预约演示
更新于：2026-04-04
Tamoxifen
更新于：2026-04-04
概要
基本信息
非在研机构- |
权益机构- |
最高研发阶段临床1期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C26H29NO |
InChIKeyNKANXQFJJICGDU-QPLCGJKRSA-N |
CAS号10540-29-1 |
关联
100 项与 Tamoxifen 相关的临床结果
登录后查看更多信息
100 项与 Tamoxifen 相关的转化医学
登录后查看更多信息
100 项与 Tamoxifen 相关的专利（医药）
登录后查看更多信息
25,868
项与 Tamoxifen 相关的文献（医药）2026-12-31·JOURNAL OF INVESTIGATIVE SURGERY
Laparoscopic Ultrasound-Guided Biopsy: A Safe and Effective Approach for Diagnosing Idiopathic Retroperitoneal Fibrosis
Article
作者: Li, Zhi-De ; Ma, Zhi-Gang ; Chen, Xiong ; Zhuo, Qian ; Meng, Yuan ; Li, Yu-Peng
BACKGROUND:
Idiopathic retroperitoneal fibrosis (IRPF) is a rare fibroinflammatory condition that is challenging to distinguish from retroperitoneal malignancies based solely on imaging. We evaluated laparoscopic ultrasound-guided biopsy for diagnosing IRPF.
METHODS:
We retrospectively analyzed 12 patients with suspected retroperitoneal fibrosis who underwent laparoscopic ultrasound-guided biopsy. The surgical technique involved systematic laparoscopic exploration, intraoperative ultrasound to delineate the mass and its relation to great vessels, and targeted biopsy.
RESULTS:
Preoperative imaging suggested retroperitoneal masses in all 12 patients but failed to provide a definitive diagnosis in any case. Laparoscopic biopsy was successfully performed in all patients without conversion to laparotomy. Pathological examination confirmed IRPF in 11 patients and retroperitoneal adenocarcinoma in one. The procedure was safe, with minimal blood loss (20.4 ± 14.8 mL) and a short operative time (68.3 ± 19.0 min). All IRPF patients were treated with a combination of prednisone, tamoxifen, and mycophenolate mofetil, leading to significant lesion regression on follow-up imaging (median 37.9 months).
CONCLUSIONS:
Laparoscopic ultrasound-guided biopsy is a safe and highly effective diagnostic procedure for IRPF. It provides definitive pathological diagnosis to guide appropriate therapy and should be considered when percutaneous biopsy is not feasible.
2026-12-31·Gut Microbes
Tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion and Farnesoid X receptor signaling disruption
Article
作者: Mo, Yongshi ; Du, Haiyan ; Chen, Yuchun ; Xia, Jiaxuan ; Xie, Zhiyong ; Jin, Yibao ; Hong, Yanjun ; Qin, Meirong ; Xu, Yaning ; Chen, Ning ; Zhou, Wenxin ; Wang, Ping ; Huang, Houshuang ; Li, Hao ; Li, Meifang ; Ma, Chong
Tamoxifen (TAM) is a widely used estrogen receptor modulator for breast cancer treatment. However, TAM exhibits significant hepatotoxicity in the clinic, affecting nearly 50% of patients and thereby limiting its clinical utility. The specific mechanisms underlying TAM-induced liver injury remain poorly understood. In this study, we elucidated the mechanistic role of the gut microbiota in the hepatotoxicity associated with TAM. TAM administration induced substantial liver injury and gut microbiota dysbiosis in mice, characterized by an increased abundance of Escherichia and a reduction in Lachnospiraceae NK4A136 group. These microbial shifts resulted in decreased levels of total fecal bile acids (BA), particularly hyodeoxycholic acid (HDCA), which was inversely correlated with TAM-induced liver injury. Additionally, TAM disrupted BA homeostasis by enhancing intestinal Farnesoid X receptor (FXR) activity and concurrently stimulating hepatic BA synthesis through an alternative nonintestinal FXR mechanism. Notably, gut microbiota depletion reversed these effects, demonstrating the critical role of the microbiota in modulating the gut‒liver FXR axis in TAM-induced liver injury. Fecal microbiota transplantation (FMT) further confirmed that TAM directly stimulated hepatic BA synthesis through a microbiota-dependent mechanism. The disruption of the gut‒liver BA‒FXR axis impaired enterohepatic BA circulation, contributing to the liver toxicity associated with TAM administration. Importantly, HDCA supplementation restored the gut‒liver BA‒FXR axis and alleviated TAM-induced liver injury. These findings highlight the intricate relationship between TAM, gut microbiota, and BA metabolism, suggesting that targeting the gut-liver FXR axis with HDCA may serve as a promising therapeutic strategy for alleviating TAM-associated liver injury.
2026-06-01·BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
RTN4IP1 drives breast tumorigenesis: Molecular mechanisms linking elevated expression to enhanced proliferation, suppressed apoptosis, and therapeutic resistance
Article
作者: He, Weijie ; Liao, Xiaolin ; Luo, Lunqi ; Wu, Sixuan ; Jiang, Yiling ; Jiang, Baohong ; Tang, Yuanbin ; Li, Yuehua ; Zeng, Lijun ; Tan, Yeru
Abnormal expression of RTN4IP1 is implicated in diverse pathologies, including malignant tumors, yet its role in breast cancer (BC) remains insufficiently defined. This study integrated TCGA-based bioinformatics analysis with experimental validation to characterize RTN4IP1-related phenotypes. RTN4IP1 mRNA and protein levels were elevated in BC tissues compared to normal breast tissue, with higher expression correlating with advanced T/N stages, HER2 positivity, aggressive PAM50 subtypes, and lower PR/ER status. Clinically, increased RTN4IP1 expression was more frequent in Black/African American patients, postmenopausal women, and invasive ductal carcinoma cases. Elevated expression was also linked to poorer overall survival in both the TNBC and HER2-positive subgroups. Functional assays showed that RTN4IP1 silencing was accompanied by reduced proliferation, increased apoptosis, and inhibited xenograft growth in MCF-7 and MDA-MB-453 models, whereas overexpression exhibited the opposite pattern. RTN4IP1 expression was further linked to features of the tumor immune microenvironment and to differential responses to Tamoxifen and Paclitaxel; inhibition of RTN4IP1 was associated with greater drug sensitivity, while overexpression coincided with reduced response. Together, these findings indicate that RTN4IP1 is closely associated with BC progression, prognosis, and treatment response, supporting its potential relevance as a biomarker and a candidate target for further investigation.
47
项与 Tamoxifen 相关的新闻（医药）2026-03-13
·汇聚南药
刘晓东
中国药科大学药学院教授，博士研究生导师。中国药理学会数学药理学会理事、中国药理学会药物代谢动力学专业委员会副主任委员、江苏省青蓝工程跨世纪省级学术带头人培养对象和江苏省“333 工程”培养对象（第二层次）。主要研究方向：中药药物代谢动力学、血脑屏障与药物转运、创新药物药代动力学。主持多项国家自然科学基金项目，发表 SCI 论文近百篇；获得国家科技进步奖二等奖（ 2007）、江苏省科技进步奖一等奖（ 2004）等荣誉。
芳香化酶抑制剂与选择性雌激素受体调节剂的眼部不良反应及其机制的研究进展PPS
戴一栋，刘李，刘晓东 *
（中国药科大学药学院，江苏 南京 211198）
[摘要]芳香化酶抑制剂和选择性雌激素受体调节剂是治疗雌激素受体阳性乳腺癌的关键药物。芳香化酶抑制剂通过抑制雌激素的生成，而选择性雌激素受体调节剂则通过拮抗雌激素受体，降低细胞周期蛋白 D1 基因、细胞周期蛋白依赖性激酶 4/6 基因等原癌基因的表达，从而抑制乳腺癌细胞的增殖。雌激素受体主要分布于乳腺、子宫、骨骼和眼部等组织。在眼部，雌激素受体存在于泪腺、晶状体和视网膜等部位。雌激素在维持泪液分泌、保持晶状体透明度以及视网膜稳定中发挥重要作用。因此，这两类药物会影响眼部生理功能，导致患者出现干眼症、白内障和视网膜病变等眼部不良反应。综述了芳香化酶抑制剂和选择性雌激素受体调节剂引发的眼部不良反应及发生机制，旨在为这两类药物治疗方案的改进和新型抗乳腺癌药物的开发提供参考。
1
乳腺癌临床治疗的现状
乳腺癌因其发病人数众多，成为全球女性面临的主要公共卫生问题。据世界卫生组织统计， 2022年全球有 230 万女性被诊断为乳腺癌， 66.6 万人因此死亡，占当年女性因癌症死亡人数的 16%[1]。自1990 年至 2021 年，乳腺癌发病率逐年上升，医疗成本随之增加，造成了严重的社会负担 [2]。
乳腺癌上皮细胞通常过量表达芳香化酶，将雄激素转化为雌激素，从而导致乳腺癌组织中雌激素水平升高。此外，这些细胞还能主动从血液中摄取雌激素，进一步引起雌激素在乳腺癌组织中蓄积 [3]。过高的雌激素水平可上调细胞周期蛋白 D1 （Cyclin D1）基因、细胞周期蛋白依赖性激酶 4/6 （ Cyclin dependent kinase 4/6， CDK4/6）基因等原癌基因的转录，同时下调 Bcl-2 相互作用杀伤蛋白（ Bcl-2 interacting killer， BIK）基因、半胱氨酸天冬氨酸蛋白酶 -9（ cysteine-aspartic acid protease 9， Caspase 9）基因等促凋亡基因的转录，促进乳腺癌细胞的增殖 [4]。
大多数乳腺癌细胞的生长依赖于雌激素受体（estrogen receptor， ER）、孕激素受体（progesterone receptor， PR）和人类表皮生长因子受体 2（ human epidermal growth factor receptor 2， HER2）的表达。因此，乳腺癌依据受体类型分为 ER 阳性（ ER+）乳腺癌、 PR 阳性（ PR+）乳腺癌、 HER2 阳性（ HER2+）乳 腺 癌 及 三 阴 性 乳 腺 癌（ triple-negative breast cancer， TNBC）等 [5]。
不同分子亚型的乳腺癌治疗方式不同： ER+/PR+乳腺癌主要采用内分泌治疗（如他莫昔芬、阿那曲唑等）； HER2+ 乳腺癌以靶向治疗为主（如帕妥珠单抗及其偶联药物）； TNBC 则依赖化疗（如紫杉醇、阿霉素等），具体治疗药物详见表 1。
ER+ 乳腺癌在所有患者中占比最高（ 80%），且这类患者对芳香化酶抑制剂（ aromatase inhibitor， AI）和选择性雌激素受体调节剂（selective estrogen receptor modulator， SERM）的治疗应答良好 [6]。目前获批上市的 AI 和 SERM 的化学结构详见图 1。对于绝经前女性，乳腺雌激素主要来自于卵巢， SERM 可拮抗 ER，抑制乳腺癌细胞增殖。早期 ER+乳腺癌患者连续使用 5 年的 SERM，可使乳腺癌复发率降低 50%，同时在 15 年内因乳腺癌所致的死亡率降低 33.3%[7]。而对于绝经后女性，乳腺雌激素主要来源于外周芳香化酶转化， AI 能够显著降低雌激素浓度，抑制 ER+ 乳腺癌细胞增殖。绝经后早期ER+ 乳腺癌患者分别服用 5 年的 SERM 和 AI 后， AI 组的乳腺癌复发率相比 SERM 组降低约 30%，且 AI 组因乳腺癌所致的死亡率相比 SERM 组减少了28.9%[8]。因此， AI 更适合绝经后的 ER+ 乳腺癌治疗。
而随着 AI 和 SERM 的广泛应用，患者眼部不良反应的报道逐渐增多，主要包括干眼症、视网膜损伤和白内障等。在一项随机、双盲的临床研究中， Cuzick 等 [9] 对绝经后女性口服 AI 5 年的不良反应展开调查，发现治疗组的干眼症发生率（4%）显著高于安慰剂组（ 2%）。 Moschos 等 [10] 研究了早期 ER+乳腺癌患者服用 AI 3 年后的眼部改变，发现其视神经纤维层变薄，提示视神经轴突丢失； P100 波幅降低和潜伏期延长，第 1、 2 环视网膜反应密度降低，提示视网膜功能受到损伤，证实了 AI 可导致视网膜损伤。 Yoon 等 [11] 对口服 SERM 6 年的 ER+ 乳腺癌患者的眼部不良反应进行了总结，发现患者眼部不良反应（包括白内障等）发生率为 13.86%。这些不良反应严重影响患者的生活质量，降低了治疗依从性，甚至导致患者停药。
因此，探讨 SERM 和 AI 引发眼部不良反应的机制具有重要意义。通过文献综述和分析，期望提高对这些药物所致的眼部不良反应的理解，为临床安全用药提供依据，以及为开发更安全的抗乳腺癌新药提供参考。
2
芳香化酶抑制剂的作用机制及分类
芳香化酶通过脱去雄激素 19 位碳并诱导 A 环芳构化，实现雄激素向雌激素的关键转化。因此，芳香化酶作为调控雌激素水平的关键酶，是治疗ER+ 乳腺癌的重要靶点。通过抑制芳香化酶的活性， AI 可减少外周雌激素的生成，抑制雌激素依赖性肿瘤的生长 [12]。绝经后，女性卵巢功能衰竭，外周组织的雌激素主要由芳香化酶催化雄激素转化为雌激素 [13]。因此， AI 用于绝经后 ER+ 乳腺癌患者，作为术后辅助治疗可降低复发风险、延长生存期；用于转移性乳腺癌可控制病情、改善生活质量并延长生存时间 [14]。
常见的 AI 有 2 种。类固醇芳香化酶抑制剂（steroidal aromatase inhibitor， SAI） 以 雄 烯 二 酮为支架，核心为环戊烷四氢苯蒽，能够以不可逆的方式与芳香化酶发生共价结合，如依西美坦；而非类固醇芳香化酶抑制剂（ non-steroidal aromatase inhibitor， NSAI）则不含任何类固醇部分，通过非共价相互作用可逆地与芳香化酶结合，如阿那曲唑、来曲唑 [13]。
依西美坦作为自杀性底物，其结构与芳香化酶的天然底物雄烯二酮相似。在临床应用中，依西美坦主要用于绝经后 ER+ 乳腺癌患者的治疗 [15]。
阿那曲唑作为苯基三唑衍生物，与芳香化酶的细胞色素 P450（ cytochrome P450， CYP）亚基中的血红素基团竞争性结合，从而抑制芳香化酶的活性。在临床应用中，阿那曲唑主要用于绝经后局部侵袭性或转移性 ER+ 乳腺癌的一线治疗和他莫昔芬无效的绝经后晚期 ER+ 乳腺癌的辅助治疗 [16]。
来曲唑与阿那曲唑的作用机制相似。来曲唑主要用于绝经后 ER+ 乳腺癌的辅助治疗和转移性 ER+乳腺癌的一线治疗 [17]。
3
选择性雌激素受体调节剂的作用机制及分类
SERM 通过调节 ER 下游基因的转录实现其组织选择性作用 [18]。这种选择性源于多个因素的综合结果：包括组织特异性表达的 ERα 和 ERβ、不同组织共调节因子的差异表达，以及配体诱导的 ER 构象的变化。正是这种复杂的调控网络使得 SERM 在不同组织中表现出截然不同的生物学效应 [19]。例如，在乳腺组织中，它们通常发挥抗雌激素作用，而在骨骼和子宫等组织中则可能发挥雌激素样作用。其中，在乳腺癌治疗中， SERM 通过拮抗 ER，阻止雌激素与受体结合，从而抑制乳腺癌细胞的增殖，减少雌激素依赖性肿瘤的生长和复发风险 [20]。
从化学结构角度来看，常用的 SERM 可以分为两大类：三苯乙烯类和苯并噻吩类结构。三苯乙烯类以 3 个苯环为核心骨架，分子呈扁平构象，具有酚羟基和与核心平面夹角较小的 N， N-二甲基氨基乙氧基侧链，如他莫昔芬、托瑞米芬；而苯并噻吩类则以苯并噻吩环系统为核心， 2 位连接苯环，其碱性侧链与核心骨架呈垂直取向，如雷洛昔芬 [20-21]。
他莫昔芬为第 1 代 SERM 的代表药物，开创了SERM 在乳腺癌预防和治疗领域的应用。其临床应用主要包括早期 ER+ 乳腺癌的辅助治疗和晚期 ER+乳腺癌的治疗，特别适用于绝经前 ER+ 乳腺癌患者，可采用单药治疗或与卵巢功能抑制剂联合使用的方案 [22]。
托瑞米芬作为第 1 代 SERM，其疗效与他莫昔芬相当，但在血脂代谢方面显示出更有利的作用，可降低总胆固醇和低密度脂蛋白胆固醇，同时提高高密度脂蛋白胆固醇水平。该药主要应用于绝经后早期 ER+ 乳腺癌的治疗 [23]。
雷洛昔芬作为第 2 代 SERM，属于多羟基酚苯并噻吩类化合物。虽然最初为治疗乳腺癌而开发，但由于在骨质疏松防治方面表现出色，最终成为首个获得美国食品药品监督管理局（ Food and Drug Administration， FDA）批准用于治疗和预防绝经后骨质疏松症的 SERM 类药物。其主要应用于 ER+ 乳腺癌合并骨质疏松患者的治疗 [24]。
4
芳香化酶抑制剂所致的眼部不良反应及相关机制
AI 在治疗 ER+ 乳腺癌时，引发多种眼部不良反应，包括干眼症、黄斑囊样水肿、视网膜动脉阻塞及视神经病变等 [25]。其中，干眼症是最具特征性的表现，通常表现为患者眼睛干涩、眼睛疼痛、视力模糊等。
4.1 干眼症
干眼症是一种多因素疾病，其特征是眼部结构（包括泪腺、睑板腺和角膜）的功能障碍导致泪膜稳态丧失，继而引发眼表炎症和组织损伤，形成自我持续的恶性循环 [26]。
Inglis 等 [27] 通过眼表疾病指数（ ocular surface disease index， OSDI）问卷对服用 AI 3 个月的绝经后乳腺癌患者进行评估，发现 AI 治疗组的干眼症发生率为 35%，这一比例显著高于未使用 AI 的对照组（ 8%）。 Ağın 等 [28] 对服用 6 个月 AI 的乳腺癌患者进行随访，发现患者的 OSDI 评分随服药时间延长而逐渐升高（治疗前 10.4 分、治疗 3 个月 20.8 分、治疗 6 个月 31.2 分）。这些研究结果表明， AI 治疗与干眼症状之间存在显著相关性，且症状随用药时间的延长而加重。
Bicer 等 [29] 对使用 AI 治疗 3 年的乳腺癌患者进行研究，通过荧光素泪膜破裂时间（ fluorescein tear film break-up time， FBUT）和施氏试验评估其泪腺功能。研究发现， AI 组的 FBUT 值为 (5.8± 2.1) s，显著低于对照组的 (8.9± 2.9) s；同时， AI 组的施氏试验值为 (10.1± 2.7) mm/5 min，也明显低于对照组的 (15.3± 2.9) mm/5 min。这些结果表明， AI 治疗显著影响患者的泪膜稳定性和泪液分泌。
在接受 AI 治疗的乳腺癌患者中，约有 22% 出现角膜荧光素染色阳性，主要表现为浅层点状染色，通常集中在角膜中央区域，染色程度多为轻中度。这种角膜上皮损害通常在治疗开始后 2 年内出现，并与泪膜破裂时间缩短、泪液分泌减少和睑板腺功能障碍等干眼症状密切相关 [29-30]。因此，研究者建议在 AI 治疗期间应定期监测患者的泪腺功能和干眼症状。
4.2 视网膜病变
接受 AI 治疗的乳腺癌患者可能出现多种视网膜不良反应，这些不良反应范围涉及从轻微的亚临床结构和功能损伤，到严重的视网膜损害，包括视网膜出血、视网膜动脉阻塞、黄斑囊样水肿以及视神经炎等。
其中，视网膜出血和视网膜动脉阻塞是两种严重的眼部血管不良反应。绝经后乳腺癌患者连续使用AI 治疗 3 年后，视网膜出血的发生率约为 11.4%。其主要表现为视网膜神经纤维层的火焰状出血和视网膜深层的斑块状出血。此外，在同时服用抗骨质疏松药物（如双膦酸盐）或解热镇痛药物（如阿司匹林）的患者中，视网膜出血的风险显著增加 [31]。同时，在使用 AI 治疗 13 个月的乳腺癌患者中，荧光素血管造影显示患者出现视网膜中央动脉阻塞 [32]。
黄斑囊样水肿是 AI 治疗的常见眼部不良反应。在服用 4 年 AI 后，患者出现视力下降、视物模糊和光敏感等症状，光学相干断层扫描（ optical coherence tomography， OCT）检查可见双侧黄斑区囊腔形成，荧光素血管造影呈现典型的花瓣样渗漏 [33]。值得注意的是，停用 AI 后水肿通常得到改善，这表明 AI 与黄斑囊样水肿之间存在明确的因果关系 [34]。
AI 也可导致玻璃体视网膜界面的病理性改变。使用 AI 超过 2 年的乳腺癌患者，往往会出现玻璃体对视网膜牵引力增加的情况，导致黄斑区从颞侧向鼻侧发生偏移。增强的牵引力还可能增加后部玻璃体脱离（ posterior vitreous detachment， PVD）和黄斑裂孔的风险，从而对视力造成损害 [35]。
AI 还可引起多种视神经改变，主要包括视神经缺失、视神经纤维层厚度减少以及视神经功能异常。一名乳腺癌患者在使用阿那曲唑 3 年后，出现右眼视野缺失。经过 OCT 检查， Velez Oquendo 等 [36]发现患者右侧视神经缺失并伴有炎症反应。为此，患者接受了玻璃体内类固醇注射，治疗后视野逐渐恢复。另一项研究显示，使用依西美坦 3 年的患者视觉诱发电位（ visual evoked potentials， VEP）的P100 波幅降低和潜伏期延长，同时多焦视网膜电图（ multifocal-electroretinogram， mfERG） 的 环 1 和环 2 反应密度下降，提示视神经功能紊乱 [10]。这些改变提示 AI 可能影响视神经的结构和功能，需要在治疗过程中进行定期监测，以及时发现并处理潜在的视神经损伤。
4.3 不良反应机制
雌激素在泪液分泌、血管保护、玻璃体形态维持和视网膜神经保护等生理功能中发挥着重要作用 [37]。绝经后女性的雌激素主要来源于外周芳香化酶转化，而 AI 可通过抑制芳香化酶，降低眼部雌激素含量，进而下调雌激素介导的生理功能，导致干眼症和视网膜病变等眼部不良反应的发生 [25]。
雌激素在维持眼表微环境的平衡方面起着重要作用。它不仅促进泪液分泌，保持泪膜的连续性，还能促进白细胞介素（ interleukin， IL） -10 和转化生长因子-β（ transforming growth factor-β， TGF-β）等抗炎因子的释放，有效减轻眼部炎症，从而共同维护眼表微环境的稳定 [28]。 Deo 等 [38] 发现，绝经期及绝经后女性干眼症风险高于年轻女性。这可能是由于眼内雌激素水平的下降，导致泪液分泌功能受损，增加了干眼症发生的风险。在接受 AI 治疗乳腺癌的绝经后女性中，随着雌激素水平的进一步降低，患者发生干眼症的风险也随之增加。
雌激素具有保护血管内皮细胞和维持血管舒张功能的作用 [39]。雌激素通过激活 ER，激活内皮型一氧化氮合酶（ endothelial nitric oxide synthase， eNOS），促进一氧化氮（ nitric oxide， NO）合成并作用于血管平滑肌，增强血管舒张能力，改善局部血流。此外，雌激素还通过上调抗氧化酶表达，降低氧化应激，减少 NO 与超氧化物结合生成的有害的过氧亚硝酸盐，从而保护并维持内皮细胞的结构 [40]。当这种保护作用受到 AI 的干扰时，可能导致视网膜血管功能异常，引发视网膜出血及其他血管源性病变。
雌激素对血眼屏障具有重要的保护作用，其通过增强血管内皮细胞和色素上皮细胞的紧密连接和黏附连接，提高内外屏障的完整性，调节水盐平衡，保护视网膜免受有害物质的侵害 [41]。 Chen 等 [42]发现，在血管内皮生长因子（ vascular endothelial growth factor， VEGF）诱导的血眼屏障损伤中，雌激素增加色素上皮细胞间的闭锁蛋白（ occludin）和紧密连接蛋白（ claudin3）的表达，从而保护血眼屏障完整性。当血眼屏障完整性被 AI 破坏时，视网膜内细胞间液蓄积，患者出现黄斑囊样水肿。
雌激素对玻璃体的影响主要体现在维持其结构完整性和功能稳定性。雌激素有助于促进胶原纤维和酸性黏多糖的合成，防止玻璃体液化加速 [43]。缺乏雌激素会导致玻璃体的退行性病变，增加视网膜牵引力，从而提高后部玻璃体脱离和黄斑裂孔的风险，最终可能导致视力损害 [35]。因此，当这种调节作用被 AI 干扰时，可能导致玻璃体形态异常，引起玻璃体与视网膜牵扯力增加，从而增加黄斑裂孔与玻璃体后脱离的风险。
雌激素具有显著的抗氧化和抗炎作用。它能够上调抗氧化酶的表达，如超氧化物歧化酶和谷胱甘肽过氧化物酶，同时抑制促炎因子的产生，如肿瘤坏死因子-α（ tumor necrosis factor-α， TNF-α）和 IL- 1β。Wei等 [44]发现，在光照诱导的视网膜退化模型中，雌激素通过激活抗氧化酶，减少活性氧簇（ reactive oxygen species， ROS）的生成和清除过量的自由基，减少视网膜神经细胞凋亡，从而保护视力。 Li 等 [45]发现，在 H2O2 诱导的视网膜损伤模型中，雌激素通过降低 Toll 样受体 2（Toll-like receptor 2， TLR2）水平，抑制促炎因子 TNF-α、干扰素-γ（ interferon-γ， IFN-γ）和IL-1β的释放，减少视网膜神经细胞的损伤。AI 干扰这一过程后，会导致视网膜内氧化应激增加，炎症反应加重，最终损害视网膜神经细胞，引发视神经炎等多种疾病。
4.4 小结
AI 相关眼部不良反应及机制的详细总结见表 2。
5
选择性雌激素受体调节剂所致的眼部不良反应及相关机制
SERM 在治疗 ER+ 乳腺癌时，可引发多种眼部不良反应，主要包括角膜混浊、晶状体病变与视网膜病变。其中，最具特征性的改变是晶样视网膜病变，表现为视网膜纤维层和内丛状层的细小白色沉积 [46]。
5.1 角膜混浊
连续使用 SERM 2 年可导致特征性角膜混浊，主要表现为基底层下沉积。角膜混浊分为涡旋状混浊和线状混浊。角膜混浊通常在双眼对称出现，颜色范围从白色到棕色，主要集中在角膜的下部区域，偶尔也会出现在中央区域。值得注意的是，这些角膜改变具有可逆性，在停用 SERM 后可能逐渐改善或消退 [47]。
5.2 晶状体病变
在长期使用 SERM 的患者中，晶状体可能出现多种不良反应，这些反应主要包括核性白内障、皮质下白内障和后囊膜下白内障 [48]。这些变化通常会导致患者出现视觉模糊和视力下降，影响日常生活质量。其中，核性白内障是最常见的表现，通常表现为双眼的轻度至中度核硬化。在停用药物后，部分患者的晶状体病变可能会有所改善 [49]。
5.3 视网膜病变
SERM 相关的视网膜病变是一类需要特别关注的药物相关性眼部并发症。根据流行病学研究，其发生率在 0.9% ~ 12% 之间；发病风险主要与用药时间、剂量及患者年龄等因素相关。该病变主要表现为 4 种典型的病理改变：晶样视网膜病变、黄斑囊样水肿、视网膜色素上皮异常和视神经病变 [46, 50]。
晶样视网膜病变是 SERM 相关视网膜病变中最具特征性的表现，其表现为细小、有光泽的白色晶状物。这些晶状物主要分布于视网膜的神经纤维层和内丛状层，尤其是在黄斑区周围。其病变早期呈散在的点状分布，随病程进展可逐渐融合。而黄斑区是中心视野和视力分辨率最高的地方。因此，随着沉积物累积，患者逐渐出现视力下降和视物变形的症状 [51-52]。
黄斑囊样水肿是另一种严重眼部不良反应。SERM 导致视网膜细胞间隙液体异常积聚，形成黄斑囊样水肿。临床上表现为中心视力进行性下降、视物变形、中心暗点及对比敏感度降低。 OCT 可见视网膜增厚和囊腔形成，荧光素血管造影呈现典型的花瓣状渗漏 [53]。治疗上需考虑调整用药方案，必要时可联合使用抗 VEGF 药物或糖皮质激素 [54]。
视网膜色素上皮异常主要表现为色素上皮细胞的结构和功能改变。色素上皮细胞通过介导水、离子和营养物质的摄取来维持光感受器细胞的生存和功能，其异常可导致光感受器细胞损伤，进而引起视野模糊和视力下降 [55]。一名乳腺癌患者服用 6.3年 SERM 后，其右眼视力逐渐下降，经过频域光学相干断层扫描（ spectral-domain optical coherence tomography， SD-OCT）检查发现，其色素上皮层和视网膜变薄。停药 1 年后，患者视网膜色素上皮层厚度和视力逐渐恢复 [56]。这表明 SERM 与视网膜色素上皮异常之间存在明确的因果关系。
视神经病变常与视网膜色素上皮异常相互影响。视神经的损伤会引起炎症反应，损伤视网膜色素上皮层。而色素上皮功能异常则影响视网膜的营养代谢，进一步损伤视神经，两者形成恶性循环 [57]。因此，患者可同时出现视神经病变和视网膜色素上皮异常等症状。临床诊疗中需进行多种检查评估，包括眼底检查、 OCT、视野检查、自发荧光和荧光素血管造影等。同时，定期随访监测对预防和控制视神经病变的进展至关重要 [58]。
5.4 不良反应机制
5.4.1 药物蓄积引起脂质代谢紊乱 SERM 因其同时具有亲水性和亲脂性的特殊物理化学性质，能够轻易透过生物膜屏障，在角膜和视网膜组织中持续累积并与细胞中脂质形成稳定复合物。当局部药物浓度超过其溶解度时，会与极性脂质结合形成晶样沉积物，这些沉积物不仅造成机械性损伤，还会干扰局部组织的正常功能 [47,51]。
这种药物蓄积会干扰细胞的脂质代谢，影响膜脂质组成，导致线粒体膜完整性受损。这些改变会损害线粒体功能，导致氧化磷酸化效率下降、 ATP产生减少、电子传递链功能受损，最终引发细胞能量供应不足和一系列细胞损伤反应。这些变化严重影响角膜和视网膜的正常功能，引起角膜混浊和晶样视网膜病变，最终导致视野模糊和视力下降 [59]。
5.4.2 阻断氯离子通道，引起晶状体混浊 氯离子在维持晶状体生理功能中发挥着关键作用，其机制主要包括以下 2 个方面：首先，通过调节水合平衡来维持晶状体的正常含水量，既防止脱水又避免过度水合；其次，通过稳定晶状体蛋白的空间构象来保障其光学透明度。当氯离子稳态被破坏时，可能导致晶状体脱水及蛋白质构象异常，进而引发晶状体混浊并显著增加白内障的发病风险。 Yu 等 [60] 发现，在甲状腺细胞中，临床剂量下的 SERM 可以阻断氯离子通道；在晶状体细胞中， SERM 也可阻断氯离子通道，增加白内障发生的风险。
5.4.3 拮抗雌激素受体，引起眼部损伤 ERα 和 ERβ是两种雌激素核受体，在眼部组织中广泛表达，主要分布于角膜、晶状体和视网膜等部位 [61]。雌激素通过这些受体参与眼部组织的生理功能调节，包括晶状体透明度维持，血管保护和神经保护等作用 [37]。因此， SERM 拮抗 ER 的作用可能引发多种眼部不良反应，包括白内障、黄斑囊样水肿、视网膜色素上皮异常和视神经病变等 [46]。
雌激素可通过 ER 作用于色素上皮细胞和视网膜血管细胞，维持血眼屏障的完整性。当 SERM 拮抗 ER，会引起血眼屏障泄露，导致细胞间液蓄积，从而诱发黄斑囊样水肿 [53]。此外，视网膜色素上皮细胞的损伤被认为是 SERM 引起视网膜病变的关键步骤。 Hwang 等 [62] 发现，雌激素可以通过 ER，降低促凋亡蛋白（如 Bax、 Caspase-3）的表达，同时上调抗凋亡蛋白（如 Bcl-2），减少色素上皮细胞凋亡，维持视网膜内微环境的稳定。
雌激素还通过 ER 作用于穆勒（ Müller）细胞和视网膜神经节细胞，减轻氧化应激，抑制细胞凋亡，促进轴突再生。例如， Tawarayama 等 [63] 在 H2O2 诱导的视网膜损伤模型中发现，雌激素通过 ER 受体，刺激 Müller 细胞分泌成纤维生长因子 2（ fibroblast growth factor 2， FGF2），减少氧化应激引起的视网膜神经节细胞的丢失。 Zhu 等 [64] 发现，在光照诱导的视网膜退化模型中，雌激素通过 ER 受体，激活磷脂酰肌醇 3-激酶（phosphoinositide 3-kinase， PI3K） -蛋白激酶 B（ protein kinase B， AKT）通路，减少视网膜神经细胞凋亡，从而防止视网膜退化。当 SERM 拮抗 ER 时，这些保护通路被抑制，导致视网膜神经节细胞的凋亡和功能障碍，从而引发视神经炎。
此外，雌激素还参与调节神经细胞的代谢。其通过影响线粒体功能和能量代谢，维持视网膜神经细胞的正常生理活动。 Peng 等 [65] 发现， ERβ 在视网膜神经节细胞线粒体中表达，在 Leber 遗传性视神经病变中，类雌激素通过 ERβ 保护线粒体结构，降低氧化应激，从而显著提高了视网膜神经节细胞的活力。当 SERM 干扰这些过程后，会导致视网膜细胞代谢紊乱，损伤视网膜神经节细胞。
5.5 小结
SERM 相关眼部不良反应及其机制的详细总结见表 3。
6
结语
AI 和 SERM 在眼部组织蓄积后，可引发干眼症、角膜混浊、白内障及视网膜病变等不良反应。其机制包括 AI 因雌激素下降导致泪液分泌减少、引发干眼症，以及玻璃体变性引起黄斑裂孔和玻璃体后脱离； SERM 通过药物蓄积引发脂质代谢紊乱，导致角膜和视网膜损伤，以及阻断氯离子通道诱发白内障。两者共同机制表现为拮抗 ER 引起的视网膜血管损伤、黄斑水肿及视神经病变。
目前， AI 和 SERM 引起的眼部不良反应缺乏明确的检测指标，主要依赖于患者的主动报告。其发生受年龄、性别和服药时间等多种因素影响，个体差异显著。临床中需定期监测患者视力变化、眼压、视网膜形态，及时关注患者反馈并依据具体情况调整用药方案，以减少眼部不良反应的发生。同时，为了优化对这些药物相关眼部不良反应的管理，亟需更多临床研究来确定最佳治疗策略和监测方法。
参考文献 ：
[1] Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022:globocan estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2024, 74(3): 229-263.
[2] Sha R, Kong X M, Li X Y, et al. Global burden of breast cancer and attributable risk factors in 204 countries and territories, from 1990 to 2021: results from the Global Burden of Disease Study 2021[J].Biomark Res, 2024, 12(1): 87.
[3] Corti C, Binboğa Kurt B, Koca B, et al. Estrogen signaling in earlystage breast cancer: impact on neoadjuvant chemotherapy and immunotherapy[J]. Cancer Treat Rev, 2025, 132: 102852.
[4] Clusan L, Ferrière F, Flouriot G, et al. A basic review on estrogen receptor signaling pathways in breast cancer[J]. Int J Mol Sci, 2023,24(7): 6834.
[5] Katsika L, Boureka E, Kalogiannidis I, et al. Screening for breast cancer: a comparative review of guidelines[J]. Life (Basel), 2024,14(6): 777.
[6] Ahn S, Park J H, Grimm S L, et al. Metabolomic rewiring promotes endocrine therapy resistance in breast cancer[J]. Cancer Res, 2024,
84(2): 291-304.
[7] Early Breast Cancer Trialists' Collaborative Group (EBCTCG),Davies C, Godwin J, et al. Relevance of breast cancer hormone receptors and other factors to the efficacy of adjuvant tamoxifen:patient-level meta-analysis of randomised trials[J]. Lancet, 2011,378(9793): 771-784.
[8] Early Breast Cancer Trialists' Collaborative Group (EBCTCG).Aromatase inhibitors versus tamoxifen in early breast cancer:patient-level meta-analysis of the randomised trials[J]. Lancet, 2015,386(10001): 1341-1352.
[9] Cuzick J, Sestak I, Forbes J F, et al. Anastrozole for prevention of breast cancer in high-risk postmenopausal women (IBIS-II): an international, double-blind, randomised placebo-controlled trial[J].Lancet, 2014, 383(9922): 1041-1048.
[10] Moschos M M, Chatziralli I P, Sergentanis T, et al.Electroretinographic and optical coherence tomography findings in breast cancer patients using aromatase inhibitors[J]. Cutan Ocul Toxicol, 2016, 35(1): 13-20.
[11] Yoon C I, Lee H S, Jeon S, et al. Relationship between tamoxifen and cataracts: a nationwide cohort study of women in South Korea[J].Breast Cancer Res Treat, 2023, 197(3): 603-612.
[12] Ghosh D. Structures and functions of human placental aromatase and steroid sulfatase, two key enzymes in estrogen biosynthesis[J].Steroids, 2023, 196: 109249.
[13] Bhatia N, Thareja S. Aromatase inhibitors for the treatment of breast cancer: an overview (2019-2023)[J]. Bioorg Chem, 2024, 151:107607.
[14] Christensen H S. Aromatase inhibitor musculoskeletal syndrome and bone loss: a review of the current literature[J]. Curr Oncol Rep, 2023,25(7): 825-831.
[15] Teslenko I, Watson C J W, Chen G, et al. Inhibition of the aromatase enzyme by exemestane cysteine conjugates[J].Mol Pharmacol, 2022,102(5): 216-222.
[16] Haddad T C, Suman V J, Giridhar K V, et al. Anastrozole dose escalation for optimal estrogen suppression in postmenopausal earlystage breast cancer: a prospective trial[J]. Clin Cancer Res, 2024,30(15): 3147-3156.
[17] Mukherjee A G, Wanjari U R, Nagarajan D, et al. Letrozole:pharmacology, toxicity and potential therapeutic effects[J]. Life Sci,2022, 310: 121074.
[18] Cerutti C, Shi J R, Vanacker J M. Multifaceted transcriptional network of estrogen-related receptor alpha in health and disease[J]. Int J Mol Sci, 2023, 24(5): 4265.
[19] Bhatia N, Hazra S, Thareja S. Selective estrogen receptor degraders (SERDs) for the treatment of breast cancer: an overview[J]. Eur J
Med Chem, 2023, 256: 115422.
[20] Gombos A, Goncalves A, Curigliano G, et al. How I treat endocrinedependent metastatic breast cancer[J]. ESMO Open, 2023, 8(2):100882.
[21] Pagliuca M, Donato M, D'Amato A L, et al. New steps on an old path:novel estrogen receptor inhibitors in breast cancer[J]. Crit Rev Oncol Hematol, 2022, 180: 103861.
[22] Howell A, Howell S J. Tamoxifen evolution[J]. Br J Cancer, 2023,128(3): 421-425.
[23] Li X, Li Z, Li L, et al. Toremifene, an alternative adjuvant endocrine therapy, is better than tamoxifen in breast cancer patients with CYP2D6*10 mutant genotypes[J]. Cancer Res Treat, 2024, 56(1):134-142.
[24] Wang Y, Sauvage M, Diennet M, et al. Design, synthesis and antiproliferative activity of raloxifene/histone deacetylase inhibitor hybrids in breast cancer[J]. Eur J Med Chem, 2024, 274: 116533.
[25] Feng Z X, Sriranganathan A, Lo C, et al. Risk of ocular adverse events with aromatase inhibitors[J]. Can J Ophthalmol, 2024, 59(5):e431-e434.
[26] Sheppard J, Shen Lee B, Periman L M. Dry eye disease: identification and therapeutic strategies for primary care clinicians and clinical
specialists[J]. Ann Med, 2023, 55(1): 241-252.
[27] Inglis H, Boyle F M, Friedlander M L, et al. Dry eyes and AIs: if you don’t ask you won’t find out[J]. Breast, 2015, 24(6): 694-698.
[28] Ağın A, Kocabeyoglu S, Yucel Gencoglu A, et al. The effects of systemic aromatase inhibitors on meibomian glands and corneal structure[J]. Eye (Lond), 2022, 36(6): 1185-1193.
[29] Bicer T, Imamoglu G I, Dogan A S, et al. The effects of adjuvant hormonotherapy on tear functions in patients with breast cancer[J].Int Ophthalmol, 2020, 40(8): 2077-2083.
[30] Machairoudia G, Kazantzis D, Chatziralli I, et al. Prevalence and risk factors of dry eye disease in patients treated with aromatase inhibitors for breast cancer[J]. Clin Exp Optom, 2024, 107(4): 415-419.
[31] Eisner A, Falardeau J, Toomey M D, et al. Retinal hemorrhages in anastrozole users[J]. Optom Vis Sci, 2008, 85(5): 301-308.
[32] Karagöz B, Ayata A, Bilgi O, et al. Hemicentral retinal artery occlusion in a breast cancer patient using anastrozole[J]. Onkologie,
2009, 32(7): 421-423.
[33] Azeem S, Al Hinai A, Al Kharousi N, et al. A case report on letrozolerelated maculopathy[J]. Oman J Ophthalmol, 2023, 16(2): 322-325.
[34] Nguyen K H, Smith A K, Kim B T, et al. A case report of cystoid macular edema, uveitis and vitreomacular traction in a patient taking anastrozole[J]. Am J Ophthalmol Case Rep, 2022, 25: 101339.
[35] Eisner A, Thielman E J, Falardeau J, et al. Vitreo-retinal traction and anastrozole use[J]. Breast Cancer Res Treat, 2009, 117(1): 9-16.
[36] Velez Oquendo G. Optic neuritis as a consequence of long-term medical treatment using anastrozole: a case report[J]. Am J Case Rep,2023, 24: e939026.
[37] Valero-Ochando J, Cantó A, López-Pedrajas R, et al. Role of gonadal steroid hormones in the eye: therapeutic implications[J].Biomolecules, 2024, 14(10): 1262.
[38] Deo N, Nagrale P. Dry eye disease: an overview of its risk factors, diagnosis, and prevalence by age, sex, and race[J]. Cureus, 2024,16(2): e54028.
[39] Gersh F, O'Keefe J H, Elagizi A, et al. Estrogen and cardiovascular disease[J]. Prog Cardiovasc Dis, 2024, 84: 60-67.
[40] SenthilKumar G, Katunaric B, Bordas-Murphy H, et al. Estrogen and the vascular endothelium: the unanswered questions[J].Endocrinology, 2023, 164(6): bqad079.
[41] Hellinen L, Hongisto H, Ramsay E, et al. Comparison of barrier properties of outer blood-retinal barrier models - Human stem cellbased models as a novel tool for ocular drug discovery[J]. Eur J Pharm Biopharm, 2023, 184: 181-188.
[42] Chen X F, Zhang M N, Jiang C H, et al. Estrogen attenuates VEGFinitiated blood-retina barrier breakdown in male rats[J]. Horm Metab Res, 2011, 43(9): 614-618.
[43] Ueki S, Suzuki Y, Nakamura Y, et al. Age-dependent changesin regulation of water inflow into the vitreous body[J]. Invest Ophthalmol Vis Sci, 2023, 64(12): 22.
[44] Wei Q, Liang X, Peng Y, et al. 17β-Estradiol ameliorates oxidativestress and blue light-emitting diode-induced retinal degeneration by decreasing apoptosis and enhancing autophagy[J]. Drug Des Devel Ther, 2018, 12: 2715-2730.
[45] Li H, Zhu C, Wang B, et al. 17β-Estradiol protects the retinalnerve cells suppressing TLR2 mediated immune-inflammation and apoptosis from oxidative stress insult independent of PI3K[J]. J Mol Neurosci, 2016, 60(2): 195-204.
[46] Fortes B H, Tailor P D, Dalvin L A. Ocular toxicity of targetedanticancer agents[J]. Drugs, 2021, 81(7): 771-823.
[47] Sahyoun J Y, Sabeti S, Robert M C. Drug-induced corneal deposits:an up-to-date review[J]. BMJ Open Ophthalmol, 2022, 7(1): e000943.
[48] Tenney S, Oboh-Weilke A, Wagner D, et al. Tamoxifen retinopathy: acomprehensive review[J]. Surv Ophthalmol, 2024, 69(1): 42-50.
[49] Henzi B C, Schmidt S, Nagy S, et al. Safety and efficacy oftamoxifen in boys with Duchenne muscular dystrophy (TAMDMD):a multicentre, randomised, double-blind, placebo-controlled, phase 3trial[J]. Lancet Neurol, 2023, 22(10): 890-899.
[50] Bazvand F, Mahdizad Z, Mohammadi N, et al. Tamoxifenretinopathy[J]. Surv Ophthalmol, 2023, 68(4): 628-640.
[51] Zhao E, Lin M, Marti J, et al. Prevalence and spectrum ofmanifestations of tamoxifen retinopathy as assessed by multimodal and ultra-widefield retinal imaging[J]. Can J Ophthalmol, 2025, 60(3): 186-191.
[52] Somisetty S, Santina A, Sarraf D, et al. The impact of systemicmedications on retinal function[J]. Asia Pac J Ophthalmol (Phila), 2023, 12(2): 115-157.
[53] Kwon H Y, Kim J, Ahn S J. Drug exposure and risk factors ofmaculopathy in tamoxifen users[J]. Sci Rep, 2024, 14(1): 16792.
[54] Li C, Xiao J, Zou H, et al. The response of anti-VEGF therapy andtamoxifen withdrawal of tamoxifen-induced cystoid macular edemain the same patient[J]. BMC Ophthalmol, 2021, 21(1): 201.
[55] O'Leary F, Campbell M. The blood-retina barrier in health anddisease[J]. FEBS J, 2023, 290(4): 878-891.
[56] Ghassemi F, Masoomian B, Khodabandeh A, et al. Tamoxifeninduced pachychoroid pigment epitheliopathy with reversible changes after drug discontinuation[J]. Int Med Case Rep J, 2020, 13: 285-289.
[57] Akash R, Panimalar A V, Puri S K, et al. A rare case of tamoxifeninduced bilateral optic neuritis[J]. Med J Malaysia, 2025, 80(Suppl 1): 7-9.
[58] Chiang T K, White K M, Kurup S K, et al. Use of visualelectrophysiology to monitor retinal and optic nerve toxicity[J]. Biomolecules, 2022, 12(10): 1390.
[59] Debisschop A, Bogaert B, Muntean C, et al. Beyond chloroquine:cationic amphiphilic drugs as endosomal escape enhancers for nucleic acid therapeutics[J]. Curr Opin Chem Biol, 2024, 83: 102531.
[60] Yu M, Wei Y, Zheng Y, et al. 17β-Estradiol activates Cl- channels viathe estrogen receptor α pathway in human thyroid cells[J]. Channels (Austin), 2021, 15(1): 516-527.
[61] Somers F M, Malek G. Estrogen related receptor alpha: potentialmodulator of age-related macular degeneration[J]. Curr Opin Pharmacol, 2024, 75: 102439.
[62] Hwang N, Chung S W. Sulfasalazine attenuates tamoxifen-inducedtoxicity in human retinal pigment epithelial cells[J]. BMB Rep, 2020, 53(5): 284-289.
[63] Tawarayama H, Uchida K, Hasegawa H, et al. Estrogen, via ESR2receptor, prevents oxidative stress-induced Müller cell death and stimulates FGF2 production independently of NRF2, attenuating retinal degeneration[J]. Exp Eye Res, 2024, 248: 110103.
[64] Zhu C, Wang S, Wang B, et al. 17β-Estradiol up-regulates Nrf2 viaPI3K/AKT and estrogen receptor signaling pathways to suppress light-induced degeneration in rat retina[J]. Neuroscience, 2015, 304: 328-339.
[65] Peng S Y, Chen C Y, Chen H, et al. Inhibition of angiogenesisby the secretome from iPSC-derived retinal ganglion cells with Leber's hereditary optic neuropathy-like phenotypes[J]. Biomed Pharmacother, 2024, 178: 117270.
信息来源：药学进展
往期推荐
!
免责声明
“汇聚南药”公众号所转载文章来源于其他公众号平台，主要目的在于分享行业相关知识，传递当前最新资讯。图片、文章版权均属于原作者所有，如有侵权，请在留言栏及时告知，我们会在24小时内删除相关信息。
本平台不对转载文章的观点负责，文章所包含内容的准确性、可靠性或完整性提供任何明示暗示的保证。
喜欢的点个“看一看”和"喜欢"吧
不然微信推送规则改变，有可能每天都会错过我们哦~
临床研究
2026-02-12
– Top-Line Data from the Phase 3 SENTRY Trial in Myelofibrosis on Track for March 2026 –
– Top-Line Data from the Phase 3 XPORT-EC-042 Trial in Endometrial Cancer on Track for Mid-2026 –
– Total Revenue was $146 Million and U.S. XPOVIO® (selinexor) Net Product Revenue was $115 Million for Full Year 2025 –
– Company Provides Full-Year 2026 Total Revenue Guidance of $130 Million to $150 Million Including U.S. XPOVIO Net Product Revenue Guidance of $115 Million to $130 Million –
– Conference Call Scheduled for Today at 8:00 a.m. ET –
NEWTON, Mass., Feb. 12, 2026 /PRNewswire/ -- Karyopharm Therapeutics Inc. (Nasdaq: KPTI), a commercial-stage pharmaceutical company pioneering novel cancer therapies, today reported financial results for the fourth quarter and full year ended December 31, 2025 and highlighted progress on key clinical development programs.
"As we enter 2026, Karyopharm is approaching a defining period marked by important upcoming clinical milestones and a continued focus on disciplined execution, positioning the Company at a potential inflection point," said Richard Paulson, President and Chief Executive Officer of Karyopharm. "While selinexor has established a durable commercial foundation in multiple myeloma within a highly competitive treatment landscape, our late-stage programs in myelofibrosis and endometrial cancer represent an opportunity to fundamentally expand the impact and scale of our franchise."
"Top-line data from our Phase 3 SENTRY trial in myelofibrosis are expected in March, and our organization is energized and well positioned to support the next phase of this program. If SENTRY is successful, we have the potential to meaningfully improve outcomes for patients and introduce the first-ever combination therapy in myelofibrosis, a setting with significant unmet need. In endometrial cancer, we remain on track to report top-line data in mid-2026 from our Phase 3 trial evaluating selinexor in a defined, biomarker-driven patient population with limited effective treatment options. With the upcoming myelofibrosis readout as a key near-term catalyst and endometrial cancer representing a subsequent opportunity for further expansion, 2026 positions Karyopharm at a potential inflection point as we work to translate our science into durable patient impact and long-term value creation," added Mr. Paulson.
Fourth Quarter 2025 Highlights
XPOVIO Commercial Performance
U.S. net product revenue was $114.9 million for the year ended December 31, 2025 compared to $112.8 million for the year ended December 31, 2024. U.S. net product revenue for the fourth quarter of 2025 was $32.1 million compared to $29.3 million for the fourth quarter of 2024.
Demand for XPOVIO was consistent in 2025 versus 2024 in the highly competitive multiple myeloma marketplace, with the community setting continuing to drive approximately 60% of overall net product revenue.
Global patient access for selinexor expanded in 2025, with favorable reimbursement decisions in Spain and China, and additional regulatory approvals in multiple countries with selinexor now approved in more than 50 countries.
Research and Development (R&D) Highlights
Myelofibrosis
Completed enrollment in early September 2025 of the Phase 3 SENTRY trial (XPORT-MF-034; NCT04562389) which is evaluating 60 mg once-weekly selinexor in combination with ruxolitinib compared to ruxolitinib plus placebo in 353 JAKi-naïve patients with myelofibrosis. The preliminary baseline characteristics for patients enrolled in SENTRY as presented at the American Society of Hematology 2025 Annual Meeting (n=320) are representative of the intended patient population. In addition, preliminary blinded aggregate safety data from the first 61 patients with a median follow-up of greater than 12 months may suggest improvements in both hematologic and non-hematologic treatment-emergent adverse events as compared to the Phase 1 data evaluating selinexor 60 mg weekly in combination with standard of care ruxolitinib in JAKi-naïve myelofibrosis patients, as well as historical ruxolitinib monotherapy data. The Company cautions that preliminary baseline characteristics and preliminary blinded aggregate safety data from the Phase 3 SENTRY trial may not ultimately be reflective of the actual trial results.
Endometrial Cancer
Enrollment continues in the Phase 3 XPORT-EC-042 trial (NCT05611931) evaluating selinexor as a maintenance-only therapy following systemic therapy versus placebo in patients with TP53 wild-type advanced or recurrent endometrial cancer.
Multiple Myeloma
Enrollment in the Phase 3 XPORT-MM-031 trial (EMN29; NCT05028348) was completed in the fourth quarter of 2024 (n=117). The trial is being conducted in collaboration with the European Myeloma Network and is evaluating the all-oral combination of selinexor 40 mg, pomalidomide and dexamethasone (SPd40) in patients with previously treated multiple myeloma who received an anti-CD38 in their immediate prior line of therapy.
Anticipated Catalysts and Operational Objectives
Myelofibrosis
Top-line data from the Phase 3 SENTRY trial is expected in March 2026.
Top-line data from all patients in the 60 mg cohort of the Phase 2 SENTRY-2 trial (NCT05980806) with at least 24 weeks of follow-up is expected in the second half of 2026. The Company continues to enroll patients into the Phase 2 SENTRY-2 trial.
Endometrial Cancer
Top-line data from the event-driven, Phase 3 XPORT-EC-042 trial is expected in mid-2026. The Company continues to enroll patients into the XPORT-EC-042 trial of selinexor as a maintenance monotherapy for patients with TP53 wild-type advanced or recurrent endometrial cancer.
Multiple Myeloma
Maintain the Company's commercial foundation in the increasingly competitive multiple myeloma marketplace and drive increased XPOVIO revenues.
Continue to support global launches by our partners following regulatory and reimbursement approvals for selinexor in ex-U.S. territories.
Top-line data from the event-driven, Phase 3 XPORT-MM-031 (EMN29) trial is expected in the second half of 2026.
2026 Financial Outlook
Based on its current operating plans, Karyopharm expects the following for full year 2026:
Total revenue to be in the range of $130 million to $150 million. Total revenue consists of U.S. XPOVIO net product revenue and license, royalty and milestone revenue earned from partners.
U.S. XPOVIO net product revenue to be in the range of $115 million to $130 million.
R&D and selling, general and administrative (SG&A) expenses to be in the range of $230 million to $245 million.
The Company expects its existing liquidity, including cash, cash equivalents and investments, as well as cash flow from net product revenue and license and other revenue, will enable it to fund its current operating plans into the second quarter of 2026.
Full Year and Fourth Quarter 2025 Financial Results
Total revenue: Total revenue for the fourth quarter of 2025 was $34.1 million, compared to $30.5 million for the fourth quarter of 2024, and $146.1 million for the year ended December 31, 2025, compared to $145.2 million for the prior year.
Net product revenue: Net product revenue was $32.1 million for the fourth quarter of 2025, compared to $29.3 million for the fourth quarter of 2024, and $114.9 million for the year ended December 31, 2025, compared to $112.8 million for the prior year.
License and other revenue: License and other revenue was $2.0 million for the fourth quarter of 2025, compared to $1.3 million for the fourth quarter of 2024, and $31.2 million for the year ended December 31, 2025, compared to $32.4 million for the prior year.
Cost of sales: Cost of sales was $1.5 million for the fourth quarter of 2025, compared to $1.3 million for the fourth quarter of 2024, and $5.9 million for the year ended December 31, 2025 compared to $6.0 million for the prior year.
R&D expenses: R&D expenses were $27.7 million for the fourth quarter of 2025, compared to $33.3 million for the fourth quarter of 2024, and $125.6 million for the year ended December 31, 2025, compared to $143.2 million for the prior year. The decreases in both periods reflect lower personnel and stock-based compensation costs and reduced overall clinical trial spending, partially offset by increased clinical trial and related costs for our myelofibrosis program.
SG&A expenses: SG&A expenses were $22.8 million for the fourth quarter of 2025, compared to $27.2 million for the fourth quarter of 2024, and $105.2 million for the year ended December 31, 2025, compared to $115.4 million for the prior year. The decreases in both periods reflect lower personnel-related costs and reduced commercial spending as part of the Company's cost reduction initiatives.
Loss from operations: Loss from operations was $17.8 million for the fourth quarter of 2025, compared to $31.3 million for the fourth quarter of 2024, representing a 43% improvement. For the year ended December 31, 2025, loss from operations was $90.7 million, compared to $119.4 million for the prior year, representing a 24% improvement. The decreases reflect improved operating efficiency and disciplined cost management.
Interest income: Interest income was $0.6 million for the fourth quarter of 2025, compared to $1.5 million for the fourth quarter of 2024, and $2.8 million for the year ended December 31, 2025, compared to $7.4 million for the prior year. The decreases in both periods reflect lower investment balances during 2025 compared to 2024.
Interest expense: Interest expense was $12.6 million for the fourth quarter of 2025, compared to $11.2 million for the fourth quarter of 2024, and $45.8 million for the year ended December 31, 2025, compared to $37.4 million for the prior year. The increases in both periods reflect higher outstanding debt and higher interest rates following the Company's financing transactions executed in October 2025.
(Loss) gain on extinguishment of debt: (Loss) gain on extinguishment of debt was a loss of $62.4 million for the year ended December 31, 2025, compared to a gain of $44.7 million for the prior year. The change reflects the impact of financing transactions completed in 2025, compared to 2024.
Other (expense) income, net: Other (expense) income, net was $10.0 million of expense in the fourth quarter of 2025, compared to $10.1 million of income in the fourth quarter of 2024, and $0.2 million of income for the year ended December 31, 2025, compared to $28.4 million in the prior year. The amounts primarily reflect non-cash fair value remeasurements of embedded derivatives and liability-classified common stock warrants related to the refinancing transactions completed in the second quarter of 2024 and the fourth quarter of 2025.
Net loss: Net loss was $102.2 million, or $5.71 per basic and diluted share, for the fourth quarter of 2025, compared to $30.8 million, or $3.67 per basic and diluted share, for the fourth quarter of 2024. Net loss for the year ended December 31, 2025 was $196.0 million, or $17.93 per basic and diluted share, compared to $76.4 million, or $9.41 per basic share and $14.00 per diluted share, for the prior year. Net loss included non-cash stock-based compensation expense of $3.9 million in each of the fourth quarters of 2025 and 2024, and $14.1 million and $18.4 million for the years ended December 31, 2025 and 2024, respectively. More than half of the full-year loss was driven by below-the-line items, primarily the loss on extinguishment of debt and interest expense, which are largely non-cash in nature.
Cash position: Cash, cash equivalents, restricted cash and investments as of December 31, 2025 totaled $64.1 million, compared to $109.1 million as of December 31, 2024.
Conference Call Information
Karyopharm will host a conference call today, February 12, 2026, at 8:00 a.m. Eastern Time, to discuss the fourth quarter 2025 financial results, the financial outlook for 2026 and to provide other business updates. To access the conference call, please dial (800) 836-8184 (local) or (646) 357-8785 (international) at least 10 minutes prior to the start time and ask to be joined into the Karyopharm Therapeutics call. A live audio webcast of the call, along with accompanying slides, will be available under "Events & Presentations" in the Investor section of the Company's website. An archived webcast will be available on the Company's website approximately two hours after the event.
About the Phase 3 SENTRY Trial
SENTRY (XPORT-MF-034; NCT04562389) is a Phase 3 clinical trial evaluating a once-weekly dose of 60 mg of selinexor in combination with ruxolitinib compared to placebo plus ruxolitinib in JAKi-naïve myelofibrosis patients with platelet counts >100 x 10
9/L. Patients are randomized 2-to-1 to the selinexor arm. The co-primary endpoints for this trial are spleen volume reduction ≥ 35% (SVR35) at week 24 and the average change in absolute total symptom score (Abs-TSS) over 24 weeks relative to baseline.
About Myelofibrosis
Myelofibrosis is a rare blood cancer that affects approximately 20,000 patients in the United States and 17,000 patients in the European Union1. The disease causes bone marrow fibrosis (scarring in the bone marrow), which makes it difficult for the bone marrow to make healthy blood cells, splenomegaly (enlarged spleen), progressive anemia which often leads to symptoms like fatigue and weakness, and other disease associated symptoms including abdominal discomfort, pain under the left ribs, early satiety, night sweats and bone pain. The only approved class of therapies to treat myelofibrosis are JAK inhibitors, including ruxolitinib. Patients treated with the most commonly prescribed JAK inhibitor often require blood transfusions, and more than 30% will discontinue treatment due to anemia.2 Anemia and transfusion dependence are correlated with poor prognosis and shortened survival.3
About the Phase 3 XPORT-EC-042 Trial
EC-042 (XPORT-EC-042; NCT05611931) is a global, Phase 3, randomized, double-blind clinical trial evaluating selinexor as a maintenance therapy following systemic therapy in patients with TP53 wild-type advanced or recurrent endometrial cancer. The EC-042 trial is expected to enroll approximately 276 patients who will be randomized 1:1 to receive either a 60 mg, once-weekly, administration of oral selinexor or placebo until disease progression. The trial includes two patient populations, for which, the primary endpoint of progression free survival will be tested sequentially: 1) a modified intent to treat population (mITT) that will include patients with either, a) TP53 wild-type tumors with proficient mismatch repair status (pMMR); or, b) TP53 wild-type tumors with deficient mismatch repair status (dMMR), who are medically ineligible to receive checkpoint inhibitors; and, 2) the trial's original intent to treat (ITT) population, which includes all patients enrolled in the trial whose tumors are TP53 wild-type, regardless of MMR status. The key secondary endpoint of overall survival will be evaluated in the ITT population. The mITT population is expected to include approximately 220 patients. In connection with the EC-042 trial, Karyopharm entered into a global collaboration with Foundation Medicine, Inc. to develop FoundationOne®CDx, a tissue-based comprehensive genomic profiling test to identify and enroll patients whose tumors are TP53 wild-type.
About Endometrial Cancer
Endometrial cancer (EC) is the most common gynecologic malignancy in the U.S.1 In 2026, approximately 68,000 uterine cancers (predominantly endometrial) are expected to be diagnosed, with approximately 14,000 deaths.1 Worldwide there were about 420,368 cases with 97,723 deaths in 2022.2 Both incidence and mortality have continued to rise.3,4 Key risk factors include obesity, type 2 diabetes, high-fat diets, tamoxifen or oral estrogen use, and delayed menopause.5 TP53 is a well-recognized prognostic marker for EC; >50% of advanced or recurrent EC tumors are TP53wt (gene for tumor protein P53; wild-type), and ~40%-55% are both TP53wt and mismatch repair-proficient (pMMR).6-8 While immune checkpoint inhibitors have shown benefit in patients with mismatch repair–deficient (dMMR) and pMMR, the magnitude of benefit is greater for patients with dMMR tumors versus pMMR tumors.9-10 There remains an unmet need for targeted therapies for patients with pMMR EC.11
About XPOVIO® (selinexor)
XPOVIO is a first-in-class, oral exportin 1 (XPO1) inhibitor compound for the treatment of cancer. XPOVIO functions by selectively binding to and inhibiting the nuclear export protein XPO1. XPOVIO is approved in the U.S. and marketed by Karyopharm in multiple oncology indications, including: (i) in combination with VELCADE® (bortezomib) and dexamethasone (XVd) in adult patients with multiple myeloma after at least one prior therapy; (ii) in combination with dexamethasone in adult patients with heavily pre-treated multiple myeloma; and (iii) under accelerated approval in adult patients with diffuse large B-cell lymphoma (DLBCL), including DLBCL arising from follicular lymphoma, after at least two lines of systemic therapy. XPOVIO® (also known as NEXPOVIO® in certain countries) has received regulatory approvals in various indications in a growing number of ex-U.S. territories and countries, including but not limited to the European Union, the United Kingdom, Mainland China, Taiwan, Hong Kong, Australia, South Korea, Singapore, Israel, and Canada. XPOVIO®/NEXPOVIO® is marketed in these respective ex-U.S. territories by Karyopharm's partners: Antengene, Menarini, Neopharm, and FORUS. Selinexor is also being investigated in several other mid- and late-stage clinical trials across multiple high unmet need cancer indications, including in myelofibrosis and endometrial cancer.
For more information about Karyopharm's products or clinical trials, please contact the Medical Information department at: Tel: +1 (888) 209-9326; Email: [email protected]
XPOVIO® (selinexor) is a prescription medicine approved:
In combination with bortezomib and dexamethasone for the treatment of adult patients with multiple myeloma who have received at least one prior therapy (XVd).
In combination with dexamethasone for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least four prior therapies and whose disease is refractory to at least two proteasome inhibitors, at least two immunomodulatory agents, and an anti‐CD38 monoclonal antibody (Xd).
For the treatment of adult patients with relapsed or refractory diffuse large B‐cell lymphoma (DLBCL), not otherwise specified, including DLBCL arising from follicular lymphoma, after at least two lines of systemic therapy. This indication is approved under accelerated approval based on response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trial(s).
SELECT IMPORTANT SAFETY INFORMATION
Warnings and Precautions
Thrombocytopenia: Monitor platelet counts throughout treatment. Manage with dose interruption and/or reduction and supportive care.
Neutropenia: Monitor neutrophil counts throughout treatment. Manage with dose interruption and/or reduction and granulocyte colony‐stimulating factors.
Gastrointestinal Toxicity: Nausea, vomiting, diarrhea, anorexia, and weight loss may occur. Provide antiemetic prophylaxis. Manage with dose interruption and/or reduction, antiemetics, and supportive care.
Hyponatremia: Monitor serum sodium levels throughout treatment. Correct for concurrent hyperglycemia and high serum paraprotein levels. Manage with dose interruption, reduction, or discontinuation, and supportive care.
Serious Infection: Monitor for infection and treat promptly.
Neurological Toxicity: Advise patients to refrain from driving and engaging in hazardous occupations or activities until neurological toxicity resolves. Optimize hydration status and concomitant medications to avoid dizziness or mental status changes.
Embryo‐Fetal Toxicity: Can cause fetal harm. Advise females of reproductive potential and males with a female partner of reproductive potential, of the potential risk to a fetus and use of effective contraception.
Cataract: Cataracts may develop or progress. Treatment of cataracts usually requires surgical removal of the cataract.
Adverse Reactions
The most common adverse reactions (≥20%) in patients with multiple myeloma who receive XVd are fatigue, nausea, decreased appetite, diarrhea, peripheral neuropathy, upper respiratory tract infection, decreased weight, cataract and vomiting. Grade 3‐4 laboratory abnormalities (≥10%) are thrombocytopenia, lymphopenia, hypophosphatemia, anemia, hyponatremia and neutropenia. In the BOSTON trial, fatal adverse reactions occurred in 6% of patients within 30 days of last treatment. Serious adverse reactions occurred in 52% of patients. Treatment discontinuation rate due to adverse reactions was 19%.
The most common adverse reactions (≥20%) in patients with multiple myeloma who receive Xd are thrombocytopenia, fatigue, nausea, anemia, decreased appetite, decreased weight, diarrhea, vomiting, hyponatremia, neutropenia, leukopenia, constipation, dyspnea and upper respiratory tract infection. In the STORM trial, fatal adverse reactions occurred in 9% of patients. Serious adverse reactions occurred in 58% of patients. Treatment discontinuation rate due to adverse reactions was 27%.
The most common adverse reactions (incidence ≥20%) in patients with DLBCL, excluding laboratory abnormalities, are fatigue, nausea, diarrhea, appetite decrease, weight decrease, constipation, vomiting, and pyrexia. Grade 3‐4 laboratory abnormalities (≥15%) are thrombocytopenia, lymphopenia, neutropenia, anemia, and hyponatremia. In the SADAL trial, fatal adverse reactions occurred in 3.7% of patients within 30 days, and 5% of patients within 60 days of last treatment; the most frequent fatal adverse reactions was infection (4.5% of patients). Serious adverse reactions occurred in 46% of patients; the most frequent serious adverse reaction was infection (21% of patients). Discontinuation due to adverse reactions occurred in 17% of patients.
Use In Specific Populations
Lactation: Advise not to breastfeed.
For additional product information, including full prescribing information, please visit
.
To report SUSPECTED ADVERSE REACTIONS, contact Karyopharm Therapeutics Inc. at 1‐888‐209‐9326 or FDA at 1‐800‐FDA‐1088 or .
About Karyopharm Therapeutics
Karyopharm Therapeutics Inc. (Nasdaq: KPTI) is a commercial-stage pharmaceutical company whose dedication to pioneering novel cancer therapies is fueled by a belief in the extraordinary strength and courage of patients with cancer. Since its founding, Karyopharm has been an industry leader in oral compounds that address nuclear export dysregulation, a fundamental mechanism of oncogenesis. Karyopharm's lead compound and first-in-class, oral exportin 1 (XPO1) inhibitor, XPOVIO® (selinexor), is approved in the U.S. and marketed by the Company in three oncology indications. It has also received regulatory approvals in various indications in 50 ex-U.S. territories and countries, including the European Union, the United Kingdom (as NEXPOVIO®) and China. Karyopharm has a focused pipeline targeting indications in multiple high unmet need cancers, including in multiple myeloma, endometrial cancer, myelofibrosis, and diffuse large B-cell lymphoma (DLBCL). For more information about our people, science and pipeline, please visit , and follow us on LinkedIn and on X at @Karyopharm.
Forward-Looking Statements
This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. Such forward-looking statements include those regarding Karyopharm's guidance on its 2026 total revenue, 2026 U.S. net product revenue and 2026 R&D and SG&A expenses; expected cash runway and liquidity; Karyopharm's beliefs about the market opportunity and annual peak revenue opportunities for selinexor; expectations with respect to commercialization efforts; expectations regarding the timing of reporting top-line data from ongoing clinical trials; the ability of selinexor to treat patients with multiple myeloma, endometrial cancer, myelofibrosis, diffuse large B-cell lymphoma and other diseases; and expectations with respect to the clinical development plans and potential regulatory submissions of selinexor. Such statements are subject to numerous important factors, risks and uncertainties, many of which are beyond Karyopharm's control, that may cause actual events or results to differ materially from Karyopharm's current expectations. For example, there can be no guarantee that Karyopharm will successfully commercialize XPOVIO or that any of Karyopharm's drug candidates, including selinexor, will successfully complete necessary clinical development phases or that development of any of Karyopharm's drug candidates will continue. Further, there can be no guarantee that any positive developments in the development or commercialization of Karyopharm's drug candidate portfolio will result in stock price appreciation. Management's expectations and, therefore, any forward-looking statements in this press release could also be affected by risks and uncertainties relating to a number of other factors, including the following: the adoption of XPOVIO in the commercial marketplace, the timing and costs involved in commercializing XPOVIO or any of Karyopharm's drug candidates that receive regulatory approval; the ability to obtain and retain regulatory approval of XPOVIO or any of Karyopharm's drug candidates that receive regulatory approval; Karyopharm's results of clinical trials and preclinical trials, including subsequent analysis of existing data and new data received from ongoing and future trials; the content and timing of decisions made by the U.S. Food and Drug Administration and other regulatory authorities, investigational review boards at clinical trial sites and publication review bodies, including with respect to the need for additional clinical trials; the ability of Karyopharm or its third party collaborators or successors in interest to fully perform their respective obligations under the applicable agreement and the potential future financial implications of such agreement; Karyopharm's ability to enroll patients in its clinical trials; unplanned cash requirements and expenditures; substantial doubt exists regarding Karyopharm's ability to continue as a going concern; development or regulatory approval of drug candidates by Karyopharm's competitors for products or product candidates in which Karyopharm is currently commercializing or developing; and Karyopharm's ability to obtain, maintain and enforce patent and other intellectual property protection for any of its products or product candidates. These and other risks are described under the caption "Risk Factors" in Karyopharm's Quarterly Report on Form 10-Q for the quarter ended September 30, 2025, which was filed with the Securities and Exchange Commission (SEC) on November 3, 2025, and in other filings that Karyopharm may make with the SEC in the future. Any forward-looking statements contained in this press release speak only as of the date hereof, and, except as required by law, Karyopharm expressly disclaims any obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise.
XPOVIO® and NEXPOVIO® are registered trademarks of Karyopharm Therapeutics Inc.
SOURCE Karyopharm Therapeutics Inc.
21%
more press release views with
Request a Demo
临床3期上市批准财报临床2期免疫疗法
2026-01-12
– Top-Line Data from the Phase 3 SENTRY Trial in Myelofibrosis on Track for March 2026 –
– Top-Line Data from the Phase 3 XPORT-EC-042 Trial in Endometrial Cancer on Track for Mid-2026 –
– Preliminary Unaudited Full Year 2025 Total Revenue and U.S. XPOVIO® (selinexor) Net Product Revenue Expected to be Approximately $145 Million and $115 Million, Respectively –
NEWTON, Mass., Jan. 12, 2026 /PRNewswire/ -- Karyopharm Therapeutics Inc. (Nasdaq: KPTI), a commercial-stage pharmaceutical company pioneering novel cancer therapies, today announced preliminary unaudited fourth quarter and full year 2025 total revenue and U.S. XPOVIO net product revenue estimates and outlined its 2025 achievements and 2026 objectives.
"2026 has the promise to be a transformative year for Karyopharm and the patient communities that we intend to serve, with top-line data from our Phase 3 SENTRY trial in myelofibrosis expected in March. Positive data from our SENTRY trial could unlock our opportunity to improve patient outcomes and redefine the standard-of-care in myelofibrosis. Our teams are actively preparing for regulatory filings, commercialization and the opportunity to rapidly launch with the first ever combination therapy in a multi-billion dollar market," said Richard Paulson, President and Chief Executive Officer of Karyopharm. "In endometrial cancer, we remain focused and on track to report top-line data from our Phase 3 XPORT-EC-042 trial in mid-2026, representing a significant opportunity to transform patient outcomes in a targeted, biomarker driven patient population. With two high-potential data readouts this year, 2026 is expected to be a catalyst-rich year that could position us for tremendous long-term value creation."
Key Program Highlights in 2025
Selinexor in Multiple Myeloma
Demand for XPOVIO was consistent in 2025 versus 2024 in the increasingly competitive multiple myeloma marketplace, with the community setting continuing to drive approximately 60% of overall net product revenue.
Global patient access for selinexor expanded in 2025, with favorable reimbursement decisions in Spain and China, and additional regulatory approvals in multiple countries where selinexor is now approved in more than 50 countries.
Selinexor in Myelofibrosis
Completed enrollment of the Phase 3 SENTRY trial (XPORT-MF-034; NCT04562389) with 353 patients in early September 2025. SENTRY is evaluating 60 mg once-weekly selinexor in combination with ruxolitinib compared to ruxolitinib plus placebo. The preliminary baseline characteristics for patients enrolled in SENTRY as presented at the American Society of Hematology 2025 Annual Meeting (n=320) are representative of the intended patient population. In addition, preliminary blinded aggregate safety data from the first 61 patients with a median follow-up of greater than 12 months may suggest improvements in both hematologic and non-hematologic treatment emergent adverse events as compared to the Phase 1 data evaluating selinexor 60 mg weekly in combination with standard of care ruxolitinib in JAKi-naïve myelofibrosis patients, as well as historical ruxolitinib monotherapy data. The Company cautions that preliminary baseline characteristics and preliminary blinded aggregate safety data from the Phase 3 SENTRY trial may not ultimately be reflective of the actual trial results.
Presented data from the XPORT-MF-035 (NCT04562870) Phase 2, randomized, open-label trial of selinexor versus physician's-choice in hard-to-treat patients with heavily pretreated myelofibrosis (n=24) at the European Hematology Association 2025 Congress. The data suggest the potential for single-agent clinical activity with selinexor, including spleen volume reduction, symptom improvement, hemoglobin stabilization, reduced transfusion burden, and evidence of disease modification.
Selinexor in Endometrial Cancer
Modified the design of the Phase 3 XPORT-EC-042 (NCT05611931) trial to: a) focus enrollment on patients with either: i) proficient mismatch repair status (pMMR) tumors; or ii) patients with deficient mismatch repair status (dMMR) tumors who are medically ineligible for checkpoint inhibitors; b) introduce a new modified intent-to-treat (ITT) population of approximately 220 patients comprised of this focused population; and, c) increase the ITT sample size to approximately 276 patients.
Enrollment continues in the Phase 3 XPORT-EC-042 trial evaluating selinexor as a maintenance-only therapy following systemic therapy versus placebo in patients with TP53 wild-type advanced or recurrent endometrial cancer.
Corporate and Financial Highlights for 2025
Based on preliminary unaudited financial information, the Company expects total revenue, which includes license and royalty revenue from partners, to be approximately $33 million for the fourth quarter 2025 and approximately $145 million for the full year 2025, and U.S. XPOVIO net product revenue to be approximately $32 million for the fourth quarter 2025 and approximately $115 million for the full year 2025.
Completed strategic financing transactions that extended cash runway beyond the expected top-line readout of the Phase 3 SENTRY trial in myelofibrosis.
Cash, cash equivalents, restricted cash and investments as of December 31, 2025 were approximately $64 million. The Company expects its existing liquidity, including the revenue it expects to generate from XPOVIO net product sales and its license agreements, will be sufficient to fund its planned operations into the second quarter of 2026.
The financial information presented in this press release may be adjusted as a result of the completion of customary annual review and audit procedures.
Anticipated Catalysts and Operational Objectives in 2026
Myelofibrosis
Top-line data from the Phase 3 SENTRY trial is expected in March 2026.
The Company expects to report top-line data from all patients in the 60 mg cohort of the Phase 2 SENTRY-2 trial with at least 24 weeks of follow-up in the second half of 2026.
Endometrial Cancer
Top-line data from the event-driven, Phase 3 XPORT-EC-042 trial is expected in mid-2026. The Company continues to enroll patients into the XPORT-EC-042 trial of selinexor as a maintenance monotherapy for patients with TP53 wild-type advanced or recurrent endometrial cancer.
Multiple Myeloma
Maintain the Company's commercial foundation in the increasingly competitive multiple myeloma marketplace and drive increased XPOVIO revenues.
Continue to support global launches by our partners following regulatory and reimbursement approvals for selinexor in ex-U.S. territories.
Continue to follow patients that are enrolled in the Phase 3 XPORT-MM-031 (EMN29) trial. The Company expects to report top-line data from this event-driven trial in the second half of 2026.
Corporate Presentation
Karyopharm will be posting an updated corporate overview presentation on its website today. The presentation will be accessible under "Events & Presentations" in the Investor section of the Company's website, .
About the Phase 3 SENTRY Trial
SENTRY (XPORT-MF-034; NCT04562389) is a Phase 3 clinical trial evaluating a once-weekly dose of 60 mg of selinexor in combination with ruxolitinib compared to placebo plus ruxolitinib in JAKi-naïve myelofibrosis patients with platelet counts >100 x 10
9/L. Patients are randomized 2-to-1 to the selinexor arm. The co-primary endpoints for this trial are spleen volume reduction ≥ 35% (SVR35) at week 24 and the average change in absolute total symptom score (Abs-TSS) over 24 weeks relative to baseline.
About Myelofibrosis
Myelofibrosis is a rare blood cancer that affects approximately 20,000 patients in the United States and 17,000 patients in the European Union1. The disease causes bone marrow fibrosis (scarring in the bone marrow), which makes it difficult for the bone marrow to make healthy blood cells, splenomegaly (enlarged spleen), progressive anemia which often leads to symptoms like fatigue and weakness, and other disease associated symptoms including abdominal discomfort, pain under the left ribs, early satiety, night sweats and bone pain. The only approved class of therapies to treat myelofibrosis are JAK inhibitors, including ruxolitinib. Patients treated with the most commonly prescribed JAK inhibitor often require blood transfusions, and more than 30% will discontinue treatment due to anemia.2 Anemia and transfusion dependence are correlated with poor prognosis and shortened survival.3
1. Clarivate/DRG (2023)
2. Palandri, F., Palumbo, G.A., Elli, E.M. et al. Ruxolitinib discontinuation syndrome: incidence, risk factors, and management in 251 patients with myelofibrosis. Blood Cancer J. 11, 4 (2021).
3. Pardanani, A., & Tefferi, A. (2011). Prognostic relevance of anemia and transfusion dependency in myelodysplastic syndromes and primary myelofibrosis. Haematologica, 96(1), 8–10.
About the Phase 3 XPORT-EC-042 Trial
EC-042 (XPORT-EC-042; NCT05611931) is a global, Phase 3, randomized, double-blind clinical trial evaluating selinexor as a maintenance therapy following systemic therapy in patients with TP53 wild-type advanced or recurrent endometrial cancer. The EC-042 trial is expected to enroll approximately 276 patients who will be randomized 1:1 to receive either a 60 mg, once-weekly, administration of oral selinexor or placebo until disease progression. The trial includes two patient populations, for which, the primary endpoint of progression free survival will be tested sequentially and the key secondary endpoint of overall survival will be evaluated: 1) a modified intent to treat population (mITT) that will include patients with either, a) TP53 wild-type tumors with proficient mismatch repair status (pMMR); or, b) TP53 wild-type tumors with deficient mismatch repair status (dMMR), who are medically ineligible to receive checkpoint inhibitors; and, 2) the trial's original intent to treat (ITT) population, which will include all patients enrolled in the trial whose tumors are TP53 wild-type, regardless of MMR status. The mITT population is expected to include approximately 220 patients. In connection with the EC-042 trial, Karyopharm entered into a global collaboration with Foundation Medicine, Inc. to develop FoundationOne®CDx, a tissue-based comprehensive genomic profiling test to identify and enroll patients whose tumors are TP53 wild-type.
About Endometrial Cancer
Endometrial cancer (EC) is the most common gynecologic malignancy in the U.S.1 In 2025, approximately 69,120 uterine cancers (predominantly endometrial) are expected to be diagnosed, with 13,860 deaths.1 In 2022, there were about 420,368 cases with 97,723 deaths worldwide.2 Both incidence and mortality have continued to rise.3,4 Key risk factors include obesity, type 2 diabetes, high-fat diets, tamoxifen or oral estrogen use, and delayed menopause.5 TP53 is a well-recognized prognostic marker for EC; >50% of advanced or recurrent EC tumors are TP53wt (gene for tumor protein P53; wild-type), and ~40%-55% are both TP53wt and mismatch repair-proficient (pMMR).6-8 While immune checkpoint inhibitors have shown benefit in patients with mismatch repair–deficient (dMMR) and pMMR, the magnitude of benefit is greater for patients with dMMR tumors versus pMMR tumors.9-10 There remains an unmet need for targeted therapies for patients with pMMR EC.11
1. American Cancer Society. Cancer Facts & Figures 2025. . Accessed October 15, 2025
2. IARC GLOBOCAN 2022, Global Estimates
3. Lu KH, et al. N Engl J Med. 2020;383:2053-2064
4. NCI. Cancer stat facts: uterine cancer. . Accessed October 7, 2025
5. American Cancer Society, Endometrial Cancer Risk Factors, 2025
6. Leslie KK, et al. Gynecol Oncol. 2021;161(1):113-121.
7. Vergote I, et al. J Clin Oncol. 2023;41(35):5400-5410.
8. Mirza MR, et al. Presentation at: ESMO Congress; October 20-24, 2023
9. Mirza MR, et al. N Engl J Med. 2023; 388:2145-2158.
10. Eskander RN, et al. N Eng J Med. 2023;388:2159-2170.
11. Makker V, et al. Gynecol Oncol. 2024 Jun:185: 202-211
About XPOVIO® (selinexor)
XPOVIO is a first-in-class, oral exportin 1 (XPO1) inhibitor and the first of Karyopharm's Selective Inhibitor of Nuclear Export (SINE) compounds for the treatment of cancer. XPOVIO functions by selectively binding to and inhibiting the nuclear export protein XPO1. XPOVIO is approved in the U.S. and marketed by Karyopharm in multiple oncology indications, including: (i) in combination with VELCADE® (bortezomib) and dexamethasone (XVd) in adult patients with multiple myeloma after at least one prior therapy; (ii) in combination with dexamethasone in adult patients with heavily pre-treated multiple myeloma; and (iii) under accelerated approval in adult patients with diffuse large B-cell lymphoma (DLBCL), including DLBCL arising from follicular lymphoma, after at least two lines of systemic therapy. XPOVIO® (also known as NEXPOVIO® in certain countries) has received regulatory approvals in various indications in a growing number of ex-U.S. territories and countries, including but not limited to the European Union, the United Kingdom, Mainland China, Taiwan, Hong Kong, Australia, South Korea, Singapore, Israel, and Canada. XPOVIO®/NEXPOVIO® is marketed in these respective ex-U.S. territories by Karyopharm's partners: Antengene, Menarini, Neopharm, and FORUS. Selinexor is also being investigated in several other mid- and late-stage clinical trials across multiple high unmet need cancer indications, including in myelofibrosis and endometrial cancer.
For more information about Karyopharm's products or clinical trials, please contact the Medical Information department at: Tel: +1 (888) 209-9326; Email: [email protected]
XPOVIO® (selinexor) is a prescription medicine approved:
In combination with bortezomib and dexamethasone for the treatment of adult patients with multiple myeloma who have received at least one prior therapy (XVd).
In combination with dexamethasone for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least four prior therapies and whose disease is refractory to at least two proteasome inhibitors, at least two immunomodulatory agents, and an anti‐CD38 monoclonal antibody (Xd).
For the treatment of adult patients with relapsed or refractory diffuse large B‐cell lymphoma (DLBCL), not otherwise specified, including DLBCL arising from follicular lymphoma, after at least two lines of systemic therapy. This indication is approved under accelerated approval based on response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trial(s).
SELECT IMPORTANT SAFETY INFORMATION
Warnings and Precautions
Thrombocytopenia: Monitor platelet counts throughout treatment. Manage with dose interruption and/or reduction and supportive care.
Neutropenia: Monitor neutrophil counts throughout treatment. Manage with dose interruption and/or reduction and granulocyte colony‐stimulating factors.
Gastrointestinal Toxicity: Nausea, vomiting, diarrhea, anorexia, and weight loss may occur. Provide antiemetic prophylaxis. Manage with dose interruption and/or reduction, antiemetics, and supportive care.
Hyponatremia: Monitor serum sodium levels throughout treatment. Correct for concurrent hyperglycemia and high serum paraprotein levels. Manage with dose interruption, reduction, or discontinuation, and supportive care.
Serious Infection: Monitor for infection and treat promptly.
Neurological Toxicity: Advise patients to refrain from driving and engaging in hazardous occupations or activities until neurological toxicity resolves. Optimize hydration status and concomitant medications to avoid dizziness or mental status changes.
Embryo‐Fetal Toxicity: Can cause fetal harm. Advise females of reproductive potential and males with a female partner of reproductive potential, of the potential risk to a fetus and use of effective contraception.
Cataract: Cataracts may develop or progress. Treatment of cataracts usually requires surgical removal of the cataract.
Adverse Reactions
The most common adverse reactions (≥20%) in patients with multiple myeloma who receive XVd are fatigue, nausea, decreased appetite, diarrhea, peripheral neuropathy, upper respiratory tract infection, decreased weight, cataract and vomiting. Grade 3‐4 laboratory abnormalities (≥10%) are thrombocytopenia, lymphopenia, hypophosphatemia, anemia, hyponatremia and neutropenia. In the BOSTON trial, fatal adverse reactions occurred in 6% of patients within 30 days of last treatment. Serious adverse reactions occurred in 52% of patients. Treatment discontinuation rate due to adverse reactions was 19%.
The most common adverse reactions (≥20%) in patients with multiple myeloma who receive Xd are thrombocytopenia, fatigue, nausea, anemia, decreased appetite, decreased weight, diarrhea, vomiting, hyponatremia, neutropenia, leukopenia, constipation, dyspnea and upper respiratory tract infection. In the STORM trial, fatal adverse reactions occurred in 9% of patients. Serious adverse reactions occurred in 58% of patients. Treatment discontinuation rate due to adverse reactions was 27%.
The most common adverse reactions (incidence ≥20%) in patients with DLBCL, excluding laboratory abnormalities, are fatigue, nausea, diarrhea, appetite decrease, weight decrease, constipation, vomiting, and pyrexia. Grade 3‐4 laboratory abnormalities (≥15%) are thrombocytopenia, lymphopenia, neutropenia, anemia, and hyponatremia. In the SADAL trial, fatal adverse reactions occurred in 3.7% of patients within 30 days, and 5% of patients within 60 days of last treatment; the most frequent fatal adverse reactions was infection (4.5% of patients). Serious adverse reactions occurred in 46% of patients; the most frequent serious adverse reaction was infection (21% of patients). Discontinuation due to adverse reactions occurred in 17% of patients.
Use In Specific Populations
Lactation: Advise not to breastfeed.
For additional product information, including full prescribing information, please visit
.
To report SUSPECTED ADVERSE REACTIONS, contact Karyopharm Therapeutics Inc. at 1‐888‐209‐9326 or FDA at 1‐800‐FDA‐1088 or
.
About Karyopharm Therapeutics
Karyopharm Therapeutics Inc. (Nasdaq: KPTI) is a commercial-stage pharmaceutical company whose dedication to pioneering novel cancer therapies is fueled by a belief in the extraordinary strength and courage of patients with cancer. Since its founding, Karyopharm has been an industry leader in oral compounds that address nuclear export dysregulation, a fundamental mechanism of oncogenesis. Karyopharm's lead compound and first-in-class, oral exportin 1 (XPO1) inhibitor, XPOVIO® (selinexor), is approved in the U.S. and marketed by the Company in three oncology indications. It has also received regulatory approvals in various indications in more than 50 ex-U.S. territories and countries, including the European Union, the United Kingdom (as NEXPOVIO®) and China. Karyopharm has a focused pipeline targeting indications in multiple high unmet need cancers, including in multiple myeloma, endometrial cancer, myelofibrosis, and diffuse large B-cell lymphoma (DLBCL). For more information about our people, science and pipeline, please visit , and follow us on LinkedIn and on X at @Karyopharm.
Forward-Looking Statements
This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. Such forward-looking statements include those regarding Karyopharm's preliminary financial information for the fourth quarter and full year 2025; expected cash runway and liquidity; expectations with respect to commercialization efforts; expectations regarding the timing of reporting top-line data from ongoing clinical trials; the ability of selinexor to treat patients with multiple myeloma, endometrial cancer, myelofibrosis, diffuse large B-cell lymphoma and other diseases; and expectations with respect to the clinical development plans and potential regulatory submissions of selinexor. Such statements are subject to numerous important factors, risks and uncertainties, many of which are beyond Karyopharm's control, that may cause actual events or results to differ materially from Karyopharm's current expectations. For example, there can be no guarantee that Karyopharm will successfully commercialize XPOVIO or that any of Karyopharm's drug candidates, including selinexor, will successfully complete necessary clinical development phases or that development of any of Karyopharm's drug candidates will continue. Further, there can be no guarantee that any positive developments in the development or commercialization of Karyopharm's drug candidate portfolio will result in stock price appreciation. Management's expectations and, therefore, any forward-looking statements in this press release could also be affected by risks and uncertainties relating to a number of other factors, including the following: the adoption of XPOVIO in the commercial marketplace, the timing and costs involved in commercializing XPOVIO or any of Karyopharm's drug candidates that receive regulatory approval; the ability to obtain and retain regulatory approval of XPOVIO or any of Karyopharm's drug candidates that receive regulatory approval; Karyopharm's results of clinical trials and preclinical trials, including subsequent analysis of existing data and new data received from ongoing and future trials; the content and timing of decisions made by the U.S. Food and Drug Administration and other regulatory authorities, investigational review boards at clinical trial sites and publication review bodies, including with respect to the need for additional clinical trials; the ability of Karyopharm or its third party collaborators or successors in interest to fully perform their respective obligations under the applicable agreement and the potential future financial implications of such agreement; Karyopharm's ability to enroll patients in its clinical trials; unplanned cash requirements and expenditures; substantial doubt exists regarding Karyopharm's ability to continue as a going concern; development or regulatory approval of drug candidates by Karyopharm's competitors for products or product candidates in which Karyopharm is currently commercializing or developing; and Karyopharm's ability to obtain, maintain and enforce patent and other intellectual property protection for any of its products or product candidates. These and other risks are described under the caption "Risk Factors" in Karyopharm's Quarterly Report on Form 10-Q for the quarter ended September 30, 2025, which was filed with the Securities and Exchange Commission (SEC) on November 3, 2025, and in other filings that Karyopharm may make with the SEC in the future. Any forward-looking statements contained in this press release speak only as of the date hereof, and, except as required by law, Karyopharm expressly disclaims any obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise.
XPOVIO® and NEXPOVIO® are registered trademarks of Karyopharm Therapeutics Inc.
SOURCE Karyopharm Therapeutics Inc.
21%
more press release views with
Request a Demo
临床3期临床结果上市批准临床2期加速审批
100 项与 Tamoxifen 相关的药物交易
登录后查看更多信息
研发状态
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 阴道疾病 | 临床1期 | - | 2023-09-21 | |
| 性交困难 | 临床申请批准 | 美国 | 2023-12-07 | |
| 外阴和阴道萎缩 | 临床申请批准 | 美国 | 2023-12-07 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
| 研究 | 分期 | 人群特征 | 评价人数 | 分组 | 结果 | 评价 | 发布日期 |
|---|
N/A | - | Tamoxifen users | 簾壓餘鑰繭選願繭網觸(觸夢構夢廠願範餘衊築) = 獵蓋獵夢淵製壓鬱簾襯 餘簾艱製餘遞齋齋鏇製 (鏇簾醖繭淵憲憲簾艱壓 ) 更多 | - | 2023-09-01 | ||
Non-tamoxifen users | 簾壓餘鑰繭選願繭網觸(觸夢構夢廠願範餘衊築) = 顧範齋鏇選糧築糧窪膚 餘簾艱製餘遞齋齋鏇製 (鏇簾醖繭淵憲憲簾艱壓 ) 更多 | ||||||
N/A | - | (Uterine cancer patients) | 遞鬱選構鏇壓艱積簾夢(鏇窪糧簾醖鹹窪窪製積) = 網醖範範鏇憲積築壓齋 夢蓋選餘廠醖鹽鬱觸製 (觸遞顧糧壓鏇製齋遞窪 ) | - | 2023-09-01 | ||
N/A | 乳腺癌 ER/PR | 769 | 鏇衊範壓膚繭選鹹襯積(簾艱齋構繭壓襯蓋夢蓋) = 糧蓋觸鹽選鬱蓋齋構遞 鹽築鹹憲願獵餘憲壓製 (鑰憲膚衊膚齋鏇窪網齋 ) 更多 | 积极 | 2006-11-01 | ||
Tamoxifen + Radiation | 鏇衊範壓膚繭選鹹襯積(簾艱齋構繭壓襯蓋夢蓋) = 鑰繭鹽衊鏇艱憲糧網膚 鹽築鹹憲願獵餘憲壓製 (鑰憲膚衊膚齋鏇窪網齋 ) 更多 | ||||||
N/A | - | 觸選壓網製壓齋獵淵壓(衊齋觸壓遞網鏇糧製壓) = 糧淵積憲艱遞蓋憲壓鹽 範網積鬱觸構夢鬱繭鹹 (窪選觸淵鏇鹹鏇選醖鏇 ) 更多 | - | 2005-10-01 | |||
觸選壓網製壓齋獵淵壓(衊齋觸壓遞網鏇糧製壓) = 憲觸鬱獵簾顧艱廠鏇繭 範網積鬱觸構夢鬱繭鹹 (窪選觸淵鏇鹹鏇選醖鏇 ) 更多 | |||||||
N/A | - | - | Tamoxifen and radiation therapy (RTTAM) | 觸積蓋遞製繭鬱夢鑰獵(構製鹽齋顧鏇餘鏇鏇鏇) = 鏇製糧繭鹹夢觸積壓衊 蓋鏇構遞糧遞齋簾衊網 (鹹顧蓋壓觸憲簾淵艱遞 ) | - | 2005-10-01 | |
鏇鏇鹹範鑰顧糧構襯觸(襯範窪願積遞網夢獵築) = 鏇蓋簾製衊蓋齋膚顧糧 鹽憲餘鹹廠糧夢製鹽簾 (顧鏇願獵構構淵膚製簾 ) 更多 | |||||||
N/A | - | Tamoxifen + Radiation Therapy | 選窪鏇繭醖醖夢繭積積(廠簾齋衊膚艱獵遞遞膚) = 願遞壓齋製鹽簾範範壓 構廠網壓鑰鏇蓋簾鑰鹹 (鹽壓構範觸衊觸簾製鹹 ) 更多 | - | 2004-09-01 | ||
Tamoxifen alone | 選窪鏇繭醖醖夢繭積積(廠簾齋衊膚艱獵遞遞膚) = 齋淵糧膚鑰醖餘壓築衊 構廠網壓鑰鏇蓋簾鑰鹹 (鹽壓構範觸衊觸簾製鹹 ) 更多 | ||||||
N/A | - | 769 | 遞膚膚積構衊選蓋齋壓(襯艱蓋鹹積積膚憲淵積) = 襯選築範餘齋壓艱夢窪 網夢鹽製網廠衊鏇築齋 (醖廠願醖遞壓憲憲網鏇 ) 更多 | 积极 | 2001-11-01 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用