A PHASE 1, OPEN-LABEL, FIXED SEQUENCE, 2-PERIOD, SINGLE-DOSE, CROSS-OVER STUDY TO ESTIMATE THE ABSOLUTE BIOAVAILABILITY OF VEPDEGESTRANT (ARV-471, PF-07850327) FOLLOWING ORAL AND INTRAVENOUS DOSING OF THE DRUG TO HEALTHY PARTICIPANTS

The purpose of this study is to learn how much of the study medicine called Vepdegestrant will reach the bloodstream when given orally compared to given intravenously.
This study is seeking participants who:
* are healthy males and healthy females who cannot have children.
* are 18 years or older.
* are healthy as decided by medical tests.
* have a body mass index (BMI) of 16 to 32 kilogram per meter squared.
* have a total body weight of more than 45 kilograms (99 pounds).
In Period 1, all participants will receive one dose of Vepdegestrant by IV. In Period 2, all participants will receive one dose of Vepdegestrant by mouth following a high-fat breakfast. The levels of Vepdegestrant in Period 1 will be compared to the levels of Vepdegestrant in Period 2 and the bioavailablility of the oral formulation of Vepdegestrant will be determined.
The study duration is 22 days and includes two periods. Participants will stay in the clinical research unit for 9 days (8 nights) during each period. A follow-up visit for each participant takes place at 28 to 35 days after taking the study medicine for the last time.

开始日期2025-04-03

申办/合作机构

Pfizer Inc.

[+1]

CTR20242782

/ Active, not recruiting临床2期

一项在 18 岁及以上 ER+/HER2- 晚期或转移性乳腺癌研究参与者中评估口服蛋白水解靶向嵌合体 Vepdegestrant（ARV-471/PF-07850327）联合 PF-07220060 治疗的耐受性、PK 和抗肿瘤活性的开放标签、干预性的安全有效性 Ib/II 期研究

II期主要目的：1. 评估 Vepdegestrant 联合 PF-07220060 治疗的临床抗肿瘤活性。II期次要目的：1. 确定 Vepdegestrant 联合 PF-07220060 治疗的其他抗肿瘤活性结局。2. 进一步评价 Vepdegestrant 与 PF-07220060 联合用药的总体安全性特征和耐受性。3. 评价 Vepdegestrant 与 PF-07220060 联合给药时，Vepdegestrant、ARV-473 和 PF-07220060 的血浆药物暴露量。4. 评估治疗后血浆 ctDNA 相对于基线水平的变化。II期探索性目的：1. 探索 PF-07220060 联合 Vepdegestrant 治疗对患者报告的症状和健康相关生命质量的影响。2. 了解乳腺癌的肿瘤生物学，确定潜在的敏感性和/或耐药性机制。3. 评价分子定义的研究参与者人群中突变状态与应答之间的关系。4. 探索药物基因组学对 PF-07220060 血浆药物暴露量的影响。

开始日期2024-11-18

申办/合作机构

Pfizer Inc.

[+2]

NCT06645938

/ Completed临床1期

A PHASE I, RANDOMIZED, OPEN-LABEL, 2-PERIOD, 2-TREATMENT, 2-SEQUENCE, CROSSOVER, SINGLE-DOSE STUDY IN HEALTHY ADULT PARTICIPANTS TO ESTIMATE THE BIOAVAILABILITY OF AN VARIANT (HIGH HARDNESS) TABLET OF VEPDEGESTRANT (ARV-471, PF-07850327) RELATIVE TO THE REGISTRATIONAL TABLET

The purpose of the study is to compare the amount vepdegestrant available from two different tablet formulations under fed conditions in healthy adult participants; 200 mg vepdegestrant alternative tablet formulation compared to 200 mg vepdegestrant standard tablet formulation.
This study is seeking male or female participants of non-childbearing potential age who:
* are 18 years or older
* are healthy as decided by medical tests.
* have a Body mass index (BMI) of 16 to 32 kilogram per meter squared; and a total body weight of more than 45 kilograms (99 pounds).
All participants will be put into groups to receive one of the 2 treatments in each period. This study will consist of 2 treatment sequences:
* Sequence 1: Single 200 mg dose of vepdegestrant registrational tablet in Period 1, followed by a single 200 mg dose of vepdegestrant variant tablet in Period 2.
* Sequence 2: Single 200 mg dose of vepdegestrant variant tablet in Period 1, followed by a single 200 mg dose of vepdegestrant registrational tablet in Period 2.
Participants will be in the study for about 11 weeks.

开始日期2024-10-16

申办/合作机构

Pfizer Inc.

[+1]

100 项与 Vepdegestrant 相关的临床结果

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100 项与 Vepdegestrant 相关的转化医学

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100 项与 Vepdegestrant 相关的专利（医药）

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项与 Vepdegestrant 相关的文献（医药）

2025-06-01·EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS

A comprehensive mechanistic investigation of factors affecting intestinal absorption and bioavailability of two PROTACs in rats

Article

作者: Dahlgren, David ; Koziolek, Mirko ; Borchardt, Thomas ; Arendt, Nathalie ; Sjöblom, Markus ; Indulkar, Anura ; Hedeland, Mikael ; Niessen, Janis ; Dubbelboer, Ilse R ; Lennernäs, Hans

AIM:

Proteolysis targeting chimeras (PROTACs) exhibit a unique and promising pharmacology. However, this comes with molecular properties exceeding the 'drug-like' rule of five chemical space, which often limits gastrointestinal absorption. This in vivo study aimed to investigate the contribution of luminal and plasma stability, intestinal effective permeability, P-glycoprotein (P-gp) efflux, and bile excretion, on the rat intestinal absorption and systemic exposure of two PROTACs, ARV-110 (812 Da, LogD_7.4 4.8) and ARV-471 (724 Da, LogD_7.4 4.6).

METHODS:

Luminal stability and effective intestinal permeability were determined directly from luminal disappearance using single-pass intestinal perfusion, with and without a protease inhibitor, or a P-gp/Cytochrome P450 CYP3A inhibitor (ketoconazole) in rats. Plasma stability was tested by in vitro incubations. Intestinal absorption, systemic exposure, and biliary excretion were examined after intraduodenal and intravenous dosing with ketoconazole or the P-gp selective inhibitor (encequidar).

RESULTS AND DISCUSSION:

Both PROTACs were degraded in the intestinal lumen and in plasma by peptidases. The intestinal effective permeability in rats was moderate for ARV-110 (0.62 × 10^-4 cm/s) and low for ARV-471 (0.23 × 10^-4 cm/s). P-gp inhibition increased the permeability 1.6- and 2.3-fold for ARV-110 and ARV-471, respectively. After intraduodenal dosing with the P-gp inhibitors a corresponding increase in systemic exposure was observed for both PROTACs. There was only a minor difference in the increased systemic exposure induced by the two inhibitors, suggesting that the mechanisms were primarily P-gp inhibition, rather than gut-wall and hepatic extraction. Biliary excretion was a minor pathway and did not affect the absorption and systemic exposure of the PROTACs to a large extent.

CONCLUSION:

In the rat, ARV-110 and ARV-471 were enzymatically degraded in the intestinal lumen and in plasma, and their intestinal permeability and systemic exposure seem to be reduced due to P-gp efflux.

2025-05-31·NEW ENGLAND JOURNAL OF MEDICINE

Vepdegestrant, a PROTAC Estrogen Receptor Degrader, in Advanced Breast Cancer.

Article

作者: Hu, Xichun ; Parameswaran, Janaki ; Mouret-Reynier, Marie-Ange ; Lu, Dongrui R ; Jerzak, Katarzyna J ; Hamilton, Erika P ; Patsouris, Anne ; Zhi, Xin ; Valota, Olga ; Cui, Jiuwei ; Guarneri, Valentina ; Sezer, Ahmet ; De Laurentiis, Michelino ; Jhaveri, Komal ; Fontana, Andrea ; Yoshinami, Tetsuhiro ; Zamagni, Claudio ; Cil, Timucin ; Martignoni, Marcella ; Molckovsky, Andrea ; Ladoire, Sylvain ; Rodriguez-Lescure, Alvaro ; Zhang, Yongqiang ; Fuentes, Christian ; Demirci, Umut ; Campone, Mario ; Cazzaniga, Marina

BACKGROUND:

Vepdegestrant is an oral proteolysis-targeting chimera (PROTAC) estrogen receptor (ER) degrader that directly harnesses the ubiquitin-proteasome system.

METHODS:

In this phase 3, open-label, randomized trial, we enrolled patients with ER-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer who had received one previous line of cyclin-dependent kinase 4 and 6 inhibitor therapy plus one line of endocrine therapy (and up to one additional line of endocrine therapy). Patients were randomly assigned in a 1:1 ratio to receive vepdegestrant at a dose of 200 mg orally once every day of each 28-day cycle or fulvestrant at a dose of 500 mg, administered intramuscularly, on day 1 and day 15 of cycle 1 and on day 1 of subsequent cycles, with randomization stratified according to ESR1-mutation status and presence or absence of visceral disease. The primary end point was progression-free survival as assessed by blinded independent central review among the patients with ESR1 mutations and among all the patients who underwent randomization. Progression-free survival was estimated with Kaplan-Meier methods and hazard ratios with a stratified Cox proportional-hazards model.

RESULTS:

A total of 624 patients underwent randomization; 313 were assigned to receive vepdegestrant, and 311 to receive fulvestrant. Among the 270 patients with ESR1 mutations, the median progression-free survival was 5.0 months (95% confidence interval [CI], 3.7 to 7.4) with vepdegestrant and 2.1 months (95% CI, 1.9 to 3.5) with fulvestrant (hazard ratio, 0.58 [95% CI, 0.43 to 0.78]; P<0.001). Among all the patients, the median progression-free survival was 3.8 months (95% CI, 3.7 to 5.3) with vepdegestrant and 3.6 months (95% CI, 2.6 to 4.0) with fulvestrant (hazard ratio, 0.83 [95% CI, 0.69 to 1.01]; P = 0.07). Adverse events of grade 3 or higher occurred in 23.4% of the patients in the vepdegestrant group and in 17.6% of the patients in the fulvestrant group. Adverse events led to treatment discontinuation in 2.9% and 0.7% of the patients, respectively.

CONCLUSIONS:

Among patients with ER-positive, HER2-negative advanced breast cancer, vepdegestrant was associated with significantly longer progression-free survival than fulvestrant in the subgroup with ESR1 mutations but not in the full patient population. (Funded by Pfizer and Arvinas Estrogen Receptor; VERITAC-2 ClinicalTrials.gov number, NCT05654623.).

2025-05-03·EXPERT OPINION ON PHARMACOTHERAPY

Vepdegestrant for the treatment of HR+/HER2– breast cancer

Review

作者: Mukohara, Toru

INTRODUCTION:

The treatment of advanced hormone receptor-positive (HR+) and human epidermal growth factor receptor 2-negative (HER2-) breast cancer has been improved through the development of endocrine therapy (ET) and targeted agents. However, resistance to ET, particularly caused by ESR1 mutations, has not been fully addressed.

AREAS COVERED:

Vepdegestrant is a first-in-class, selective, and orally bioavailable PROteolysis TArgeting Chimera (PROTAC) estrogen receptor (ER) degrader. Preclinical studies have suggested promising activity of vepdegestrant irrespective of ESR1 genotypes. Phase I and II clinical studies have revealed a favorable safety profile and encouraging efficacy of vepdegestrant as a single agent and in combination with other targeted agents.

EXPERT OPINION:

The results of the phase III VERITAC-2 study, comparing vepdegestrant with fulvestrant, are expected to be available in 2025, and will provide the first data on the true clinical significance of vepdegestrant. Several phase III studies of combinations with vepdegestrant including + atirimociclib (a cyclin-dependent kinase 4 inhibitor) have been or are planned to be conducted. The results of these may not only transform the treatment landscape for advanced HR+/HER2- breast cancer but may pave the way for PROTAC as a new class of anti-cancer drugs that may make previously undruggable targets druggable.

285

项与 Vepdegestrant 相关的新闻（医药）

2025-06-11

·GlobeNewswire-Health Care

Arvinas to Present Preclinical Data for PROTAC BCL6 Degrader, ARV-393, at the 2025 European Hematology Association (EHA) Annual Meeting

– Company to showcase preclinical studies of ARV-393, an investigational oral PROTAC BCL6 degrader, as a single agent in models of nodal T-follicular helper cell lymphoma, angioimmunoblastic-type (AITL) and transformed follicular lymphoma, and in combination with small molecule inhibitors in models of diffuse large B-cell lymphoma – June 05, 2025 -- Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company working to develop a new class of drugs based on targeted protein degradation, today announced that new preclinical data for ARV-393 will be presented at the European Hematology Association (EHA) meeting, June 12-15, 2025 in Milan, Italy. ARV-393 is Arvinas’ investigational orally bioavailable PROteolysis TArgeting Chimera (PROTAC) degrader targeting the B-cell lymphoma 6 protein (BCL6), a transcriptional repressor and major driver of B-cell lymphomas. Poster Title: ARV-393, a PROteolysis TArgeting Chimera (PROTAC) BCL6 Degrader, is Efficacious in Preclinical Models of Diffuse Large B-Cell Lymphoma, Nodal T-Follicular Helper Cell Lymphoma, and Transformed Follicular Lymphoma Abstract: PF1000 Session Title: Lymphoma biology & translational research Date: Thursday, June 13, 2025 Time: 6:30-7:30 p.m. CEST ARV-393 is an investigational orally bioavailable PROteolysis TArgeting Chimera (PROTAC) designed to degrade B-cell lymphoma 6 protein (BCL6), a transcriptional repressor and major driver of B-cell lymphomas. The BCL6 protein facilitates B cell tolerance of rapid proliferation and somatic gene recombination via repressing cell cycle checkpoints, terminal differentiation, apoptosis, and the DNA damage response. PROTAC-mediated degradation has the potential to address the traditional undruggable nature of BCL6. ARV-393 is currently being evaluated in a Phase 1 clinical trial in patients with relapsed/refractory non-Hodgkin lymphoma. Arvinas (Nasdaq: ARVN) is a clinical-stage biotechnology company dedicated to improving the lives of patients suffering from debilitating and life-threatening diseases. Through its PROTAC protein degrader platform, Arvinas is pioneering the development of protein degradation therapies designed to harness the body’s natural protein disposal system to selectively and efficiently degrade and remove disease-causing proteins. Arvinas is currently progressing multiple investigational drugs through clinical development programs, including vepdegestrant, targeting the estrogen receptor for patients with locally advanced or metastatic ER+/HER2- breast cancer; ARV-393, targeting BCL6 for relapsed/refractory non-Hodgkin Lymphoma; and ARV-102, targeting LRRK2 for neurodegenerative disorders. Arvinas is headquartered in New Haven, Connecticut. The content above comes from the network. if any infringement, please contact us to modify.

蛋白降解靶向嵌合体

2025-06-10

·药智网

历经24年，这类药物「全球首款」上市在即

经过24年科学探索，PROTAC技术终于迈出从实验室到商业化的关键一步。近日，Arvinas与辉瑞共同宣布，已向美国FDA提交了Vepdegestrant（ARV-471）的新药上市申请，用于治疗携带ESR1突变的ER+/HER2-晚期或转移性乳腺癌患者。这是全球首个申报上市的PROTAC药物，标志着靶向蛋白降解技术从概念验证走向临床应用的重大突破。全球首款蓄势待发蛋白降解靶向嵌合体（PROTAC）技术代表了一种革命性的药物开发范式。与传统药物抑制靶蛋白功能不同，PROTAC分子通过双头结构设计，一端结合目标蛋白，另一端招募E3泛素连接酶，将目标蛋白和E3泛素连接酶拉近，形成稳定的三元复合物，从而促使靶蛋白发生泛素化修饰并最终被蛋白酶体降解。图1 PROTAC作用机制图片来源：参考资料[2]Vepdegestrant是一种基于PROTAC技术研发的潜在“first-in-class”口服选择性雌激素受体降解剂，可通过激活细胞内泛素-蛋白酶体系统直接介导野生型和突变型ER蛋白降解。它已经获得美国FDA授予的突破性疗法认定，用于治疗经治ER阳性、HER2阴性乳腺癌。图2 ARV-471对野生型和突变型ER均具有较高降解效率图片来源：参考资料[3]在临床前研究中，vepdegestrant对MCF7、T47D等ER依赖性乳腺癌细胞系表现出高效降解能力，72小时内可诱导≥90%的ER降解，半数降解浓度（DC50）低至0.9 nmol/L，最大降解率（Dmax）达95%。此次vepdegestrant上市申请基于关键III期VERITAC-2研究的积极结果。试验共纳入了624例既往接受过CDK4/6抑制剂和内分泌治疗的ER+/HER2-晚期乳腺癌患者。研究发现：在全人群中，Vepdegestrant组中位无进展生存期（PFS）为3.7个月，与氟维司群组的3.6个月相比未达统计学显著性差异。图3 全人群中Vepdegestrant组中位无进展生存期图片来源：参考资料[4]但在携带ESR1突变的亚组中，Vepdegestrant展现出突破性疗效：患者中位PFS达5.0个月，显著优于氟维司群组的2.1个月，疾病进展或死亡风险降低43%。次要终点同样令人鼓舞：Vepdegestrant组的临床获益率（CBR）达42.1%，显著高于氟维司群组的20.2%；客观缓解率（ORR）分别为18.6%vs.4.0%。总生存期（OS）数据尚未成熟（20%成熟度），有待进一步随访评估。图4 Vepdegestrant组的临床获益率及客观缓解率图片来源：参考资料[4]安全性方面，Vepdegestrant表现出可控的安全性特征：两组3级及以上不良事件发生率分别为23.4%vs.17.6%，最常见不良事件为疲劳（26.6%vs.15.6%）、ALT水平升高（14.4%vs 9.8%）和恶心（13.5%vs.8.8%）。因TEAE导致停药的比例较低（2.9%vs.0.7%）。24年潜心耕耘Vepdegestrant的申报是PROTAC技术商业化的里程碑事件。这项颠覆性技术历经24年潜心耕耘，终迎爆发临界点。2001年，耶鲁大学Craig Crews教授设计了首个由磷酸肽片段和与蛋白靶相互作用的小分子片段组成双功能分子PROTAC-1；图5 PROTAC-1的作用机制图片来源：参考资料[5]2003年，PROTAC被应用于靶向降解ER和AR受体；2004年，随着E3连接酶小分子配体的突破，PROTAC进入小分子化阶段；2008年，Crews教授团队开发出首款双功能小分子药物并将其命名为“PROTAC”，“PROTAC”命名由此而来。这是PROTAC发展的早期阶段，从最初的肽类PROTAC到小分子化，解决了PROTAC成药性的分子量过大和细胞渗透性问题，是PROTAC技术从概念走向潜在药物的基石。图6 首款双功能小分子药物PROTAC图片来源：参考资料[6]2013年，Crews联合创办Arvinas公司，加速技术转化；2015年，首个基于VHL和CRBN的PROTAC出现，PROTAC迈入纳摩尔级降解活性时代；同年，C4Therapeutics成立，聚焦蛋白质降解剂研发领域。这一时期，则是PROTAC技术发展的技术进步阶段，标志着靶向蛋白降解（TPD）领域开始形成产业生态。2019年，全球首个PROTAC药物ARV-110进入临床试验，开启临床转化纪元；2020年，赛诺菲与KymeraTherapeutics达成合作协议，共同开发蛋白降解管线KT-474；2021年，辉瑞以高达24亿美元的总交易额获得Vepdegestrant的全球权益；2024年，Arvinas继续扩大商业版图，以1.5亿美元预付款加10.1亿美元潜在付款将第二代雄激素受体降解剂ARV-766授权给诺华。这一期间，TPD领域蓬勃发展，从临床转化阶段逐渐过渡至全球合作阶段。不仅如此，资本市场对靶向蛋白降解（TPD）领域也热情高涨。2022年全球靶向蛋白降解（TPD）市场规模达1138亿美元，据MarketDigits预测，2030年全球靶向蛋白降解（TPD）市场规模将飙升至2475亿美元，年复合增长率高达10%。风险资本敏锐捕捉这一趋势，五年内投入从2017年的3300万美元飙升至2022年的7.07亿美元，增长超过2000%；2024年第一季度更延续高热，单季融资超2.77亿美元，较2023年同期增长15倍以上。谁将引领风骚？随着PROTAC技术的发展，全球医药行业正上演着一场竞逐大戏。国际舞台上，以Nurix、Arvinas、Kymera、C4T四大技术先驱为核心的Biotech军团已构筑起显著的技术壁垒与差异化优势。在其推动下，疗法管线从初代雄激素受体靶向药物ARV-110不断裂变，衍生出ARV-471、NX2127、KT-474等众多明星候选药物，展现出靶点拓展与适应症覆盖的巨大潜能。与此同时，拜耳、罗氏、赛诺菲、辉瑞、诺华等跨国巨头纷纷携重资入局，其战略合作不仅为PROTAC技术注入了强劲的研发动能与资源支持，更标志着整个领域正从艰难证明成药性的探索期，迈向检验市场价值的商业化验证新阶段。此外，中国力量亦在此浪潮中强势崛起。据不完全统计，国内已有超过30家公司投身PROTAC研发领域。海思科、百济神州、开拓药业、睿跃生物等领跑者，凭借相关项目的快速推进进入临床开发阶段，已然构成国内PROTAC领域的第一方阵。表1 全球处于临床II期及以上阶段的PROTAC数据来源：药智数据、公开资料整理整体来看，当前已有超过200款PROTAC新药处于研发阶段，33款已步入临床，占比16.3%。其中，Arvinas的ARV-471作为唯一处于新药上市申请阶段的产品，肩负着验证PROTAC市场价值的重任。临床II期阵营中，8款产品正蓄势待发，从Kymera与赛诺菲联手推进的免疫炎症药物KT-474，到开拓药业全球首创外用的雄激素受体降解剂GT20029，再到Arvinas/诺华合作的重磅KRAS G12D降解剂ASP-3082，无不代表着各自领域突破性进展的前沿方向。值得注意的是，KT-474在完成I期后，其针对化脓性汗腺炎和特应性皮炎的II期研究正被赛诺菲加速扩大；GT20029在中国II期临床试验中成功达到主要终点；而ASP-3082作为全球首个进入临床的KRAS G12D降解剂，其精准靶向特性已在临床前研究中展现卓越潜力。结语随着首款PROTAC分子申报上市，未来十年，靶向蛋白降解领域或将迎来爆发式增长。参考资料[1]https://ir.arvinas.com/news-releases/news-release-details/arvinas-announces-submission-new-drug-application-us-fda[2]Garber,Ken.“How protein-slayer drugs could beat some of the cruellest cancers.”Nature vol.641,8062(2025):300-302.[3]Smith,J.,&Doe,A.(2024).Preclinical and Clinical Evaluation of Vepdegestrant(ARV-471)in ER+Breast Cancer.Clinical Cancer Research,30(5),1234-1245.[4]https://www-nejm-org.libproxy1.nus.edu.sg/doi/full/10.1056/NEJMoa2505725[5]Sakamoto,K M et al.“Protacs:chimeric molecules that target proteins to the Skp1-Cullin-F box complex for ubiquitination and degradation.”Proceedings of the National Academy of Sciences of the United States of America vol.98,15(2001):8554-9.[6]Schneekloth,Ashley R et al.“Targeted intracellular protein degradation induced by a small molecule:En route to chemical proteomics.”Bioorganic&medicinal chemistry letters vol.18,22(2008):5904-8.声明：本内容仅用作医药行业信息传播，为作者独立观点，不代表药智网立场。如需转载，请务必注明文章作者和来源。对本文有异议或投诉，请联系maxuelian@yaozh.com。责任编辑 | 史蒂文合作、投稿、转载开白 | 马老师 18323856316（同微信）阅读原文，是受欢迎的文章哦

临床结果蛋白降解靶向嵌合体突破性疗法临床3期

2025-06-10

·癌度

《癌度早报2025年6月10日》

癌度临床试验病友交流群（点击）一、新药快讯1、双免疫疗法为黑色素瘤脑转移患者带来希望，脑肿瘤控制率63%在2025年美国临床肿瘤学年会上，一项早期临床试验结果表明，将LAG-3抗体药物瑞拉利单抗，与PD-1抑制剂纳武利尤单抗联合，治疗晚期脑转移的黑色素瘤患者，63%的患者用药后脑肿瘤得以控制，18.5%的患者脑病灶大幅度缩小，达到了部分缓解，3.7%的患者脑病灶完全消失，达到了完全缓解。用药后平均3.2个月脑病灶发生变化，对于几乎无药可用的患者来说，这两款药物的联合治疗效果可谓惊艳。2、明星PROTAC药物申报上市，用于治疗乳腺癌近日，全球首款PROTAC药物在美国申报上市，这是一款名为Vepdegestrant的药物，用于治疗既往接受过内分泌治疗且携带ESR1突变，激素受体阳性HER2阴性乳腺癌，基于一项三期临床试验结果，这款药对比氟维司群具有显著的无进展生存期改善，该药的中位无进展生存期是5个月，而氟维司群的中位无进展生存期仅为2.1个月，该药将疾病或死亡风险降低了43%。3、新型抗体偶联药MRG003治疗鼻咽癌，亮相ASCO大会2025年美国临床肿瘤学会年会上，中山大学肿瘤防治中心韩非教授发布口头报告，介绍抗体偶联药MRG003治疗复发转移性鼻咽癌的疗效，173名患者入组用药，治疗组治疗应答率为30.2%，而对照组治疗应答率仅为11.5%，治疗组的中位无进展生存期为5.8个月，对照组仅为2.8个月，死亡风险降低了37%。该药将中位总生存期延长了5个月，具有明显的生存获益。二、抗癌前沿1、PD-1的K药皮下注射版本在中国申报上市2025年6月7日，CDE官网显示，PD-1抑制剂帕博利珠单抗皮下注射剂型上市申请获得受理，这是首款在国内申报上市的皮下注射PD-1抗体，2024年11月，关键性三期临床试验证实皮下注射剂型疗效，不劣于静脉输注剂型。皮下注射剂型为每6周注射一次，中位注射时间为2分钟，每次注射4.8毫升。皮下注射可以让患者在门诊用药治疗，而非在医院里住院静脉输注。欢迎关注癌度，肿瘤用药基因检测，临床试验免费用药欢迎联系癌度咨询!

免疫疗法临床3期ASCO会议临床结果蛋白降解靶向嵌合体

100 项与 Vepdegestrant 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
ER阳性/HER2阴性/ESR1突变乳腺癌	申请上市	美国	Arvinas, Inc.	2025-06-06
ER阳性/HER2阴性乳腺癌	临床3期	美国	Arvinas Estrogen Receptor, Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	美国	Pfizer Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	中国	Arvinas Estrogen Receptor, Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	中国	Pfizer Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	日本	Arvinas Estrogen Receptor, Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	日本	Pfizer Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	阿根廷	Pfizer Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	阿根廷	Arvinas Estrogen Receptor, Inc.	2023-03-03
ER阳性/HER2阴性乳腺癌	临床3期	澳大利亚	Arvinas Estrogen Receptor, Inc.	2023-03-03

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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


NCT05654623 (VERITAC-2, ASCO2025 \| Company_Website) 人工标引	临床3期	ER阳性/HER2阴性乳腺癌 ER Positive \| HER2 Negative	624	Vepdegestrant	願遞選窪憲範繭壓鏇醖(鬱獵鑰簾鹹窪膚窪膚願) = 範壓選積網構觸鏇膚艱顧窪廠蓋淵窪顧繭構獵 (選窪憲淵選醖觸鹹醖壓, 3.6–5.3) 更多	积极	2025-05-30
				fulvestrant	願遞選窪憲範繭壓鏇醖(鬱獵鑰簾鹹窪膚窪膚願) = 鏇廠構繭窪積艱憲簾膚顧窪廠蓋淵窪顧繭構獵 (選窪憲淵選醖觸鹹醖壓, 2.2–3.8) 更多
NCT05654623 (VERITAC-2, Company_Website) 人工标引	临床3期	ER阳性/HER2阴性乳腺癌 ESR1 Mutation	-	Vepdegestrant (ESR1 mutant)	齋構憲膚製衊窪鏇窪鑰(膚簾製淵廠艱夢蓋鬱憲) = The results exceeded the pre-specified target hazard ratio of 0.60 in the ESR1m population. The trial did not reach statistical significance in improvement in PFS in the intent-to-treat (ITT) population. 範夢蓋襯醖積鹽餘築蓋 (蓋壓鬱構觸糧艱獵齋繭 )	不佳	2025-03-11
				fulvestrant (ESR1 mutant)
NCT05548127 (TACTIVE-U, GlobeNewswire) 人工标引	临床1期	ER阳性/HER2阴性乳腺癌三线	16	Vepdegestrant + Abemaciclib	淵繭獵襯廠遞鏇範願製(憲衊襯鹽築選鬱顧積醖) = None 膚網壓獵顧鬱鬱醖鑰夢 (窪範範壓廠憲簾壓鬱窪 ) 更多	积极	2024-12-10
				Vepdegestrant + Abemaciclib (mutant ESR1)
NCT05463952 (Pubmed \| Int J Clin Oncol)	临床1期	局部晚期不能切除的乳腺癌 \| 乳腺癌 \| ER阳性乳腺癌 ... estrogen receptor (ER) 更多	6	Vepdegestrant 200 mg QD	網積網網衊襯遞齋鏇衊(窪製構襯網襯膚鑰廠窪) = Four (66.7%) patients experienced adverse events; none led to dose reduction or discontinuation 鬱齋選範網繭獵獵築壓 (淵鹹糧製獵蓋憲獵遞鹽 ) 更多	-	2024-11-20
NCT05463952 (CTgov)	临床1期	局部晚期不能切除的乳腺癌 \| 乳腺癌 \| ER阳性乳腺癌 ... 更多	6	ARV-471	繭積鹽夢壓網製衊觸遞 = 繭鹹繭繭觸獵壓積繭窪壓遞鏇艱遞餘廠顧範窪 (廠網鑰觸願壓鹽糧艱壓, 窪醖鑰製觸憲遞鏇淵顧 ~ 積壓窪淵壓醖衊襯鑰鬱) 更多	-	2024-09-23
NCT05538312 (CTgov)	临床1期	-	12	ARV-471 (Period 1: ARV-471 200 mg)	鹹醖顧簾廠築艱衊廠顧(襯齋夢遞鏇廠窪蓋鬱蓋) = 鹹遞膚觸壓範蓋鏇襯齋願築觸廠範蓋蓋壓選窪 (壓鏇顧窪顧鏇顧鬱繭餘, 23) 更多	-	2024-09-23
				Itraconazole+ARV-471 (Period 2: ARV-471 200 mg + Itraconazole 200 mg)	鹹醖顧簾廠築艱衊廠顧(襯齋夢遞鏇廠窪蓋鬱蓋) = 衊廠鏇築壓簾構獵膚膚願築觸廠範蓋蓋壓選窪 (壓鏇顧窪顧鏇顧鬱繭餘, 24) 更多
NCT05673889 (CTgov)	临床1期	-	24	Dabigatran (Period 1: Dabigatran 75 mg)	積範鏇獵遞壓願艱淵鹹(鬱網網製膚蓋壓顧遞醖) = 鏇壓顧網淵遞壓衊築繭製鏇鹽醖憲衊積築選鏇 (鑰範獵製艱廠製繭獵壓, 94) 更多	-	2024-08-16
				ARV-471+Dabigatran (Period 2: Dabigatran 75 mg + ARV-471 200 mg)	積範鏇獵遞壓願艱淵鹹(鬱網網製膚蓋壓顧遞醖) = 鏇選窪襯網簾網醖觸遞製鏇鹽醖憲衊積築選鏇 (鑰範獵製艱廠製繭獵壓, 66) 更多
NCT05652660 (CTgov)	临床1期	-	12	Rosuvastatin (Period 1: Rosuvastatin)	壓淵積網製鹹獵鏇選鬱(窪膚遞顧積鹹獵繭觸鑰) = 鹽廠鹽鑰齋鏇繭夢選願餘選鹹構網範蓋餘憲膚 (鹽鏇糧餘觸選廠顧積築, 53) 更多	-	2024-07-26
				Rosuvastatin+ARV-471 (Period 2: ARV-471 + Rosuvastatin)	壓淵積網製鹹獵鏇選鬱(窪膚遞顧積鹹獵繭觸鑰) = 製獵觸糧網餘顧鑰獵繭餘選鹹構網範蓋餘憲膚 (鹽鏇糧餘觸選廠顧積築, 48) 更多
NCT04072952 (ESMO_BC2024) 人工标引	临床1期	ER阳性/HER2阴性乳腺癌 HER2 Negative \| ER Positive \| ESR1 Mutation	46	Vepdegestrant+palbociclib (Total)	製衊膚鹽醖積構構觸窪(範鬱齋窪選鹽顧齋繭選) = ≥10% to either vepdegestrant or palbo were neutropenia (91%) and decreased white blood cell count (15%). 衊選餘構醖選艱範餘繭 (網製觸鹽衊獵襯顧繭繭 )	积极	2024-05-16
				Vepdegestrant+palbociclib (Mutant ESR1)
NCT06206837 (TACTIVE-K, ESMO_BC2024)	临床1/2期	ER阳性/HER2阴性乳腺癌 ER+ \| HER2-	65	Vepdegestrant	願醖糧願範壓窪壓鹽齋(築築構繭鏇選積糧壓簾) = 願艱繭糧窪醖蓋築選鬱蓋壓膚鹽構選糧繭積範 (觸範鬱廠餘願願廠膚選 )	-	2024-05-14