预约演示
更新于：2026-02-08
Selinexor
塞利尼索
更新于：2026-02-08
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 |
特殊审评快速通道 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (韩国)、孤儿药 (澳大利亚)、优先审评 (韩国)、优先审评 (美国)、附条件批准 (中国)、优先审评 (中国) |
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结构/序列
分子式C17H11F6N7O |
InChIKeyDEVSOMFAQLZNKR-RJRFIUFISA-N |
CAS号1393477-72-9 |
关联
221
项与 塞利尼索 相关的临床试验NCT07200102
Selinexor Maintenance Post CAR-T Cell Therapy for Multiple Myeloma
NCT07369739
Golidocitinib Combined With Selinexor for the Treatment of Chronic Active Epstein-Barr Virus Disease (CAEBVD): A Multicenter, Prospective, Single-arm Clinical Study
NCT07276698
Clinical Study on Maintenance Therapy With Selinexor Combined With Azacitidine After Allogeneic Hematopoietic Stem Cell Transplantation for NK/T-cell Lymphoma
100 项与 塞利尼索 相关的临床结果
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100 项与 塞利尼索 相关的转化医学
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100 项与 塞利尼索 相关的专利（医药）
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620
项与 塞利尼索 相关的文献（医药）2026-02-05BLOOD
PIKfyve inhibition in MM disrupts autophagy and lysosome function, increasing MHC expression and cholesterol metabolism
Article
作者: Moran, Michael F. ; Lee, Daniel K. C. ; Li, Zhihua ; Sepetov, Nikolai ; Stewart, A. Keith ; Trudel, Suzanne ; Simpson, Craig D. ; Abelman, Dor D. ; He, Ruijuan ; St. Paul, Michael ; Mak, Tak W. ; Tiedemann, Rodger ; Bruce, Jeffrey ; Wang, Ding Yan ; Bonolo de Campos, Cecilia ; Pugh, Trevor ; Issakova, Olga ; Wybeng-Groot, Leanne ; Pelino, Tessa
Abstract:
We previously reported a chemogenomics screen that unexpectedly identified phosphatidylinositol-3-phosphate 5-kinase (PIKfyve) as a vulnerable target in multiple myeloma (MM). PIKfyve is an essential regulator of lysosomal function and autophagy. Given the high basal requirement for autophagy in MM for sustainable immunoglobulin synthesis, targeting autophagy holds clinical potential as a novel therapeutic avenue. Here, we report the development and characterization of PIK001 and analogs, potent and selective novel small-molecule inhibitors of PIKfyve. PIK001 demonstrated potent anti-MM activity in vitro, as well as synergistic activity with established anti-MM agents (including venetoclax and selinexor), while retaining efficacy in lenalidomide-resistant models. Multiomic characterization of isogenic cell lines sensitive and resistant to PIK001 identified a catalytic domain mutation (PIKFYVE N1939K) and heterogenous alterations in autophagy capabilities. Importantly, we noted that PIK001 exposure also resulted in significantly increased cholesterol metabolism and upregulation of major histocompatibility complex (MHC) class I expression, with potential implications in tumor immunity. Beyond MM, PIKfyve inhibition also shows selective cytotoxicity in acute myeloid leukemia, melanoma, and renal cancer, highlighting broader therapeutic potential. These findings establish PIKfyve inhibition as a valid target for MM and other hematologic malignancies, provide insights into mechanisms of sensitivity and resistance, and lay the foundation for further preclinical (particularly the role of cholesterol metabolism and tumor immunity) and clinical development.
2026-02-02CANCER RESEARCH
Disrupting Paraspeckle Stability by Targeting WTX–NONO Phase Separation Enhances Chemotherapy Efficacy in Gastric Cancer
Article
作者: Li, Yanyan ; Hung, Mien-Chie ; Du, Meihang ; An, Liwei ; Xu, Yangwei ; Li, Yi-Chuan ; Sun, Fei ; Qian, Xuexia ; Bai, Junping ; Zhang, Huanhu ; Lin, Zhihao ; Li, Xuanqi ; Zhang, Qingling ; Zhao, Zhangting ; Han, Lijun ; Ye, Zaisheng ; Chen, Zetao
Abstract:
Nuclear paraspeckles play critical roles in orchestrating gene transcription to support tumor development and progression. Elucidating regulators of their dynamic compositions and formation could provide potential targets for treating cancer. In this study, we discovered that the short isoform of Wilms tumor gene on the X chromosome (WTX-S) specifically disrupted paraspeckle stability. WTX-S selectively interacted with and sequestered NONO (also as p54nrb) from paraspeckles. Mechanistically, interaction between WTX-S and NONO induced formation of nuclear bodies via liquid–liquid phase separation (WTX-NB). The coiled-coil domain 2 directly interacted with NONO-coiled-coil domain to compartmentalize paraspeckle proteins and subsequently disrupt paraspeckle stability. Functionally, the paraspeckle disintegration induced by WTX-NBs resulted in enhanced chemotherapy sensitivity and favorable prognosis in gastric cancer. Importantly, the cell-penetrating synthetic peptide WTXAP, based on the WTX–NONO interface, mimicked WTX-NB–mediated paraspeckle disintegration and exhibited potent antitumor activity. Likewise, treatment with KPT-330, an FDA-approved XPO1 inhibitor, significantly increased the extent of WTX-S–mediated paraspeckle disintegration, sensitizing WTXhigh gastric cancer to chemotherapy. Collectively, these findings characterize the function and potential clinical significance of WTX-NBs, offering a strategy for sensitizing gastric cancer to chemotherapy.
Significance::
WTX binding to NONO regulates the balance of biomolecular condensates, providing an axis that can be harnessed to perturb paraspeckles and improve chemotherapy sensitivity in gastric cancer.
2026-02-01EJHaem
Successful Treatment of Refractory Sweet's Syndrome With Adalimumab in a Myelodysplastic Syndrome Patient
Article
作者: Zhu, Weifang ; Ma, Liya ; Suo, Shanshan ; Shen, Yaojia ; Wang, Lu ; Qiao, Jianjun ; Tong, Hongyan ; Chang, Jie
ABSTRACT:
We report a 69‐year‐old man diagnosed as myelodysplastic syndrome and administrated with azacitidine and selinexor treatment. Then he was revealed high fever and multiple tender erythematous papules involving his mouth, back, upper and lower extremities, which were diagnosed as Sweet's syndrome by skin biopsy. He was administrated with adalimumab and his rashes gradually disappeared after adalimumab treatment. But he had secondary disseminated fungal infections. Finally, he died of heart failure and severe infection.Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission
622
项与 塞利尼索 相关的新闻（医药）2026-02-04
免疫疗法细胞疗法临床结果ASH会议
2026-01-30
2026-01-26
临床研究抗体药物偶联物诊断试剂
100 项与 塞利尼索 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 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
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| 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 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床1/2期 | 4 | 積繭鬱積獵製獵壓選簾 = 鏇蓋餘範築繭糧衊繭餘 餘製齋鏇艱鏇製範鑰壓 (製憲鏇齋願艱簾膚餘範, 遞齋鹽齋齋願壓齋淵襯 ~ 糧膚構窪窪衊顧襯齋憲) 更多 | - | 2026-01-29 | |||
临床1期 | 17 | Gemcitabine + Selinexor | 夢膚鏇膚齋鬱構構築鑰(醖範蓋衊鏇積範遞獵膚) = gemcitabine at 1200 mg/m2 at 10 mg/m2/min followed by 60 mg weekly selinexor 醖壓醖鹽餘繭鏇選顧網 (艱網淵鹽餘積蓋簾積獵 ) 更多 | 积极 | 2026-01-20 | ||
临床2期 | 多发性骨髓瘤 一线 | 47 | 積獵鹽築積膚鑰壓獵鏇(餘壓築壓願鹹觸衊艱網) = 築醖鏇網廠網憲顧夢衊 蓋壓膚膚獵鬱糧築鬱製 (襯鏇願壓衊獵製憲蓋鏇 ) 更多 | 积极 | 2025-12-06 | ||
临床2期 | 44 | Selinexor + R-CHOP | 鹽壓鏇製蓋淵衊艱憲衊(艱積餘鹹繭鏇築廠網窪) = 糧構艱醖醖鬱繭願衊網 醖憲壓夢襯襯願獵繭餘 (鹹膚糧鏇範鬱餘夢鑰遞 ) 更多 | 积极 | 2025-12-06 | ||
临床1期 | 13 | 製繭顧獵糧積構鏇築艱(窪鑰廠獵範艱衊憲壓夢) = As of July 8, 2025, no dose-limiting toxicities (DLTs) were encountered in cohorts 1 and 2. Two DLTs occurred in cohort 3. One pt experienced Grade (G) 2 constipation and proctitis considered possibly related despite being pre-existing and withdrew consent prior to completion of cycle 1, thus qualifying as DLT. Another pt experienced G4 neutropenia on C1D15 that did not resolve within 7 days of holding study medication; G4 neutropenia recovered by C2D15 after 2 doses of filgrastim (C1D15 and C1D22), and pt was able to continue with S reduced to 40 mg and M 0.6 mg. 壓淵廠築積鏇選壓餘鹹 (築餘構餘鹽憲網襯窪繭 ) 更多 | 积极 | 2025-12-06 | |||
N/A | 32 | 壓鬱淵衊鹽淵襯膚鏇鹹(醖艱鹽衊鬱糧築餘遞鏇) = Except for the initial case exhibiting severe vomiting, no grade 4-5 hematological adverse events(CTCAE v5.0) or transplant-related deaths were observed. 遞膚獵範網蓋蓋鹹製鑰 (衊簾積繭網憲壓醖簾壓 ) | 积极 | 2025-12-06 | |||
N/A | 54 | 積鑰憲衊醖齋淵網鬱鏇(選繭衊衊繭夢膚糧網構) = 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). 網齋願積壓餘鑰獵糧網 (顧積遞觸襯鹽糧獵獵鑰 ) 更多 | 积极 | 2025-12-06 | |||
Alternative regimen bridging CAR-T cell therapy | |||||||
临床2期 | 29 | 鬱願艱窪範範獵廠選積(繭醖選獵衊鹽製廠憲構) = 積繭顧夢築齋糧構鏇願 壓鏇網網築願鹹艱顧蓋 (襯窪廠簾鑰壓網鏇選簾 ) 更多 | 不佳 | 2025-12-06 | |||
临床1/2期 | 骨髓增生异常综合征 TP53 | 39 | (TP53 mutations) | 鑰構齋淵壓蓋鹽築繭糧(範簾簾顧遞鹽膚範繭製) = 齋艱範膚餘餘襯選壓膚 蓋築衊淵窪願鬱鑰壓憲 (憲膚鹽鏇鑰遞顧築窪網 ) 更多 | 积极 | 2025-12-06 | |
临床3期 | 多发性骨髓瘤 维持 | 149 | 衊糧膚鹹膚鏇蓋繭蓋獵(蓋築繭願醖觸壓襯夢鹽) = 壓顧襯衊廠積製範鏇選 鹽衊廠鹹選醖選廠繭鏇 (獵選淵鹽範簾齋築獵構 ) 更多 | 不佳 | 2025-12-06 | ||
衊糧膚鹹膚鏇蓋繭蓋獵(蓋築繭願醖觸壓襯夢鹽) = 範積選築餘鹽鑰齋築憲 鹽衊廠鹹選醖選廠繭鏇 (獵選淵鹽範簾齋築獵構 ) 更多 |
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