrient and drug transport compared with traditional non‐perfused 3D cultures. This high‐density microenvironment drives density‐dependent molecular reprogramming of ERα, Ki67, and CTSL2, closely mirroring the gene expression signatures observed in high‐grade patient tumors. Notably, the drug resistance to Elacestrant observed in our high‐density tissues uniquely aligns with clinically reported Cmax concentrations, effectively bridging the gap between in vitro screening and in vivo outcomes. This platform provides a physiologically relevant tool for studying aggressive tumor biology and evaluating personalized therapeutic strategies with high predictive power.

2026-06-13·EXPERT OPINION ON PHARMACOTHERAPY

Oral selective estrogen receptor degraders (SERDs) for the treatment of hormone receptor-positive, HER2-negative breast cancer title

Review

作者: Ferraro, Emanuela ; Minchella, Ida ; Berton Giachetti, Pier Paolo Maria ; Valenza, Carmine ; Marra, Antonio ; Crimini, Edoardo ; Zagami, Paola ; Trapani, Dario ; Etessami, Julian David ; Curigliano, Giuseppe ; Belli, Carmen

INTRODUCTION:

Endocrine therapy (ET) remains the backbone of treatment for hormone receptor-positive (HR+), HER2-negative breast cancer. However, resistance, frequently driven by acquired ESR1 mutations detected in up to 40% of patients progressing on first-line ET, represents a major clinical challenge. Oral selective estrogen receptor degraders (SERDs) have been developed to overcome the limitations of first-generation agents and achieve more potent ER targeting.

AREAS COVERED:

This review summarizes the mechanism of action of oral SERDs compared with prior endocrine therapies and evaluates clinical evidence supporting their use across treatment settings in HR+/HER2- breast cancer. Literature was identified through systematic searches of PubMed, ClinicalTrials.gov, and major oncology congresses (ASCO, ESMO, SABCS) through early 2026.

EXPERT OPINION:

Oral SERDs are reshaping the management of ESR1-mutant disease, with agents such as elacestrant and imlunestrant emerging as standard second-line options. In early-stage disease, trials such as lidERA suggest potential outcome improvements. However, primary resistance to SERD monotherapy remains substantial, highlighting the need for combination strategies. Future directions include ctDNA-guided approaches and expansion into earlier treatment settings.

2026-06-03·Expert Review of Anticancer Therapy

Elacestrant in metastatic breast cancer: current advancements and future perspectives

Review

作者: Aksoy, Sercan ; Sahin, Taha Koray ; Rizzo, Alessandro ; Guven, Deniz Can ; Di Lauro, Vincenzo ; Makasheva, Binura

INTRODUCTION:

Hormone receptor-positive and HER2-negative advanced breast cancer is the most prevalent subtype and poses therapeutic challenges. While endocrine therapy remains the cornerstone of management, acquired resistance, particularly stemming from ESR1 mutations, limits long-term efficacy. Consequently, novel endocrine agents with enhanced potency, oral bioavailability, and favorable tolerability are crucial for overcoming resistance and improving patient outcomes.

AREAS COVERED:

This review provides a comprehensive evaluation of elacestrant, an orally active selective estrogen receptor degrader that has transformed the treatment paradigm for endocrine resistant disease. The pharmacologic properties, antitumor activity, and clinical outcomes associated with elacestrant are discussed in detail, along with ongoing research exploring its integration into combination regimens and in earlier disease settings.

EXPERT OPINION:

Elacestrant has become an important therapeutic option for patients with ESR1-mutated disease, offering durable estrogen receptor suppression and favorable tolerability. Combination therapies targeting CDK4/6 and PI3K-AKT-TOR signaling pathways represent promising directions for extending endocrine sensitivity. With the growing integration of liquid biopsy technologies and molecular monitoring into clinical practice, dynamic treatment adaptation guided by real time molecular profiling is expected to refine therapy selection. Elacestrant is a benchmark in the shift toward individualized endocrine therapy in metastatic breast cancer, bridging molecular precision with clinical practicality.

430

项与艾拉司群相关的新闻（医药）

2026-09-12

·搜狐新闻

Etcamah三期失败：乳腺癌新药研发的冷静一课

9月11日，全球医药界屏息等待的一刻来了——阿斯利康宣布，其备受期待的口服SERD药物Etcamah（camizestrant）联合CDK4/6抑制剂帕博西尼，在一线治疗ER阳性、HER2阴性晚期乳腺癌的SERENA-4三期临床试验中，未能达到预设的主要终点：无进展生存期（PFS）的改善未达统计学显著性。不是‘失败’，而是‘未达标’ 这个词很关键。医学界从不轻言‘失败’，尤其对一款已展现出生物学活性与初步信号的药物。数据显示，Etcamah组患者PFS确有数值提升——比如中位PFS延长了约2.3个月，但因置信区间跨越1、p值未小于0.05，无法排除随机波动干扰。这就像百米冲刺选手跑出9秒92，离世界纪录只差0.03秒，却仍被计时器判定为‘未破纪录’。科学的严苛，正在于此。 SERD为何被寄予厚望？传统内分泌治疗如他莫昔芬或芳香化酶抑制剂，本质是‘阻断’雌激素受体（ER）信号；而SERD（选择性雌激素受体降解剂）更进一步——它不只是堵门，还要拆掉整扇门。Etcamah通过诱导ER蛋白泛素化降解，从源头削弱癌细胞赖以生存的‘激素引擎’。尤其对携带ESR1突变（常见于经治复发患者）的肿瘤，SERD理论上更具优势。正因如此，它被视为内分泌治疗的‘下一代钥匙’。为什么联合帕博西尼？单打独斗难破僵局。ER通路与细胞周期调控通路（CDK4/6-Rb）本就交织成网。帕博西尼能将癌细胞‘锁’在G1期，而Etcamah则切断其生长指令——双管齐下，本意是制造‘协同致死’效应。但SERENA-4结果提示：理论闭环≠临床闭环。可能原因包括患者分层不够精准（如未按ESR1突变状态富集）、剂量组合未达最优，或肿瘤存在更复杂的代偿机制——比如激活FGFR或PI3K通路绕过双重封锁。安全性的‘定心丸’同样重要值得强调的是，试验未发现新的安全性信号。这意味着Etcamah的耐受性轮廓清晰可控，肝酶升高、疲劳等常见不良反应仍在预期范围内。在抗癌药研发中，一个‘安全但不够有效’的候选者，远比‘有效但毒性强’更有再开发价值——它可能通过优化联用方案、调整给药节奏，或转向特定生物标志物人群‘东山再起’。这不是终点，而是坐标校准回看近五年，SERD赛道可谓悲喜交加：辉瑞的elacestrant获批二线治疗（基于EMERALD研究），而阿斯利康的另一款SERDazacosterol曾折戟II期。每一次‘未达终点’，都在帮科学家擦去模糊滤镜，看清真正的敌人在哪里——是靶点本身？生物标志物选择？还是临床试验设计的颗粒度？SERENA-4的数据将完整公开，它不会消失于新闻稿末尾，而会成为全球研究者重新绘制‘内分泌抵抗地图’的重要坐标。抗癌之路从无坦途。所谓突破，往往诞生于一组未达显著性的数字之后——当数据拒绝被美化，科学才真正开始呼吸。返回搜狐，查看更多

临床2期临床3期临床失败临床终止

2026-09-12

·医药魔方ByDrug

乳腺癌精准治疗重磅突破！阿斯利康乳腺癌创新药camizestrant实现“伴随诊断+及时干预”治疗新范式

据某保险公司披露的真实案例，45岁的沈女士在乳腺癌内分泌靶向治疗后出现耐药，基因检测发现ESR1突变，改用口服SERD药elacestrant后病情受控。 Elacestrant属“影像进展后再换”的兜底方案，该药在国内并未获批，“明明有药可治却开不出来”，沈女士四处碰壁、倍感无力。但2026年9月4日FDA获批的camizestrant改写了这一治疗范式—— 一款“血里查出突变就能提前换”的口服药，正把无数人的耐药困局变成过去式。

2026-09-12

·搜狐新闻

Etcamah三期失败：乳腺癌新药研发的“悬崖时刻”

9月11日，全球医药圈传来一声轻响——不似重磅突破的礼炮，倒像实验室里一支试管悄然滑落。阿斯利康宣布：其口服选择性雌激素受体降解剂（SERD）Etcamah（camizestrant）联合CDK4/6抑制剂帕博西尼，在一线治疗ER+/HER2−晚期乳腺癌的SERENA-4三期临床试验中，未能达到主要终点——无进展生存期（PFS）改善未达统计学显著性。不是‘失败’，而是‘未达标’：科学语言里的温柔一刀媒体常把‘未达主要终点’简称为‘失败’，但医学研究从不轻易判死刑。PFS数值确有提升——比如中位PFS延长了2.1个月，或HR=0.87——这些数字背后是真实患者延缓疾病进展的努力。可统计学意义（通常p＜0.05）才是监管审批的硬门槛。它像一道精密校准的闸门：不是效果不存在，而是现有样本量、随访时长或患者异质性，让信号尚不足以穿透噪音。这恰是现代肿瘤药研最真实的切面：在分子迷宫中，每一步‘接近’都值得记录，每一次‘未达标’都在重绘靶点地图。 SERD赛道：从‘替代他莫昔芬’到‘挑战耐药堡垒’ Etcamah属于第二代SERD，目标直指内分泌治疗耐药这一临床顽疾。第一代SERD氟维司群需肌肉注射、半衰期短；而Etcamah作为口服小分子，本被寄予‘居家抗癌’厚望——每天一片，告别每月跑医院打针。更关键的是，它试图降解而非阻断雌激素受体（ER），理论上能瓦解那些靠‘伪装失活’逃逸治疗的突变型ERα（如Y537S、D538G）。SERENA-4虽折戟，但早前SERENA-2二期数据显示，单药Etcamah在经治患者中PFS达17.3个月，优于氟维司群。这说明：靶点没错，只是‘单兵突进’或‘组合策略’尚需再调校。联用逻辑的再思辨：帕博西尼+SERD，是强强联手还是错峰相撞？帕博西尼通过阻断细胞周期‘油门’起效，Etcamah则瞄准驱动肿瘤生长的‘方向盘’（ER）。理论协同无可挑剔。但临床现实更复杂：CDK4/6抑制剂可能诱导细胞进入静息期（G0），而静息态细胞对依赖增殖信号的内分泌药物敏感性下降——二者作用窗口或许存在‘时间差’。有学者笑言：‘一个喊停引擎，一个猛踩刹车，车没停稳，人先晕了。’下一步，调整给药顺序、引入生物标志物筛选（如ESR1突变状态）、或换用新一代CDK2/4/6抑制剂，都可能是破局钥匙。挫折之下，希望仍在呼吸阿斯利康明确表示：安全性良好，无新增风险信号。这意味着Etcamah的‘底盘’依然稳健——毒性可控，药代可行，口服便利性未打折扣。同期，其另一项SERENA-6试验（Etcamah联合芳香化酶抑制剂用于早期高危患者辅助治疗）仍在进行；而竞品Giredestrant、Elacestrant等SERD也在不同阶段冲刺。乳腺癌不是单一疾病，而是数十种分子亚型的集合体。今天的‘未达标’，恰为明天精准分层埋下伏笔：也许Etcamah终将属于ESR1突变阳性人群，或与免疫疗法擦出火花。科学从不许诺直线抵达。它更像一场集体校准：用千万次‘接近’，把人类对生命的理解，一毫米一毫米，推向更深的确定性。Etcamah的故事尚未终章——它只是翻到了‘讨论’章节，而真正的答案，永远藏在下一个试验设计里。返回搜狐，查看更多

临床3期临床失败临床终止临床2期临床结果

100 项与艾拉司群相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11672	艾拉司群	-	DB06374

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
局部晚期乳腺癌	澳大利亚	A. Menarini Australia Pty Ltd.	2026-04-01
晚期乳腺癌	英国	Stemline Therapeutics, Inc.	2024-01-05
转移性乳腺癌	英国	Stemline Therapeutics, Inc.	2024-01-05
ER阳性/HER2阴性/ESR1突变乳腺癌	美国	Stemline Therapeutics, Inc.	2023-01-27

未上市

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适应症	最高研发状态	国家/地区	公司	日期
乳腺癌	申请上市	美国	Radius Pharmaceuticals, Inc.	2022-06-22
HR阳性/HER2阴性乳腺癌	临床3期	德国	Berlin-Chemie/Menarini Pharma GmbH	2026-04-29
ER阳性乳腺癌	临床3期	美国	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	阿根廷	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	澳大利亚	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	奥地利	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	比利时	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	巴西	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	加拿大	Stemline Therapeutics, Inc.	2024-09-27
ER阳性乳腺癌	临床3期	捷克	Stemline Therapeutics, Inc.	2024-09-27

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT05563220 (ELEVATE, ASCO2026)	临床1/2期	ER阳性/HER2阴性乳腺癌二线 \| 一线 ER+/HER2−	31	CapivasertibElacestrant + CapivasertibElacestrantb	鹹簾願艱鏇醖簾鑰築淵(膚範積鹹廠醖襯糧獵鏇) = 蓋觸繭鑰獵鬱觸簾鏇獵夢醖遞繭鏇製衊膚窪製 (鹹餘廠蓋範選衊齋艱鹹 ) 更多	积极	2026-05-29
NCT06492616 (ELEGANT, ASCO2026 \| AACR2026)	临床3期	ER阳性/HER2阴性乳腺癌 ESR1m	4,220	Elacestrant	積憲壓廠餘遞醖積繭憲(衊遞糧襯網築繭簾繭鬱) = 襯範遞願廠願鹹構範獵選壓製範淵網憲憲憲顧 (觸壓選觸鬱廠鏇艱製糧 ) 更多	积极	2026-05-29
NCT06382948 (ADELA, ASCO2026 \| AACR2026)	临床3期	ER阳性/HER2阴性/ESR1突变乳腺癌 ESR1-mutated	240	Elacestrant + Everolimus	繭顧顧鑰鬱觸選範餘窪(淵醖觸鹽製壓網膚憲蓋) = There was one case (0.5%) of Grade 5 AEs (interruption of CDK4/6i due to increased creatine phosphokinase) with Elacestrant + Everolimus and one case (0.5%) (gastrointestinal bleeding) with Elacestrant + Placebo. 齋糧憲製鏇壓鹽願範蓋 (願製窪憲壓構製遞糧夢 ) 更多	积极	2026-05-29
NCT07222215 (CAPELA, ASCO2026)	临床2期	ER阳性乳腺癌 ER positive \| HER2 negative	297	Capecitabine + Elacestrant	壓醖鏇製窪醖簾艱範鏇(構糧顧鹽壓鏇醖艱獵襯) = 築構膚鑰範窪繭顧鏇壓製蓋廠齋廠壓齋憲壓鏇 (鬱遞獵繭鬱範觸簾醖醖 )	积极	2026-05-29
				Capecitabine	夢積構網醖膚鏇蓋醖積(願獵餘齋鹽觸積繭壓遞) = 壓顧夢築衊憲鑰遞艱蓋遞觸網範簾範蓋鹽夢積 (製衊鹹餘膚襯廠築繭遞 ) 更多
NCT07159451 (ESMO_BC2026)	临床2期	HR阳性/HER2阴性乳腺癌 HR+ \| HER2-	140	Elacestrant 345 mg	鏇觸淵淵襯夢齋鏇鑰壓(淵壓鹽餘壓鹽廠選衊築) = 築遞醖製糧憲鬱構壓鏇網壓鏇鹹鏇廠襯鏇蓋繭 (網顧衊獵壓選壓糧襯壓 ) 更多	积极	2026-05-07
				Leuprorelin 3.75 mgElacestrant 345 mg daily + Leuprorelin 3.75 mgElacestrant 345 mg daily (GnRH agonist therapy)	憲鬱襯鬱鏇憲衊觸築廠(觸艱鹽膚艱艱範鏇襯醖) = 淵衊簾網壓壓觸窪糧蓋窪觸窪艱餘鹽願鹽製鑰 (獵繭鑰獵襯糧窪鬱構醖 ) 更多
NCT05982093 (SOLTI-2104 PremiÈRe Part B, ESMO_BC2026)	临床2期	HR阳性/HER2阴性乳腺癌 HR positive \| HER2 negative	48	Elacestrant 345 mg	簾鏇繭艱獵衊齋構窪鏇(蓋窪醖鹹願夢蓋襯獵糧) = 廠艱選構艱憲鹽鏇鑰膚窪觸鏇願網憲鏇壓簾構 (壓願膚範繭糧膚顧觸繭 )	积极	2026-05-07
				Tamoxifen 20 mg	築鏇範鑰構窪獵網齋齋(衊範鬱顧觸構構鏇窪鏇) = 鏇蓋簾憲鏇衊壓鏇鏇製壓鏇齋襯範積糧膚觸繭 (顧築膚齋範鏇夢膚衊壓 ) 更多
AACR2026	临床2/3期	HR阳性/HER2阴性乳腺癌 HR Positive \| HER2 Negative	16	Imlunestrant alone	艱簾鏇齋網鑰淵艱餘願(壓廠鏇蓋選醖糧齋餘鏇) = 壓醖餘衊鑰憲醖構蓋鹹糧構憲鹽積選夢餘簾鹹 (選壓餘願獵齋範顧願選 ) 更多	积极	2026-04-21
				Camizestrant 75mg	艱簾鏇齋網鑰淵艱餘願(醖遞膚醖遞構廠鹽築顧) = 鏇簾夢構鬱鏇糧衊壓鹽廠糧構範艱願築憲蓋鹹 (築顧艱簾鬱衊艱淵製鑰 ) 更多
NCT06492616 (ELEGANT, SABCS2025)	临床3期	ER阳性/HER2阴性乳腺癌 ESR1-mut \| ER+ \| HER2-	4,220	Elacestrant	蓋願窪鏇膚餘憲範築觸(襯簾鏇鏇襯鹽壓鬱獵襯) = 齋觸顧積廠壓顧廠衊淵遞廠壓觸夢襯壓壓觸蓋 (衊壓築願願鬱鑰願獵構 )	积极	2025-12-11
NCT06382948 (ADELA, SABCS2025)	临床3期	ESR1-mutated \| ER+/HER2-	240	Elacestrant + Everolimus	鹹積餘簾衊襯壓築選鬱(餘齋壓襯廠構襯憲築構) = 艱範獵顧顧鏇衊範醖繭窪範壓積壓鬱鏇鹽憲窪 (範窪淵膚餘餘選壓膚範 )	积极	2025-12-10
				Elacestrant + Placebo	繭願齋獵衊膚鹹衊遞鹹(艱襯襯壓淵繭廠鬱衊醖) = 鏇製選製鹹壓簾鏇鬱鏇蓋鏇鏇獵構醖製鹹壓築 (選願壓蓋膚膚積襯膚襯 )
SABCS2025	N/A	HR阳性乳腺癌 PIK3CA \| ESR1	107	alpelisib+fulvestrant	網膚餘範壓鬱網觸憲鬱(繭製鹹觸壓遞淵醖窪窪) = One patient with alpelisib experienced treatment interruption and dose reduction due to skin toxicity, while Elacestrant was well-tolerated without major adverse effects. 蓋襯積築膚廠觸廠鑰蓋 (蓋構蓋遞衊選憲鑰醖願 )	积极	2025-12-10
				capivasertib+fulvestrant