A Phase 1 First-in-human Study of BMS-986500 as Monotherapy in Advanced Solid Tumors and as Combination Therapy in CDK4/6 Inhibitor Pre-treated Advanced Breast Cancer

The purpose of this study is to assess BMS-986500 as monotherapy in advanced solid tumors and as combination therapy in CDK4/6 inhibitor pre-treated advanced breast cancer.

开始日期2025-08-15

申办/合作机构

Bristol Myers Squibb Co.

NCT06982521

/ Recruiting临床3期

A Phase 3 Open-Label Randomized Study Assessing the Efficacy and Safety of RLY-2608 + Fulvestrant Versus Capivasertib + Fulvestrant as Treatment for PIK3CA-mutant Hormone Receptor Positive, Human Epidermal Growth Factor Receptor 2 Negative (HR+/HER2-) Locally Advanced or Metastatic Breast Cancer Following Recurrence or Progression On or After Treatment With a CDK4/6 Inhibitor

This is a global, multicenter, open-label, randomized Phase 3 study comparing the efficacy and safety of RLY-2608 + fulvestrant to capivasertib + fulvestrant for the treatment of patients with HR+/HER2- ABC with PIK3CA mutation following recurrence or progression on or after treatment with a CDK4/6 inhibitor.

开始日期2025-07-31

申办/合作机构

Relay Therapeutics, Inc.

NCT06979596

/ Not yet recruiting临床2期

A Multicenter, Open-label, Phase 2 Basket Study of MK-5684 in Participants With Selected Solid Tumors (OMAHA-015)

Researchers want to learn if MK-5684 (the study medicine) can treat breast cancer, ovarian cancer, and endometrial cancer. MK-5684, the study medicine, is designed to treat cancer by blocking the body from making steroid hormones.
Researchers will compare MK-5684 to the standard treatments for each cancer type in this study.
The goal of this study is to learn if people who receive MK-5684 live longer without the cancer growing or spreading compared to people who receive a standard treatment.

开始日期2025-07-17

申办/合作机构

Merck Sharp & Dohme LLC

100 项与氟维司群相关的临床结果

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100 项与氟维司群相关的转化医学

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100 项与氟维司群相关的专利（医药）

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6,686

项与氟维司群相关的文献（医药）

2025-12-01·MOLECULAR BIOLOGY REPORTS

Clinical aspect of male breast cancer: a burgeoning and unaddressed issue

Review

作者: Mukherjee, Sukhes ; Ray, Suman Kumar

Rare among male cancers, male breast cancer (MBC) accounts for less than one percent of all male tumors. The prevalence of this illness and female breast cancer (FBC) have both been on the rise in recent years. While reports have implicated hormonal, environmental, and genetic variables in the development of MBC, nothing is known about its aetiology. Radiation exposure, hormonal imbalances caused by other medical conditions, and, most significantly, a positive family history of breast cancer-which indicates a hereditary predisposition-are major risk factors. While low-penetrance gene mutations (such as CHEK-2) are more prevalent, they do not enhance the risk of breast cancer development to the same extent as rare mutations in high-penetrance genes (such as BRCA1 and BRCA2). Speculated risk factors, including BRCA2 and lifestyle changes in the last few decades, are considered in light of the reasons for the rising occurrence. Topics covered include aromatase inhibitors, fulvestrant, and the prolactin and androgen receptor targeting pathways, as well as the therapeutic therapy of male breast cancer. Invasive ductal carcinomas, which account for about 90% of breast cancers in men, express many hormone receptors and show clear signs of treatment benefit. No single therapy method has been supported by published evidence from prospective randomized trials in MBC to yet. The treatment decision should be guided by the primary prognostic markers, which include tumor size and the number of axillary nodes involved. Detailed descriptions of the clinicopathologic characteristics of MBC are included in the present review. Our focus is on molecular profiling of MBC as a means to discover potential biomarkers and potential pharmacologic intervention targets. Endocrine treatment, which includes tamoxifen, aromatase inhibitors, and GnRH analogues, as well as cytotoxic chemotherapy, are characterized in light of the existing research. We also outline the possible function of targeted medications such as HER2-directed treatments, PARP inhibitors, and angiogenesis inhibitors.

2025-10-01·BIOORGANIC & MEDICINAL CHEMISTRY

Structural evolution progress of orally bioavailable selective estrogen receptor degraders

Review

作者: Lei, Hongrui ; Zhang, Jiahe ; Zhai, Xin ; Zhao, Yingtong ; Sun, Yan ; Liu, Yibo ; Zhang, Jiachen

The alpha subtype of the estrogen receptor (ERα) plays a crucial role in breast cancer as a target for endocrine therapy. Fulvestrant, developed by AstraZeneca as the first selective estrogen receptor degraders (SERDs), effectively downregulates ER levels by reducing its stability, which leads to degradation through protein degradation mechanisms. However, the administration of Fulvestrant via the intramuscular route has imposed significant limitations on its clinical application, prompting the exploration of active oral bioavailable SERDs. Furthermore, research institutes and pharmaceutical companies have evaluated the efficacy of various oral SERDs in terms of their ability to degrade the ER, binding capacity, safety profiles, and numerous other indicators. This paper reviews recent advancements in oral SERDs, discusses their evolutionary relationships, and outlines the processes of structural modification, providing valuable insights for future research and applications.

2025-10-01·BREAST

BEBT-209, a primary CDK4 selective inhibitor, for the treatment of HR+/HER2- advanced breast cancer (BECTOP1): a phase 1, multicentre, open-label study

Article

作者: Wang, Ying ; Li, Wei ; Shi, Yehui ; Zhang, Fan ; Hu, Zhe-Yu ; Liu, Liping ; Yang, Xiaohong ; Ouyang, Quchang ; Liu, Binliang ; Xie, Ning ; Li, Jing ; Xiao, Huawu ; Wu, Biao ; Tian, Can ; Ding, Boni ; Wang, Shouman ; Jiang, Kegang

PURPOSE:

Several cyclin-dependent kinase 4/6 (CDK4/6) inhibitors have been approved for the treatment of hormone receptor-positive (HR+) and human epidermal growth factor receptor 2-negative (HER2-) advanced breast cancer. Despite the side effects that affect patients' quality of life, most patients still opt for CDK4/6 inhibitors due to their significant benefits. However, to further enhance treatment efficacy and safety, new approaches are still needed.

PATIENTS AND METHODS:

This multicentre, open-label, Phase 1 trial enrolled Chinese patients with HR+, HER2-advanced breast cancers. The primary endpoints were dose-limiting toxicity (DLT), maximum tolerated dose (MTD). Secondary endpoints included the objective response rate (ORR), clinical benefit rate (CBR), progression-free survival (PFS), and pharmacokinetic parameters.

RESULTS:

During the dose-escalation phase, a DLT was observed in the 150 mg bid dose cohort, specifically, 2 patients experienced grade 4 neutropenia. MTD of BEBT-209 was 100 mg bid, and the most common adverse event (AE) was neutropenia. In Phase 1b, the median PFS of patients with BEBT-209 alone, BEBT-209 plus letrozole, and BEBT-209 plus fulvestrant was 10.38 months, 24.94 months, and not reached, respectively. At doses of 25 mg qd-150 mg bid, steady state areas under the concentration-time curve and peak concentration increased proportionally with dose. The most common grade 3 or 4 AEs were neutropenia (65.4 %), lymphocytopenia (7.4 %), and anaemia (4.9 %).

CONCLUSION:

BEBT-209 was a primary CDK4 selective inhibitor and showed an acceptable safety profile and dose-dependent plasma exposure. The results highlight the potential of combination treatments as compelling options, particularly in combination with fulvestrant.

1,475

项与氟维司群相关的新闻（医药）

2025-07-30

·GlobeNewswire-Health Care

Celcuity Inc. Announces Pricing of Concurrent Public Offerings of 2.750% Convertible Senior Notes Due 2031 and Common Stock and Pre-Funded Warrants

MINNEAPOLIS, July 30, 2025 (GLOBE NEWSWIRE) -- Celcuity Inc. (Nasdaq: CELC) (the “Company”), a clinical-stage biotechnology company pursuing development of targeted therapies for oncology, today announced the pricing of its underwritten public offering of $175,000,000 aggregate principal amount of its 2.750% convertible senior notes due 2031 (the “Convertible Notes” and such offering, the “Convertible Notes Offering”), and its underwritten public offering of 1,836,842 of shares of its common stock (the “Common Stock”) at a public offering price of $38.00 per share and, in lieu of Common Stock to investors who so choose, pre-funded warrants to purchase up to 400,000 shares of Common Stock (the “Pre-Funded Warrants”) at a public offering price of $37.999 per Pre-Funded Warrant, which represents the per share public offering price of each share of Common Stock less the $0.001 per share exercise price of each Pre-Funded Warrant (such offering, the “Common Stock Offering”). The Company has granted the underwriters of the offerings a 30-day option to purchase up to an additional $26,250,000 aggregate principal amount of Convertible Notes, solely to cover over-allotments, if any, in the Convertible Notes Offering and a 30-day option to purchase up to an additional 335,526 shares of Common Stock at the public offering price less the underwriting discounts and commissions in the Common Stock Offering. The Convertible Notes will be general, unsecured, senior obligations of the Company. The Convertible Notes will accrue interest payable semiannually in arrears on February 1 and August 1 of each year, beginning on February 1, 2026, at a rate equal to 2.750% per year. The Convertible Notes will mature on August 1, 2031, unless earlier converted, redeemed or repurchased by the Company. At any time until the close of business on the scheduled trading day immediately before the maturity date, the Convertible Notes will be convertible at the option of the holders based on an initial conversion rate of 19.4932 shares of Common Stock per $1,000 principal amount of the Convertible Notes, which is equivalent to an initial conversion price of approximately $51.30 per share of Common Stock, representing a premium of approximately 35% above the public offering price per share of Common Stock in the Common Stock Offering. In connection with the closing of the Convertible Notes Offering, the Company will irrevocably elect to settle conversions, if any, of the Convertible Notes in shares of Common Stock together with cash in lieu of any fractional share, if applicable. The Convertible Notes Offering is expected to close on August 1, 2025, while the Common Stock Offering is expected to close on July 31, 2025, in each case, subject to satisfaction of customary closing conditions. The closing of neither the Convertible Notes Offering nor the Common Stock Offering is conditioned upon the closing of the other offering. The Company estimates that the net proceeds from the Convertible Notes Offering and the Common Stock Offering will be approximately $248.7 million, after deducting underwriting discounts and commissions and the Company’s estimated offering expenses. The Company intends to use the net proceeds from the offering for working capital and general corporate purposes, which may include clinical trial expenditures, commercial launch expenditures, research and development expenditures, capital expenditures, expansion of business development activities and other general corporate purposes. If the underwriters exercise their over-allotment option, the Company expects to use any additional proceeds from the offering for the purposes described in the preceding sentence. In connection with the pricing of the Convertible Notes Offering, the Company has determined that it will not enter into the capped call transactions with one or more of the underwriters or affiliates thereof and/or other financial institutions (the “option counterparties”) as initially contemplated and as disclosed in the preliminary prospectus supplement relating to the Convertible Notes Offering and the preliminary prospectus supplement relating to the Common Stock Offering. As a result of the Company’s determination not to enter into the capped call transactions, certain investors in the Convertible Notes that were expecting to hedge their equity price risk through certain derivative transactions with the option counterparties may instead hedge their equity price risk after the pricing of the Convertible Notes Offering by entering into derivative transactions with other parties or selling shares of Common Stock, which could adversely affect the market price of our Common Stock and the Convertible Notes. Jefferies, TD Cowen and Leerink Partners are acting as joint book-running managers for the Convertible Notes Offering and the Common Stock Offering. LifeSci Capital is acting as lead manager for the Convertible Notes Offering and passive bookrunner for the Common Stock Offering. ICR Capital LLC is acting as financial advisor to the Company in connection with the Convertible Notes Offering. The Company has filed a registration statement (including a prospectus) with the Securities and Exchange Commission (the “SEC”) as well as a preliminary prospectus supplement with respect to each of the offerings to which this communication relates. Before you invest, you should read the applicable preliminary prospectus supplement and the prospectus in that registration statement and other documents the Company has filed with the SEC for more complete information about the Company and these offerings. You may obtain these documents by visiting EDGAR on the SEC’s website at www.sec.gov. Alternatively, the Company, any underwriter or any dealer participating in the applicable offering will arrange to send you the applicable preliminary prospectus supplement (or, when available, the applicable final prospectus supplement) and the accompanying prospectus upon request to: Jefferies LLC, Attention: Equity Syndicate Prospectus Department, 520 Madison Avenue, New York, New York 10022, or by telephone at (877) 821-7388, or by email at Prospectus Department@Jefferies.com; TD Securities (USA) LLC, 1 Vanderbilt Avenue, New York, NY 10017, by telephone at (855) 495-9846 or by email at TD.ECM_Prospectus@tdsecurities; or Leerink Partners LLC, Attention: Syndicate Department, 53 State Street, 40th Floor, Boston, MA 02109, by telephone at (800) 808-7525, ext. 6105 or by email at syndicate@leerink.com. This press release does not constitute an offer to sell or a solicitation of an offer to buy the Convertible Notes, any shares of Common Stock issuable upon conversion of the Convertible Notes, the shares of Common Stock, the Pre-Funded Warrants, any shares of Common Stock issuable upon the exercise of the Pre-Funded Warrants or any other securities and shall not constitute an offer, solicitation or sale in any jurisdiction in which such an offer, solicitation or sale would be unlawful prior to the registration and qualification under the securities laws of such state or jurisdiction. ABOUT CELCUITY Celcuity is a clinical-stage biotechnology company pursuing development of targeted therapies for treatment of multiple solid tumor indications. The company’s lead therapeutic candidate is gedatolisib, a potent, pan-PI3K and mTORC1/2 inhibitor that comprehensively blockades the PI3K/AKT/mTOR (“PAM”) pathway. Its mechanism of action and pharmacokinetic properties are differentiated from other currently approved and investigational therapies that target PI3Kα, AKT, or mTORC1 alone or together. A Phase 3 clinical trial, VIKTORIA-1, evaluating gedatolisib in combination with fulvestrant with or without palbociclib in patients with HR+/HER2- advanced breast cancer is currently enrolling patients. A Phase 1/2 clinical trial, CELC-G-201, evaluating gedatolisib in combination with darolutamide in patients with metastatic castration resistant prostate cancer, is ongoing. A Phase 3 clinical trial, VIKTORIA-2, evaluating gedatolisib plus a CDK4/6 inhibitor and fulvestrant as first-line treatment for patients with HR+/HER2- advanced breast cancer is currently enrolling patients. Celcuity is headquartered in Minneapolis. FORWARD-LOOKING STATEMENTS This press release contains statements that constitute "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 including statements relating to the Convertible Notes Offering, the Common Stock Offering, our ability to complete such offerings on the anticipated timeline or at all and the anticipated use of the net proceeds therefrom, together with other statements that are not historical facts, are forward-looking statements that are estimates reflecting management’s best judgment based upon currently available information. Words such as, but not limited to, “look forward to,” “believe,” “expect,” “anticipate,” “estimate,” “intend,” "confidence," "encouraged," “potential,” “plan,” “targets,” “likely,” “may,” “will,” “would,” “should” and “could,” and similar expressions or words identify forward-looking statements. The forward-looking statements included in this press release are based on management’s current expectations and beliefs which are subject to a number of risks, uncertainties and factors, including our limited operating history; our potential inability to develop, validate and commercialize gedatolisib on a timely basis or at all; the uncertainties and costs associated with clinical studies and with developing and commercializing biopharmaceuticals; the complexity and difficulty of demonstrating the safety and sufficient magnitude of benefit to support regulatory approval of gedatolisib and other products we may develop; challenges we may face in developing and maintaining relationships with pharmaceutical company partners; the uncertainty and costs associated with clinical trials; the uncertainty regarding market acceptance by physicians, patients, third-party payors and others in the medical community, and with the size of market opportunities available to us; difficulties we may face in managing growth, such as hiring and retaining a qualified sales force and attracting and retaining key personnel; changes in government regulations; tightening credit markets and limitations on access to capital; stock market volatility or other factors that may affect our ability to access capital on favorable terms or at all; and obtaining and maintaining intellectual property protection for our technology and time and expense associated with defending third-party claims of intellectual property infringement, investigations or litigation threatened or initiated against us. In addition, all forward-looking statements are subject to other risks detailed in our Annual Report on Form 10-K for the year ended December 31, 2024, and in our Quarterly Report on Form 10-Q for the quarter ended March 31, 2025, as such risks may be updated in our subsequent filings with the Securities and Exchange Commission. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. All forward-looking statements are qualified in their entirety by these cautionary statements, and we undertake no obligation to revise or update this press release to reflect events or circumstances after the date hereof. CONTACTS: Celcuity Inc.Brian Sullivan, bsullivan@celcuity.comVicky Hahne, vhahne@celcuity.com(763) 392-0123 ICR HealthcarePatti Bank, patti.bank@icrhealthcare.com(415) 513-1284

临床3期

2025-07-30

·ioncology

乳腺癌精准治疗《Prof. Liao Ning's Insight 》廖宁教授专栏——精准治疗PAM通路第一期

点击蓝字，关注我们大家好我是广东省人民医院廖宁医生，欢迎大家来到《Liao ning’s Insight与宁同行，乳腺癌精准基因靶点GENEfield》专栏，今天我将为大家解读乳腺癌经典信号通路——PAM通路。PAM通路是指PI3K-AKT-mTOR信号通路，最先由美国科学家Lewis C. Cantley教授于 1988 年发现[1]。经过科学家们不断探索和研究，PAM通路的异常激活被证实在乳腺癌的发生、发展中起到了重要作用[2]。PAM 通路的信号转导，主要是由PIK3CA、AKT1、PTEN和mTOR基因编码的蛋白完成。PAM 信号通路的激活首先由胞外配体，与跨膜蛋白RTK结合或趋化因子与GPCR受体结合，从而激活PI3K蛋白，激活的PI3K催化PIP2磷酸化为PIP3，PIP3再招募AKT到细胞膜上，并进一步激活AKT。激活后的AKT作用于mTOR等下游底物，mTOR被激活后可增强原癌基因的转录，促进血管形成并影响代谢，促进肿瘤细胞的增殖与生存。PTEN是PAM通路的负调节因子，通过将PIP3去磷酸化，实现PI3K/PIP3信号传导的阻断，当 PIK3CA、PTEN、AKT1等关键驱动基因异常，PAM 通路调节机制失调会导致细胞异常增殖[3,4]。有研究显示，PAM信号通路的异常激活与早期乳腺癌的病理完全缓解率低[5]、复发风险高、总生存期短相关[6]，与晚期乳腺癌生存预后差相关[7]。此外，PAM信号通路的异常激活还与HR+/HER2-乳腺癌内分泌治疗耐药、CDK4/6抑制剂耐药相关[8]。根据广东省人民医院的数据，62.6%的乳腺癌患者存在至少一个PAM通路基因突变[9]。其中最常见的3个基因为PIK3CA发生率可达45%、PTEN发生率可达7.5%、AKT1发生率可达5.9%[9]。PIK3CA突变是PAM通路最常见的基因突变，在总体乳腺癌的发生率约为30%-40%[7]。相较高加索人，中国乳腺癌患者PIK3CA突变发生率更高，可达45.6%[10]。ER阳性和ER低表达转移性乳腺癌中，PIK3CA突变均是发生率最高的基因突变。而在ER阴性转移性乳腺癌中，PIK3CA突变发生率也可达13%[11]。PIK3CA突变与预后不良相关。一项纳入3219例HR+/HER2-转移性乳腺癌病例的回顾性分析显示，无论进行何种治疗方案，相较 PIK3CA未突变组，PIK3CA突变组患者中位PFS更短[7]。目前，乳腺癌治疗领域靶向PIK3CA的药物包括PI3K抑制剂伊那利塞、阿培利司，其中阿培利司尚未在国内获批。PTEN蛋白功能缺陷是导致 PAM 信号通路持续激活，从而使细胞持续增殖的因素之一。在TNBC 中，PTEN蛋白功能缺陷发生率可达67%，而在Luminal型乳腺癌中发生率为29%~44%，在HER2阳性乳腺癌中发生率可达22%[2]。由于PTEN蛋白功能缺陷，可能由基因突变、启动子甲基化异常、RNA 调控异常或翻译后修饰异常等多种原因导致[12]，PTEN基因突变和PTEN蛋白功能缺陷的发生率存在较大差异。一项纳入4895例乳腺癌组织样本的回顾性研究显示，PTEN蛋白功能缺失的发生率高达54.8%。其中7.0%的样本中，携带PTEN基因突变和/或51.4%的样本存在PTEN蛋白功能缺陷[13]。根据CAPItello-291研究的探索性分析结果，内分泌治疗后进展或复发HR+/HER2-晚期乳腺癌患者中，免疫组化检测的PTEN蛋白功能缺陷发生率达19%，而这些PTEN蛋白功能缺陷患者也可从卡匹色替联合氟维司群疗法中获益[14]。因而 PTEN蛋白功能缺陷，也可能是筛选优势患者的生物标志物之一。一项回顾性研究纳入了4111例 PTEN缺失或突变的乳腺癌患者，结果显示PTEN蛋白功能缺陷与乳腺癌预后更差有关[15]。AKT处于PAM通路的关键中心环节，可激活下游因子调控细胞周期。AKT1主要突变在各亚型乳腺癌中发生率相似，为2.6%~7.4%[2]。在中国乳腺癌患者中，AKT1的突变率约为 6.4%，尤其是Luminal A型乳腺癌患者的突变率可达12.1%[16]。目前靶向AKT抑制剂卡匹色替已被证实，可为内分泌治疗经治且存在PIK3CA/AKT1/PTEN任意突变的HR+/HER2-转移性乳腺癌带来PFS获益[17]。总的来说PAM 通路相关基因突变在乳腺癌中发生率高，且目前已有相关药物可以靶向这一信号通路，从而延缓肿瘤发展、转移的进程。相信随着基因检测的普及，越来越多的乳腺癌患者可以接受个性化、精准化治疗策略，从靶向PAM通路的治疗中获益。感谢收看，我们下期再见！廖宁教授广东省人民医院外科乳腺科行政主任，医学博士，教授，博士生导师国际肿瘤学预防和治疗学会（ISOPT）公共教育主任美国肿瘤外科学会（SSO）国际理事会理事国际前哨淋巴结学会（ISNS）国际理事会理事文章发表:Zhang W, Ning L (Corresponding author) et al. An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses. Nat Commun 2024; 15: 5470. (IF=16.6)Ning L (First author), Charles Balch et al. Accuracy and Reproducibility of ChatGPT Responses to 362 Breast Cancer Tumor Board Cases. JCO Clinical Cancer Informatics 2025.Ning L (First author & corresponding author), Li C, Cao L et al. Single-cell profile of tumor and immune cells in primary breast cancer, sentinel lymph node, and metastatic lymph node. Breast Cancer 2023; 30: 77-87 etc.Hello everyone, I am Dr. Liao Ning from Guangdong Provincial People's Hospital. Welcome to the "Liao Ning's Insight & Journey with Ning – Breast Cancer Precision Gene Target GENEfield" column,where today we'll delve into a pivotal signaling pathway in breast cancer: the PAM pathway.The PAM pathway refers to the PI3K-AKT-mTOR signaling pathway, first discovered by American scientist Prof. Lewis C. Cantley in 1988[1]. Through continuous exploration and research by scientists, the abnormal activation of the PAM pathway has been confirmed to play a crucial role in the initiation and progression of breast cancer[2].Signal transduction within the PAM pathway is primarily mediated by proteins encoded by the PIK3CA, AKT1 , PTEN , and mTOR genes. Activation of the PAM signaling pathway is initiated by the binding of extracellular ligands to transmembrane receptor tyrosine kinases or by the interaction of chemokines with G protein-coupled receptors, leading to the activation of PI3K protein. Activated PI3K catalyzes the phosphorylation of PIP2 to PIP3, which subsequently recruits AKT to the cell membrane, resulting in its further activation. Activated AKT then acts on downstream substrates, including mTOR. Upon activation, mTOR enhances oncogene transcription, promotes angiogenesis, and influences metabolism, thereby facilitating tumor cell proliferation and survival. PTEN functions as a negative regulator of the PAM pathway by dephosphorylating PIP3, thereby blocking PI3K/PIP3 signal transduction. Dysregulation of the PAM pathway's regulatory mechanisms, often due to abnormalities in key driver genes such as PIK3CA, PTEN, and AKT1, contributes to aberrant cellular proliferation [3,4].Studies have demonstrated that the dysregulation and subsequent hyperactivation of the PAM signaling pathway are associated with a diminished pathological complete response rate [5], elevated recurrence risk, and reduced overall survival in patients with early-stage breast cancer [6]. Moreover, this aberrant activation is correlated with an unfavorable survival prognosis in advanced breast cancer[7].Beyond these associations, the abnormal activation of the PAM pathway has also been implicated in mediating resistance to endocrine therapy and CDK4/6 inhibitors in individuals with HR+/HER2- breast cancer [8].Data from Guangdong Provincial People's Hospital indicate that 62.6% of breast cancer patients possess at least one mutation in a PAM pathway gene [9]. Among these, the three most common mutated genes are PIK3CA, with an incidence of up to 45%, PTEN, at up to 7.5%, and AKT1, at up to 5.9% [9].PIK3CA mutations represent the most prevalent genetic alteration within the PAM pathway, with an overall incidence of approximately 30-40% in breast cancer [7]. Notably, the incidence of PIK3CA mutations is higher in Chinese breast cancer patients compared to Caucasians, reaching up to 45.6% [10]. PIK3CA mutations are the most frequent genetic alterations observed in both ER-positive and ER-low-expressing metastatic breast cancer. Even in ER-negative metastatic breast cancer, the incidence of PIK3CA mutations can reach 13% [11]. PIK3CA mutations are associated with a poor prognosis. A retrospective analysis of 3219 cases of HR+/HER2- metastatic breast cancer revealed that patients with PIK3CA mutations had a shorter median progression-free survival compared to those without the mutation, regardless of the treatment regimen [7]. Currently, drugs targeting PIK3CA in breast cancer treatment include the PI3K inhibitors Inavolisib and alpelisib. Of these, alpelisib is not yet approved in China.PTEN protein dysfunction is a contributing factor to the sustained activation of the PAM signaling pathway, which in turn drives continuous cell proliferation. The incidence of PTEN protein dysfunction can reach up to 67% in Triple-Negative Breast Cancer, while it ranges from 29% to 44% in Luminal breast cancer and up to 22% in HER2-positive breast cancer [2].Since PTEN protein dysfunction can stem from various causes, including gene mutations, abnormal promoter methylation, aberrant RNA regulation, or post-translational modifications [12], there's a significant disparity between the incidence of PTEN gene mutations and PTEN protein dysfunction. A retrospective study of 4895 breast cancer tissue samples revealed that PTEN protein loss occurred in a high proportion of cases, reaching 54.8%. Within this group, 7.0% of samples carried PTEN gene mutations and/or 51.4% exhibited PTEN protein dysfunction [13].According to exploratory analysis results from the CAPItello-291 study, the incidence of PTEN protein dysfunction, as detected by immunohistochemistry, was 19% in HR+/HER2- advanced breast cancer patients who had progressed or relapsed after endocrine therapy. Patients with this PTEN protein dysfunction also benefited from capivasertib combined with fulvestrant therapy [14]. Consequently, PTEN protein dysfunction could serve as a biomarker for selecting patients who would most benefit from targeted therapies. A retrospective study involving 4111 breast cancer patients with PTEN deletion or mutation demonstrated that PTEN protein dysfunction was associated with a poorer breast cancer prognosis [15].AKT occupies a central, pivotal position within the PAM pathway, capable of activating downstream effectors and regulating the cell cycle. The incidence of AKT1 mutations is relatively consistent across various breast cancer subtypes, ranging from 2.6% to 7.4% [2]. In Chinese breast cancer patients, the AKT1 mutation rate is approximately 6.4%, with a notably higher incidence of up to 12.1% observed specifically in Luminal A subtype breast cancer patients [16]. Currently, the AKT inhibitor capivasertib has demonstrated progression-free survival benefits in HR+/HER2- metastatic breast cancer patients who have previously undergone endocrine therapy and harbor any PIK3CA, AKT1, or PTEN mutation [17].In summary, PAM pathway-related gene mutations are highly prevalent in breast cancer, and existing targeted therapies are capable of modulating this signaling pathway to impede tumor progression and metastasis. As genetic testing becomes more widespread, it is anticipated that an increasing number of breast cancer patients will receive personalized and precision treatment strategies, thereby benefiting from PAM pathway-targeted therapies.Thank you for watching, and we'll see you next time! See you!Prof. Ning LiaoAdministrative Director, Department of Breast Surgery, Guangdong Provincial People's Hospital; MD, Professor, Doctoral SupervisorDirector of Public Education, International Society of Oncology Prevention and Treatments (ISOPT)International Board Member, Society of Surgical Oncology (SSO), USAInternational Board Member, International Society of Sentinel Node (ISNS)Publications:Zhang W, Ning L (Corresponding author) et al. An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses. Nat Commun 2024; 15: 5470. (IF=16.6)Ning L (First author), Charles Balch et al. Accuracy and Reproducibility of ChatGPT Responses to 362 Breast Cancer Tumor Board Cases. JCO Clinical Cancer Informatics 2025.Ning L (First author & corresponding author), Li C, Cao L et al. Single-cell profile of tumor and immune cells in primary breast cancer, sentinel lymph node, and metastatic lymph node. Breast Cancer 2023; 30: 77-87 etc.参考文献：（滑动查看）[1] Whitman M, Downes CP, Keeler M, Keller T, Cantley L. Type I phosphatidylinositol kinase makes a novel inositol phospholipid, phosphatidylinositol-3-phosphate. Nature. 1988;332(6165):644-646. doi:10.1038/332644a0[2] Zhu, Kunrui et al. PI3K/AKT/mTOR-Targeted Therapy for Breast Cancer. Cells vol. 11,16 2508. 12 Aug. 2022, doi:10.3390/cells11162508[3] Rasti, Aryana R et al. PIK3CA Mutations Drive Therapeutic Resistance in Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer. JCO precision oncology vol. 6 (2022): e2100370.[4] Browne IM, André F, Chandarlapaty S, Carey LA, Turner NC. Optimal targeting of PI3K-AKT and mTOR in advanced oestrogen receptor-positive breast cancer. Lancet Oncol. 2024 Apr;25(4):e139-e151.[5] Jank P, Karn T, van Mackelenbergh M, et al. An analysis of PIK3CA hotspot mutations and response to neoadjuvant therapy in breast cancer patients from four prospective clinical trials. Clin Cancer Res. Published online June 5, 2024. doi:10.1158/1078-0432.CCR-24-0459[6] Zagami P, Fernandez-Martinez A, Rashid NU, et al. Association of PIK3CA Mutation With Pathologic Complete Response and Outcome by Hormone Receptor Status and Intrinsic Subtype in Early-Stage ERBB2/HER2-Positive Breast Cancer. JAMA Netw Open. 2023;6(12):e2348814. Published 2023 Dec 1. doi:10.1001/jamanetworkopen.2023.48814[7] 赵佳宁,刘月平. 乳腺癌PIK3CA突变的临床意义及其检测研究进展[J]. 临床与实验病理学杂志,2024,40(9):973-978. DOI:10.13315/j.cnki.cjcep.2024.09.014.[8] Schagerholm, C., Robertson, S., Toosi, H. et al. PIK3CA mutations in endocrine-resistant breast cancer. Sci Rep 14, 12542 (2024).[9] Weikai Xiao, et al. J Cancer. 2021 May 27;12(14):4408-4417. [10] Jia M,Liao N,Chen B,et al. PIK3CA somatic alterations in invasive breast cancers:different spectrum from Caucasians to Chinese detected by next generation sequencing[J].Breast Cancer,2021,28(3):644-652. [11] Chiara Corti, et al. Differential genomic landscape of estrogen receptor (ER)-low versus ER-positive (ER+) and ER-negative (ER-) metastatic breast cancer (MBC).2025 ASCO 1071.[12] Lee YR, Chen M, Pandolfi PP. The functions and regulation of the PTEN tumour suppressor: new modes and prospects. Nat Rev Mol Cell Biol. 2018 Sep;19(9):547-562. doi: 10.1038/s41580-018-0015-0. PMID: 29858604. [13] Khoury K, et al. Prevalence of Phosphatidylinositol-3-Kinase (PI3K) Pathway Alterations and Co-alteration of Other Molecular Markers in Breast Cancer. Front Oncol. 2020 Aug 31;10:1475.[14] Capivasertib–fulvestrant for patients with HRpositive/HER2-negative advanced breast cancer who had relapsed or progressed during or after aromatase inhibitor treatment: exploratory analysis of PTEN deficiency by IHC from the Phase III CAPItello-291 trial.2024 SABCS P2-03-19.[15] Wang T,et al. Loss of PTEN Expression, PIK3CA Mutations, and Breast Cancer Survival in the Nurses' Health Studies. Cancer Epidemiol Biomarkers Prev. 2022 Oct 4;31(10):1926-1934. [16] Jiang YZ, Ma D, Jin X, et al. Integrated multiomic profiling of breast cancer in the Chinese population reveals patient stratification and therapeutic vulnerabilities. Nat Cancer 2024;5(4):673-690.[17] Turner NC, Oliveira M, Howell SJ, et al. Capivasertib in Hormone Receptor-Positive Advanced Breast Cancer. N Engl J Med. 2023 Jun 1;388(22):2058-2070.（来源：良医汇肿瘤资讯）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

临床1期临床结果

2025-07-30

·米内网

集采注射剂已砍掉700亿！倍特、科伦、石药迎战第十一批，18个产品成下一轮目标？

精彩内容近日，备受瞩目的#第十一批集采药品名单出炉，再有23个化药注射剂入选，倍特药业、石家庄四药、科伦药业、正大制药、石药集团等国内巨头将全力迎战。米内网数据显示，前十批集采中标的158个化药注射剂2024年在中国公立医疗机构终端的合计销售规模比2018年缩水超过700亿元，集采大刀毫不留情。目前剔除了第十一批集采相关产品后（含拟纳入和过评数量达到条件未纳入的药品），还有18个注射剂已触及集采门槛，下一轮集采依然危机四伏。第十一批集采瞄准23个重磅注射剂，倍特、科伦、石药全力迎战7月15日，上海阳光医药采购网发布了《关于开展第十一批国家组织药品集中采购相关药品信息填报工作的通知》，拟纳入55个品种，其中注射剂占了23个，比例高达41.8%。7月28日，上海阳光医药采购网发布工作提示，信息填报系统将于7月31日16:00停止填报，本轮集采已是箭在弦上。表1：拟纳入第十一批集采的注射剂来源：米内网中国公立医疗机构终端竞争格局从亚类来看，血液代用品和灌注液占了4个，阻塞性气管疾病用药、心脏病治疗用药、全身用抗细菌药、肌肉松弛药各占了2个，治疗与胃酸分泌相关疾病的药物、止吐药和止恶心药、造影剂、胃肠解痉药及抗胆碱药和胃动力药、全身用皮质激素类、其它消化道和代谢用药、麻醉剂、抗肿瘤药、抗炎药和抗风湿药、抗分枝杆菌药、咳嗽和感冒用药11个亚类各占1个。从金额来看，5个注射剂品种2024年在中国城市公立医院、县级公立医院、城市社区中心及乡镇卫生院（简称中国公立医疗机构）终端的销售额超过10亿元，其中头孢唑肟注射剂高达42亿元、法莫替丁注射剂和溴己新注射剂均超过20亿元、苯唑西林注射剂和复方醋酸钠林格注射液/钠钾镁钙葡萄糖注射液也有超过16亿元以上的销售额。23个拟纳入第十一批集采的注射剂2024年在中国公立医疗机构终端的销售额合计超过187亿元。值得注意的是，拟纳入第十一批集采的注射剂中有22个是上市超过10年的老品种，仅注射用福沙匹坦双葡甲胺为2019年上市，该产品上市1年后（2020年）在中国公立医疗机构终端的销售额突破1亿元，2021年升上6亿元水平，进入2022版国家医保目录后销售额继续稳步增长，2022-2023年均达到8亿元水平，2024年涨至9.2亿元新高，2025年Q1再有5.29%的增长。该产品纳入第十一批集采后是断层下滑还是继续走高，静待市场给予验证。图1：涉及注射剂在6个及以上的集团（二级）来源：米内网中国上市药品（MID）数据库截至7月29日，23个拟纳入第十一批集采的注射剂涉及竞争集团（按二级集团统计，含原研+过评）已超过200家，#倍特药业和#石家庄四药均以9个产品迎战排在第一梯队，#科伦药业有8个产品，#天津医药、#福安药业各有7个产品，#正大制药、#石药控股、丽彩医药集团3家集团均有6个产品备战，而遂成药业、华夏生生药业(北京)2家集团也有5个产品迎战。大战即将拉开帷幕，谁将成为大赢家？我们拭目以待。市场缩水超700亿，29个超10亿注射剂陨落了化药注射剂一直是国家集采的常客，从4+7城市试点到第十批共有158个产品中标，相关产品2018年（集采执行前）在中国公立医疗机构终端的合计销售规模达1977亿元，而到了2024年则降至1264亿元，市场缩水超过了700亿元，集采大刀毫不留情。已中标的158个化药注射剂分布在35个亚类市场，其中全身用抗细菌药占了35个、抗肿瘤药占了15个、心脏病治疗用药占了11个。值得注意的是，拟纳入第十一批集采的异烟肼注射剂，将是抗分枝杆菌药市场首个纳入集采的注射剂，集采横扫的范围正在不断扩大。表2：前十批集采已中标的化药注射剂亚类情况来源：米内网中国上市药品（MID）数据库4+7城市(2018年12月)及联盟地区(2019年9月)中标的氟比洛芬酯注射液，2018年在中国公立医疗机构终端的销售额为23.8亿元，2019-2020年连续暴跌21.45%、60.70%，随后经历了回升、下滑又回升的状态，到了2024年销售额仅有9.9亿元。昔日超10亿注射剂经历了集采后陨落，有同样经历的产品还有28个。第四批(2021年2月)中标的注射用泮托拉唑钠、丙泊酚中/长链脂肪乳注射液、注射用硼替佐米、注射用帕瑞昔布钠，4个产品2021年在中国公立医疗机构终端的销售额分别为19.9亿元、13.6亿元、12.8亿元、12.7亿元，而到了2024年仅剩5.4亿元、6.9亿元、3.5亿元、2.8亿元。第五批(2021年6月)中标的多西他赛注射液和注射用艾司奥美拉唑钠，2个产品2021年销售额均超30亿元，2024年仅剩8.1亿元、9.5亿元；注射用盐酸吉西他滨和脂肪乳氨基酸(17)葡萄糖(11%)注射液，2个产品2021年销售额均超20亿元，2024年仅剩8.6亿元、9.9亿元；注射用兰索拉唑、紫杉醇注射液、利奈唑胺葡萄糖注射液、硫辛酸注射液、盐酸帕洛诺司琼注射液，5个产品2021年销售额均超10亿元，2024年仅剩1.5亿元、5.2亿元、5.0亿元、5.1亿元、1.6亿元。第七批(2022年7月)中标的注射用奥美拉唑钠和注射用替加环素，2个产品2022年销售额在20亿元级别，2024年仅剩9.4亿元、7.2亿元；注射用头孢米诺钠、碘帕醇注射液、唑来膦酸注射液、伊班膦酸钠注射液、罗库溴铵注射液，5个产品2022年销售额在10亿元级别，2024年仅剩5.7亿元、4.5亿元、5.0亿元、2.5亿元、5.5亿元。第八批(2023年4月)中标的注射用头孢西丁钠、注射用生长抑素、左卡尼汀注射液、丙氨酰谷氨酰胺注射液、酮咯酸氨丁三醇注射液，5个产品2023年销售额均在10亿元水平，2024年分别跌至9.3亿元、9.8亿元、9.6亿元、5.6亿元、2.7亿元。第九批(2023年11月)中标的盐酸乌拉地尔注射液、氟维司群注射液、地塞米松磷酸钠注射液，3个产品2023年销售额也在10亿元水平，2024年均降至8亿元左右。图2：集采后跃升为超10亿产品的注射剂（单位：万元）来源：米内网中国公立医疗机构终端竞争格局集采如流水，能覆舟也能载舟。第五批(2021年6月)中标的注射用阿奇霉素、左氧氟沙星氯化钠注射液和奥沙利铂注射液，3个产品2021年在销售额为9.4亿元、8.1亿元、4.4亿元，在集采助力下销售持续暴涨，2024年分别涨至11亿元、20亿元、13亿元级别。16个注射剂“躲过一劫”，这18个产品成下一轮目标？表3：过评数量达到条件未纳入第十一批集采的注射剂注：销售额低于1亿元用*表示来源：米内网中国公立医疗机构终端竞争格局7月15日发布的《关于开展第十一批国家组织药品集中采购相关药品信息填报工作的通知》中有一份“过评数量达到条件未纳入第十一批集采的药品”名单，其中注射剂占了16个。腹膜透析液注射剂、复方氨基酸注射剂、碘普罗胺注射剂、曲普瑞林注射剂、万古霉素注射剂、头孢他啶阿维巴坦注射剂、亚胺培南西司他丁注射剂7个超10亿重磅品种暂时躲过一劫。表4：目前竞争集团≥7家的化药注射剂注：销售额低于1亿元用*表示来源：米内网中国公立医疗机构终端竞争格局截至2025年7月29日，已有企业过评的化药注射剂中，剔除前十批集采已中标产品（158个）、拟纳入第十一批集采的注射剂（23个）、过评数量达到条件未纳入第十一批集采的注射剂（16个），目前竞争集团（按二级集团统计，含原研+过评）在7家及以上的化药注射剂还有18个，其中卡络磺钠注射液、维生素B6注射液、左氧氟沙星注射液已有超过10家竞争集团，达肝素钠注射液是超10亿产品。集采已成为医药行业年度重要事件，化药注射剂作为关键品种面临更大转型压力，但观察规则演变，每批次都有细节调整，体现出动态优化特征，经过锤炼的化药注射剂市场有望迎来高质量新格局。资料来源：米内网数据库、上海阳光医药采购网注：米内网《中国公立医疗机构终端竞争格局》，统计范围是：中国城市公立医院、县级公立医院、城市社区中心以及乡镇卫生院，不含民营医院、私人诊所、村卫生室；上述销售额以产品在终端的平均零售价计算。数据统计截至7月29日，欢迎指正！免责声明：本文仅作医药信息传播分享，并不构成投资或决策建议。本文为原创稿件，转载文章或引用数据请注明来源和作者，否则将追究侵权责任。投稿及报料请发邮件到872470254@qq.com稿件要求详询米内微信首页菜单栏商务及内容合作可联系QQ：412539092【分享、点赞、在看】点一点不失联哦

100 项与氟维司群相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D01161	氟维司群	L02BA03	DB00947

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
HR阳性乳腺腺癌	美国	AstraZeneca Pharmaceuticals LP	2017-08-25
乳腺癌	日本	AstraZeneca KK	2011-09-26
ER阳性乳腺癌	欧盟	AstraZeneca AB	2004-03-09
ER阳性乳腺癌	冰岛	AstraZeneca AB	2004-03-09
ER阳性乳腺癌	列支敦士登	AstraZeneca AB	2004-03-09
ER阳性乳腺癌	挪威	AstraZeneca AB	2004-03-09
HR阳性/HER2阴性乳腺癌	欧盟	AstraZeneca AB	2004-03-09
HR阳性/HER2阴性乳腺癌	冰岛	AstraZeneca AB	2004-03-09
HR阳性/HER2阴性乳腺癌	列支敦士登	AstraZeneca AB	2004-03-09
HR阳性/HER2阴性乳腺癌	挪威	AstraZeneca AB	2004-03-09
HR阳性乳腺癌	美国	AstraZeneca Pharmaceuticals LP	2002-04-25

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
HER2阳性乳腺癌	临床3期	奥地利	Novartis Pharmaceuticals Corp.	2021-09-14
HER2阳性乳腺癌	临床3期	法国	Novartis Pharmaceuticals Corp.	2021-09-14
HER2阳性乳腺癌	临床3期	意大利	Novartis Pharmaceuticals Corp.	2021-09-14
HER2阳性乳腺癌	临床3期	荷兰	Novartis Pharmaceuticals Corp.	2021-09-14
HER2阳性乳腺癌	临床3期	西班牙	Novartis Pharmaceuticals Corp.	2021-09-14
HER2阳性乳腺癌	临床3期	瑞士	Novartis Pharmaceuticals Corp.	2021-09-14
HER2 阴性乳腺癌	临床3期	意大利	Novartis Pharmaceuticals Corp.	2018-02-02
6型髓鞘减少脑白质营养不良	临床3期	意大利	Novartis Pharmaceuticals Corp.	2018-02-02
早期乳腺癌	临床3期	西班牙	AstraZeneca PLC	2007-11-01
孤立性纤维瘤	临床3期	加拿大	AstraZeneca PLC	2004-01-01

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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


NCT00253422 (SoFEA, CTgov)	临床3期	乳腺癌	698	fulvestrant+anastrozole (Faslodex + Placebo)	窪襯廠簾獵鑰壓繭淵獵(築膚廠鑰網顧鑰選遞遞) = 糧淵鏇淵夢鏇膚選構蓋夢範鑰齋範憲範範網衊 (糧壓夢顧鑰憲製鹽觸積, 顧廠繭網壓廠壓憲鹽構 ~ 繭簾蓋齋廠鏇獵膚願艱) 更多	-	2025-06-04
				fulvestrant+anastrozole (Faslodex + Arimidex)	窪襯廠簾獵鑰壓繭淵獵(築膚廠鑰網顧鑰選遞遞) = 壓獵艱願構廠獵願構鑰夢範鑰齋範憲範範網衊 (糧壓夢顧鑰憲製鹽觸積, 襯淵鬱鬱網範壓製範願 ~ 願廠鑰鬱醖願膚選膚蓋) 更多
ESMO_BC2025	N/A	HR+ \| HER2-negative	1,085	Fulvestrant	顧選齋艱鹹餘構糧淵鑰(築簾獵鑰壓壓蓋構簾醖) = 網製壓遞觸顧築窪簾願顧築憲壓鏇鏇艱衊願鬱 (積壓製築淵窪淵膚壓蓋 ) 更多	不佳	2025-05-14
NCT06408168 (REPLOT Trial, AACR2025)	临床2期	HR阳性/HER2阴性小叶癌 \| 乳腺浸润性小叶癌 E-cadherin \| ROS1	58	Repotrectinib	蓋糧壓築繭壓繭糧齋願(夢衊艱憲艱蓋淵襯範網) = <10% 鬱積夢憲鬱淵廠壓齋蓋 (願蓋齋選廠鹹觸築夢鏇 ) 更多	积极	2025-04-29
NCT06757634 (VIKTORIA-2, AACR2025)	临床3期	HR阳性/HER2阴性乳腺癌一线 PIK3CA	-	Gedatolisib + CDK4/6 inhibitor + Fulvestrant	構製壓淵齋憲觸積淵醖(蓋構膚範窪艱糧蓋構鬱) = expected mPFS is 25 to 28 months 鏇鑰構範獵憲顧遞窪鏇 (夢網顧膚鑰壓襯網顧艱 ) 更多	积极	2025-04-29
NCT05169567 (postMONARCH, CTgov)	临床3期	HR阳性/HER2阴性乳腺癌	368	Fulvestrant+abemaciclib (Arm A: Abemaciclib Plus Fulvestrant)	願遞膚觸築齋淵蓋築襯(遞壓簾糧餘壓觸醖鹹構) = 選願膚餘願憲觸網鹹鹽鑰構憲獵膚蓋範積顧醖 (壓鏇窪獵簾獵廠醖膚鹹, 積壓簾觸鑰廠淵積衊選 ~ 選淵鹽築鹹衊襯積遞糧) 更多	-	2025-02-27
				Placebo+Fulvestrant (Arm B: Placebo Plus Fulvestrant)	願遞膚觸築齋淵蓋築襯(遞壓簾糧餘壓觸醖鹹構) = 糧膚夢鏇簾壓壓鏇廠壓鑰構憲獵膚蓋範積顧醖 (壓鏇窪獵簾獵廠醖膚鹹, 積築願壓窪餘願鬱憲願 ~ 齋鬱淵選選製鹹餘夢膚) 更多
NCT04256941 (CTgov)	临床2期	转移性乳腺癌	4	Fulvestrant (Fulvestrant)	積顧鏇願衊廠糧鬱觸顧(夢選齋醖糧繭蓋衊膚繭) = 襯構襯鹹積觸艱餘夢網網糧鹽壓窪網壓衊衊鏇 (壓築廠遞選鏇繭淵選鏇, 襯範窪廠鑰齋鏇壓蓋範 ~ 觸觸顧蓋衊製築簾顧積) 更多	-	2024-12-27
				fulvestrant+ribociclib (Kisqali)+abemaciclib (verzenio)+palbociclib (Ibrance) (Continuing AI After Randomization)	積顧鏇願衊廠糧鬱觸顧(夢選齋醖糧繭蓋衊膚繭) = 齋廠鏇醖繭齋廠築蓋窪網糧鹽壓窪網壓衊衊鏇 (壓築廠遞選鏇繭淵選鏇, 齋願蓋艱餘齋願構鹽構 ~ 積積鹽遞餘範淵艱壓獵) 更多
NCT02491983 (PARSIFAL, CTgov)	临床2期	转移性HER2阴性乳腺癌 \| ER阳性/HER2阴性乳腺癌 \| 转移性乳腺癌	486	Letrozole+palbociclib (Arm A)	觸構觸鹽遞淵網醖繭遞 = 遞窪鏇廠壓窪積鑰鬱夢觸鹽製壓遞繭餘網淵襯 (觸鏇廠簾顧鏇積鹽鑰觸, 鑰積糧遞餘簾糧簾淵淵 ~ 衊鹽鏇衊襯夢鹽築遞選) 更多	-	2024-12-09
				Fulvestrant+palbociclib (Arm B)	觸構觸鹽遞淵網醖繭遞 = 網鬱艱觸築築積齋壓淵觸鹽製壓遞繭餘網淵襯 (觸鏇廠簾顧鏇積鹽鑰觸, 築積願網觸鏇齋選鏇艱 ~ 壓衊鑰觸鹽願願衊蓋繭) 更多
NCT04305496 (CAPItello-291, Pubmed \| J Clin Oncol)	临床3期	PIK3CA突变/HR阳性/HER2阴性乳腺癌 PIK3CA \| AKT1 \| PTEN	708	Capivasertib 400 mg twice daily with fulvestrant	鹹夢顧顧網糧鑰齋範醖(憲製構積壓壓鏇簾蓋襯): HR = 0.6 (95% CI, 0.51 ~ 0.71) 更多	积极	2024-12-01
				Placebo with fulvestrant
NCT02860000 (TBCRC041, CTgov)	临床2期	局部晚期乳腺癌 \| 转移性乳腺癌 \| 激素难治性乳腺癌 ... 更多	96	Laboratory Biomarker Analysis+Alisertib (Arm I (Alisertib))	襯鑰壓蓋構夢壓醖構醖(蓋選壓觸膚顧獵鏇鬱艱) = 願夢遞鏇夢鏇襯膚糧築膚艱壓夢艱願壓願壓遞 (遞構淵築醖廠蓋顧齋夢, 構選齋築壓簾蓋醖憲構 ~ 顧鏇艱窪網鹽築膚鏇網) 更多	-	2024-10-18
				Laboratory Biomarker Analysis+Alisertib+fulvestrant (Arm II (Alisertib, Fulvestrant))	襯鑰壓蓋構夢壓醖構醖(蓋選壓觸膚顧獵鏇鬱艱) = 網艱襯築鹹壓築觸範簾膚艱壓夢艱願壓願壓遞 (遞構淵築醖廠蓋顧齋夢, 築憲遞鹽糧選夢夢簾選 ~ 壓淵願夢憲網築憲淵願) 更多