预约演示
更新于：2026-05-09
Selinexor
塞利尼索
更新于：2026-05-09
概要
基本信息
药物类型 小分子化药 |
别名 CRM1-nuclear-export-inhibitor、NEXPOVIO、Selinexor + [13] |
作用方式 抑制剂 |
作用机制 ACADS inhibitors(acyl-CoA dehydrogenase short chain inhibitors)、XPO1抑制剂(输出蛋白1抑制剂) |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (2019-07-03), |
最高研发阶段(中国)批准上市 |
特殊审评优先审评 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、优先审评 (中国)、附条件批准 (中国)、孤儿药 (韩国)、优先审评 (韩国)、孤儿药 (澳大利亚)、快速通道 (美国) |
登录后查看时间轴
结构/序列
分子式C17H11F6N7O |
InChIKeyDEVSOMFAQLZNKR-RJRFIUFISA-N |
CAS号1393477-72-9 |
关联
228
项与 塞利尼索 相关的临床试验NCT07479979
Phase Ib/II Study of Selinexor in Combination With Carfilzomib, Subcutaneous Isatuximab Administered Via Investigational Device and Dexamethasone (SCID) for Patients With Relapsed and/or Relapsed Refractory Multiple Myeloma
NCT07554482
A Prospective, Single-Arm, Multicenter, Phase II Clinical Study of Selinexor Combined With Reduced-Dose Radiotherapy in the Treatment of Early-Stage Extranodal NK/T-Cell Lymphoma
NCT07447817
Investigator-Initiated, Open-Label, Phase II Trial of Selinexor in Combination With Pacritinib in Patients With Myelofibrosis Who Are JAK Inhibitor-Naïve and Have Cytopenias (ILLUMINATE)
100 项与 塞利尼索 相关的临床结果
登录后查看更多信息
100 项与 塞利尼索 相关的转化医学
登录后查看更多信息
100 项与 塞利尼索 相关的专利（医药）
登录后查看更多信息
665
项与 塞利尼索 相关的文献（医药）2026-12-31ANNALS OF MEDICINE
Efficacy and safety of Ruxolitinib-based combination therapy in the patients with Myelofibrosis (MF): a systematic review and meta-analysis
Review
作者: Li, Yuxin ; Sun, Wanling ; Cao, Yaofang ; Hui, Wuhan ; Tan, Shuai
BACKGROUND:
Myelofibrosis (MF) is a chronic myeloproliferative neoplasm. Although Ruxolitinib, a JAK1/2 inhibitor, remains the cornerstone of MF treatment, it does not reverse disease progression, and resistance frequently emerges. These limitations have prompted investigation into combination therapies targeting pathways beyond the JAK-STAT axis. This meta-analysis aims to evaluate the efficacy and safety of Ruxolitinib-based combination therapies in patients with MF.
METHODS:
We conducted a systematic search of databases for studies published through August 1, 2025. Thirteen distinct Ruxolitinib-based combination regimens were included. Primary efficacy endpoints were ≥35% spleen volume reduction at 24 weeks (SVR35) and ≥50% reduction in total symptom score (TSS50). Safety endpoints focused on the incidence of grade 3/4 thrombocytopenia and anemia. Subgroup analyses were performed based on prior JAK inhibitor exposure and therapeutic mechanism of action.
RESULTS:
A total of 19 studies comprising 1,088 patients were included in the meta-analysis. Among JAK inhibitor-naïve patients, the combination of Ruxolitinib with Selinexor demonstrated the highest efficacy (SVR35: 92%; TSS50: 78%), followed by Ruxolitinib plus BMS-986158 (SVR35: 90%). For patients with prior JAK inhibitor exposure, Ruxolitinib plus Siremadlin (SVR35: 45%) showed notable activity.
CONCLUSION:
For JAK inhibitor-naïve patients, Ruxolitinib-based combination regimens demonstrated satisfactory clinical responses and the potential for meaningful disease control. For patients with prior JAK inhibitor exposure, the addition of combination therapy drugs may further enhance the efficacy. Personalized treatment selection remains essential, as therapeutic efficacy is significantly influenced by prior JAK inhibitor exposure.
2026-06-01BIOORGANIC CHEMISTRY
PET imaging of XPO1 engagement with [18F]selinexor: A pharmacodynamic theranostic strategy for multiple myeloma
Article
作者: Yan, Junjie ; Pan, Donghui ; Su, Chen ; Wang, Lizhen ; Zhong, Xinlin ; Yang, Min ; Wang, Xinyu ; Xu, Yuping ; Chen, Chongyang
Exportin 1 (XPO1), a nuclear export protein frequently overexpressed in multiple myeloma (MM), represents a validated therapeutic target. However, noninvasive imaging approaches capable of assessing XPO1 engagement and pharmacodynamic modulation during therapy remain limited. Here, we present the radiosynthesis and preclinical evaluation of [18F]selinexor, an XPO1-targeted positron emission tomography (PET) radiotracer derived from the clinically used drug selinexor via an 18F/19F isotope exchange method. This labeling approach preserves the parent drug's molecular structure and pharmacological characteristics, enabling in vivo tracking of selinexor. [18F]Selinexor was synthesized with a radiochemical yield of 23.9 ± 4.1% and molar activity of 0.41 ± 0.08 GBq/μmol. The tracer exhibited favorable stability, XPO1-specific binding, and tumor retention. PET imaging and pharmacokinetic analysis demonstrated rapid systemic distribution followed by slow elimination, closely consistent with known pharmacokinetics of selinexor. Predominant hepatobiliary clearance and prolonged blood retention supported optimal tumor uptake at delayed imaging time points, with tracer uptake peaking at 3 h post-injection in MM.1S (2.92 ± 0.30% ID/g) and NCI-H929 (2.50 ± 0.18% ID/g) xenografts. Uptake was markedly reduced upon blocking, confirming the tracer's in vivo specificity. During therapeutic intervention, repeated selinexor administration effectively suppressed tumor growth and was accompanied by a progressive reduction in tumor uptake from 3.03 ± 0.25% ID/g (day 0) to 0.93 ± 0.13% ID/g (day 15). Notably, this reduction in uptake occurred independently of changes in tumor volume and correlated with decreased XPO1 expression by immunohistochemistry. Conversely, doxorubicin reduced tumor size without affecting uptake, indicating preserved XPO1-associated signal. Together, these findings demonstrate that [18F]selinexor PET functions as a noninvasive imaging tool for evaluating the in vivo pharmacokinetics and pharmacodynamic behavior of selinexor, and capturing treatment-induced alterations in XPO1 engagement, although further structural optimization will be required prior to potential translation.
2026-05-05BRITISH JOURNAL OF CANCER
Enhanced nuclear export caused by O-GlcNAcylation of nucleoporins is a potential therapeutic target in mesothelioma
Article
作者: Sato, Tatsuhiro ; Mukai, Satomi ; Hiroshima, Kenzo ; Kato, Kagayaki ; Kamei, Yasuhiro ; Kondo-Ida, Lisa ; Yabuta, Norikazu ; Mishiro-Sato, Emi ; Sekido, Yoshitaka
BACKGROUND:
Mesothelioma is an aggressive malignancy with limited therapeutic options. Genetic alterations involving the Hippo pathway are commonly observed. O-GlcNAcylation is frequently elevated in cancer and drives tumour progression. However, its relationship with Hippo pathway dysfunction in mesothelioma remains unclear.
METHODS:
O-GlcNAcylation levels were examined in mesothelioma samples and cell lines, and O-GlcNAcylated proteins were detected by mass spectrometry. The functional impact of O-GlcNAcylation was determined by quantifying nuclear transport dynamics using light-induced live-cell imaging. Genetic and pharmacological inhibition of O-GlcNAcylation was evaluated in vitro. Treatment with the nuclear export inhibitor KPT-330 (Selinexor) was assessed in vitro and in a mouse xenograft model.
RESULTS:
O-GlcNAcylation was markedly increased in mesothelioma cells with Hippo pathway inactivation. This modification primarily targeted nuclear pore complex proteins, including NUP214 and NUP62, and significantly accelerated nuclear export rates. Suppression of O-GlcNAcylation diminished nuclear export and inhibited cell proliferation. Importantly, pharmacological blockade of nuclear export using KPT-330 suppressed cell growth in vitro and produced significant antitumour effects in vivo.
CONCLUSIONS:
These findings demonstrate O-GlcNAcylation-driven enhancement of nuclear export as a therapeutically actionable vulnerability in mesothelioma with inactivation of the Hippo pathway.
733
项与 塞利尼索 相关的新闻（医药）2026-05-08
·百度百家
100 项与 塞利尼索 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 滤泡性淋巴瘤 | 印尼 | 2025-03-05 | |
| 难治性多发性骨髓瘤 | 中国 | 2021-12-14 | |
| 复发性多发性骨髓瘤 | 中国 | 2021-12-14 | |
| 复发性弥漫性大B细胞淋巴瘤 | 以色列 | 2021-02-04 | |
| 难治性弥漫性大 B 细胞淋巴瘤 | 以色列 | 2021-02-04 | |
| 弥漫性大B细胞淋巴瘤 | 美国 | 2020-06-22 | |
| 多发性骨髓瘤 | 美国 | 2019-07-03 |
未上市
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 |
|---|---|---|---|---|
| 难治性急性髓细胞白血病 | 临床3期 | 中国 | 2023-01-29 | |
| 复发性急性髓细胞白血病 | 临床3期 | 中国 | 2023-01-29 | |
| 子宫内膜癌 | 临床3期 | 中国 | 2021-10-27 | |
| 子宫内膜癌 | 临床3期 | 中国 | 2021-10-27 | |
| 真性红细胞增多症后骨髓纤维化 | 临床3期 | 美国 | 2021-03-11 | |
| 真性红细胞增多症后骨髓纤维化 | 临床3期 | 澳大利亚 | 2021-03-11 | |
| 真性红细胞增多症后骨髓纤维化 | 临床3期 | 比利时 | 2021-03-11 | |
| 真性红细胞增多症后骨髓纤维化 | 临床3期 | 保加利亚 | 2021-03-11 | |
| 真性红细胞增多症后骨髓纤维化 | 临床3期 | 加拿大 | 2021-03-11 | |
| 真性红细胞增多症后骨髓纤维化 | 临床3期 | 捷克 | 2021-03-11 |
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
临床2期 | 18 | 遞範鑰糧艱選鏇顧繭構 = 壓遞夢齋觸糧鹹鏇積繭 淵鏇壓襯膚遞願鬱醖遞 (齋製齋築夢獵艱網夢糧, 襯餘鹽淵鏇壓構艱鹹襯 ~ 淵製選繭鹽網鹽壓齋壓) 更多 | - | 2026-03-06 | |||
临床1/2期 | 4 | 構範製醖餘願憲壓衊襯 = 繭壓顧顧憲繭遞鑰糧夢 齋糧餘構壓觸鏇鬱繭繭 (鹹鑰壓願艱顧構簾廠願, 製膚鹽醖簾遞積製顧壓 ~ 糧壓積襯獵遞鏇願顧齋) 更多 | - | 2026-01-29 | |||
临床1期 | 17 | Gemcitabine + Selinexor | 願膚簾糧鹽築淵積壓窪(憲齋鹹顧鹽淵選襯餘鏇) = gemcitabine at 1200 mg/m2 at 10 mg/m2/min followed by 60 mg weekly selinexor 衊選觸窪衊憲繭築廠製 (選簾築遞襯顧淵糧簾壓 ) 更多 | 积极 | 2026-01-20 | ||
临床2期 | 多发性骨髓瘤 一线 | 47 | 顧鬱繭鹽繭艱衊艱窪鏇(鹽觸選選築衊網艱鏇鹽) = 遞選繭艱鹹製觸遞夢餘 淵夢壓齋夢鏇願製獵餘 (憲糧製選遞餘醖積壓鹹 ) 更多 | 积极 | 2025-12-06 | ||
临床2期 | 肾功能不全 一线 | 63 | 餘範積廠餘願鏇範網膚(選鬱廠餘鏇壓積積糧壓) = 觸選繭製範憲鏇醖網鑰 窪糧鑰積願選壓膚窪壓 (艱獵蓋壓鹽簾鏇憲廠醖 ) 更多 | 积极 | 2025-12-06 | ||
临床1/2期 | 骨髓增生异常综合征 TP53 | 39 | (TP53 mutations) | 鏇淵觸艱衊窪繭艱夢蓋(簾願艱鏇積鑰繭願蓋築) = 積繭簾繭網艱廠網顧製 糧齋積膚願窪願築鹽醖 (構壓顧遞繭鬱膚齋繭獵 ) 更多 | 积极 | 2025-12-06 | |
N/A | 54 | 鏇鏇選鹽夢壓憲網艱鹹(積艱餘淵選鏇憲窪簾憲) = Grade 1 occurred in 9 patients (60%) and 28 patients (71.8%), respectively; Grade 2 in 1 patient (6.7%) and 4 patients (10.3%); Only one patient in the selinexor-based regimen group experienced Grade 4 (6.7%) CRS. There is no difference between the selinexor-based group and alternative regimen groups (grade 1-4: 73.3% vs 82.1% p=0.475; grade 3 and 4: 6.7% vs 0%; p=0.278). 繭獵鏇鹹襯鹹艱範積鑰 (醖蓋齋鬱壓獵網鏇顧鑰 ) 更多 | 积极 | 2025-12-06 | |||
Alternative regimen bridging CAR-T cell therapy | |||||||
临床2期 | 44 | Selinexor + R-CHOP | 範壓範範醖餘艱選鏇築(廠鏇獵範鹽艱遞糧獵襯) = 鬱鏇鏇憲餘觸願觸餘艱 齋範構鏇顧簾齋憲艱醖 (齋鑰蓋構觸遞選網選壓 ) 更多 | 积极 | 2025-12-06 | ||
临床2期 | 29 | 壓範鹽醖範醖醖鬱製獵(窪願膚築選醖糧廠鹹夢) = 廠夢衊鏇餘獵淵鹽獵襯 廠積遞蓋窪糧廠顧窪鬱 (夢夢憲憲範鑰觸製製網 ) 更多 | 不佳 | 2025-12-06 | |||
临床1/2期 | 多发性骨髓瘤 一线 | 21 | 壓簾壓醖蓋襯範齋廠鹽(鏇觸襯糧糧憲淵窪觸蓋) = 鹹繭淵築廠鹹醖憲淵積 襯糧壓鹽選醖範築築醖 (夢艱襯鹹醖蓋膚廠窪鹹 ) 更多 | 积极 | 2025-12-06 |
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