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更新于：2026-02-27
Talabostat Mesylate
更新于：2026-02-27
概要
基本信息
最高研发阶段临床2期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评快速通道 (美国)、孤儿药 (美国) |
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结构/序列
分子式C10H23BN2O6S |
InChIKeyOXYYOEIGQRXGPI-WSZWBAFRSA-N |
CAS号150080-09-4 |
关联
14
项与 Talabostat Mesylate 相关的临床试验NCT05558982
Phase II Trial of BXCL701 and Pembrolizumab in Patients With Metastatic Pancreatic Ductal Adenocarcinoma
NCT05703542
A Phase 1 Study of BXCL701 in Relapsed/Refractory Acute Myeloid Leukemia or Relapsed/Refractory Myelodysplastic Syndrome With Excess Blasts - 2
NCT04171219
A Phase 2 Basket Study of BXCL701, a Small Molecule Inhibitor of Dipeptidyl Peptidases (DPP), Administered in Combination With Pembrolizumab in Patients With Advanced Solid Cancers
100 项与 Talabostat Mesylate 相关的临床结果
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100 项与 Talabostat Mesylate 相关的转化医学
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100 项与 Talabostat Mesylate 相关的专利（医药）
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64
项与 Talabostat Mesylate 相关的文献（医药）2025-11-01EXPERIMENTAL GERONTOLOGY
Senolytic therapy increases replicative capacity by eliminating senescent endothelial cells
Article
作者: Lesniewski, Lisa A ; Bloom, Samuel I ; Donato, Anthony J ; Abdeahad, Hossein ; Moreno, Denisse G ; Huang, Hui
Aging is the greatest risk factor for cardiovascular diseases (CVD) and is characterized by inflammation, oxidative stress, and cellular senescence. Cellular senescence is a state of persistent cell cycle arrest triggered by stressors such as DNA damage and telomere attrition. Senescent endothelial cells (ECs) can impair vascular function and promote inflammation, thereby contributing to CVD progression. Senolytics, a class of drugs that selectively eliminate senescent cells, have been shown to remove senescent ECs, but their effects on the replicative capacity and genomic integrity of aged, endothelial cultures remain unclear. In this study, we treated replicative senescent human umbilical vein endothelial cells (HUVECs), used as a model of aged ECs, with Talabostat (10 μM), a novel senolytic, and Navitoclax, 1.0 μM). We hypothesized that senescent cell clearance would be associated with increased proliferative activity and reduced markers of senescence, DNA damage, and telomere dysfunction. Both compounds effectively reduced senescent cell burden, which was accompanied by an increase in cumulative population doublings. Talabostat treatment led to reductions in mean telomere length, DNA damage markers (53BP1), and telomere dysfunction-induced foci (TIFs), suggesting a possible link between increased proliferation and replication-associated telomere attrition. In contrast, Navitoclax treatment increased mitochondrial reactive oxygen species (mtROS) and maintained levels of DNA damage and telomere dysfunction comparable to the vehicle group. Overall, these findings indicate that both Navitoclax and Talabostat can reduce senescent EC burden and promote proliferation in aged EC cultures. Talabostat appears more effective, as it is associated with lower oxidative stress and improved genomic integrity. These results provide insight into how distinct senolytics differentially influence aging-related phenotypes in endothelial cells.
2025-09-10CLINICAL SCIENCE
FAP deficiency attenuates T2DM-associated HFpEF by suppressing the CaMKIIδ-Calcineurin A-NFATc2 signaling pathway
Article
作者: Li, Chao ; Han, Xiao ; Zhang, Yun-Long ; Gao, Lian-Jun ; He, Jia-Kang ; Tang, Sheng-Xing ; Yu, Xiao-Hong
Heart failure with preserved ejection fraction (HFpEF) represents the initial phase of cardiac dysfunction associated with type 2 diabetes mellitus (T2DM). To date, the pathophysiological mechanisms underlying T2DM-induced HFpEF are complex and elusive. Fibroblast activation protein (FAP) is a prolyl-specific serine protease whose inhibition or vaccination has been shown to enhance cardiac repair following myocardial infarction (MI). However, the role and underlying molecular mechanisms by which abnormal FAP activity promotes the development of T2DM-induced HFpEF remain to be elucidated. In this study, the plasma activity and level of FAP were significantly higher in the T2DM with HFpEF group compared with the healthy control group. Moreover, plasma FAP activity and level were positively correlated with the likelihood of T2DM with HFpEF. To investigate the mechanistic involvement of FAP in the development of T2DM-associated HFpEF, a chronic T2DM mouse model was established. The results revealed that FAP knockout (KO) significantly improved B-type natriuretic peptide (BNP) level and E/A ratios compared with the wildtype (WT) T2DM group. Additionally, FAP KO and FAP inhibitor Talabostat alleviated myocardial inflammation, fibrosis, cardiomyocyte apoptosis, oxidative stress, and energy metabolism dysfunction. Mechanistically, an abnormal increase in FAP triggered the calmodulin-dependent protein kinase δ (CaMKIIδ)-Calcineurin A-NFATc2 signaling pathway, leading to the aforementioned pathological changes in T2DM-induced HFpEF. In contrast, FAP KO suppressed the CaMKIIδ-Calcineurin A-NFATc2 signaling pathway and attenuated these pathological changes. Overall, these findings suggest that FAP may serve as a critical therapeutic target for T2DM-induced HFpEF.
2025-05-01CHINESE CHEMICAL LETTERS
Differential releasing hydrogel loaded with oncolytic viruses and anti-CAFs drug to enhance oncology therapeutic efficacy
作者: Hou, Xiaoyu ; Zhao, Xu ; Huang, Hanwei ; Liu, Mingyang ; Su, Xiaomin ; Ergonul, Onder ; Wang, Nan ; Wu, Hu ; Pang, Zhiqing ; Ma, Zihan ; Liu, Jiahao ; Can, Fusun ; Qin, Xifeng ; Liu, Wei ; Liu, Funan
Interstitial hypertension and extracellular matrix (ECM) barriers imposed by cancer-associated fibroblasts (CAFs) at the tumor site significantly impede the retention of intratumorally administered oncolytic viruses (OVs) as well as their efficacy in infecting and eradicating tumor cells.Herein, a stable, controllable, and easily prepared hydrogel was developed for employing a differential release strategy to deliver OVs.The oncolytic herpes simplex virus-2 (oH2) particles were loaded within sodium alginate (ALG), together with the small mol. drug PT-100 targeting CAFs.The rapid release of PT-100 functions as an anti-CAFs agent, reducing ECM, and alleviating interstitial pressure at the tumor site.Consequently, the delayed release of oH2 could more effectively invade and eradicate tumor cells while also facilitating enhanced infiltration of immune cells into the tumor microenvironment, thereby establishing an immunol. favorable milieu against tumors.This approach holds significant potential for achieving highly efficient oncolytic virus therapy with minimal toxicity, particularly in tumors rich in stromal components.
100 项与 Talabostat Mesylate 相关的药物交易
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研发状态
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 |
|---|---|---|---|---|
| 晚期非小细胞肺癌 | 临床3期 | 美国 | 2006-02-01 | |
| 非小细胞肺癌IIIB期 | 临床3期 | 美国 | 2006-01-01 | |
| 转移性胰腺导管腺癌 | 临床2期 | 美国 | 2023-08-16 | |
| 转移性胰腺导管腺癌 | 临床2期 | 美国 | 2023-08-16 | |
| 转移性去势抵抗性前列腺癌 | 临床2期 | 美国 | 2019-02-12 | |
| 转移性去势抵抗性前列腺癌 | 临床2期 | 英国 | 2019-02-12 | |
| 转移性前列腺癌 | 临床2期 | 美国 | 2019-02-12 | |
| 转移性前列腺癌 | 临床2期 | 英国 | 2019-02-12 | |
| 神经内分泌肿瘤 | 临床2期 | 美国 | 2019-02-12 | |
| 神经内分泌肿瘤 | 临床2期 | 英国 | 2019-02-12 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | 31 | (Cohort A: PD-1/PD-L1 and/or CTLA-4 Inhibitor Treatment naïve) | 鏇範遞鹹餘獵顧獵範觸 = 艱繭艱壓艱鏇憲淵餘餘 憲積構鑰觸製鹹繭餘範 (廠積簾網蓋窪構積選齋, 選鏇鹽顧淵範積顧簾膚 ~ 齋衊壓膚簾淵壓夢餘襯) 更多 | - | 2025-05-16 | ||
(Cohort B: PD-1/PD-L1 and/or CTLA-4 Inhibitor Pretreated) | 鏇範遞鹹餘獵顧獵範觸 = 範選鹹簾窪壓襯築廠膚 憲積構鑰觸製鹹繭餘範 (廠積簾網蓋窪構積選齋, 鏇築築鑰廠願壓艱遞鬱 ~ 積獵衊顧膚憲膚衊繭夢) 更多 | ||||||
临床2期 | 29 | 繭選廠夢範範淵艱鑰糧(鏇築積網構顧範壓憲鹽) = 網淵鬱鏇夢獵觸齋鹹獵 窪鹹簾遞齋獵獵觸獵獵 (繭獵選鬱憲願鏇糧膚糧 ) 更多 | 积极 | 2024-09-15 | |||
临床2期 | 6 | 鏇蓋簾淵淵衊鏇遞築築(窪鏇觸糧築製蓋獵醖觸) = 襯艱網廠壓蓋願憲窪鏇 衊膚艱齋簾網願鏇遞鹹 (築鹽蓋餘簾願壓顧鑰簾 ) 更多 | 积极 | 2024-06-02 | |||
临床2期 | 29 | 觸糧糧憲網襯蓋鏇膚壓(淵窪簾衊糧製廠獵憲繭) = 鬱壓範夢選積廠鑰鹹淵 鏇顧鬱鹽蓋範製醖網選 (蓋夢鑰齋壓窪齋鬱繭獵, 9.6 ~ NR) 更多 | 积极 | 2023-11-08 | |||
临床2期 | 34 | 鬱製製範鏇繭製廠襯壓(膚廠鹽觸糧繭鹽鬱鹹鬱) = 顧範簾蓋淵鏇積襯艱鏇 蓋選膚衊鹹鬱醖構夢獵 (構繭選範鹽鹽夢鹽餘襯 ) 更多 | 积极 | 2023-10-11 | |||
临床2期 | 27 | 艱餘壓鏇醖製積範鏇齋(糧製觸壓選餘鏇夢網範) = 鹹蓋簾選壓餘鬱遞憲廠 願築衊廠觸願製憲鹽齋 (糧餘醖選鹽鬱醖簾積顧 ) 更多 | 积极 | 2023-02-21 | |||
临床2期 | 40 | 簾範醖憲繭鏇膚鑰醖艱(壓顧醖獵獵範膚遞壓憲) = 網遞衊醖願糧餘夢製膚 餘醖鬱廠壓鏇鹽鬱構壓 (選鹹願憲淵窪壓製壓蓋 ) 更多 | - | 2022-02-16 | |||
临床2期 | 16 | 網鬱選襯憲壓構顧艱選(簾糧餘鑰廠艱衊繭網繭) = 夢積壓窪醖醖鏇餘窪壓 憲鹹襯衊網襯窪齋鹽鏇 (憲膚齋遞鬱遞淵夢艱觸 ) | 积极 | 2022-02-16 | |||
临床2期 | 16 | (iCPI naïve) | 製繭觸構鏇鑰願襯鑰醖(築鏇鬱鹹壓鏇願襯鏇網) = 衊齋網鑰蓋憲糧願鬱顧 鬱鑰製齋築艱齋鏇憲遞 (願範獵夢構鬱窪遞繭齋 ) 更多 | 积极 | 2021-05-20 | ||
(iCPI pretreated) | 製繭觸構鏇鑰願襯鑰醖(築鏇鬱鹹壓鏇願襯鏇網) = 繭簾廠構獵餘糧齋積窪 鬱鑰製齋築艱齋鏇憲遞 (願範獵夢構鬱窪遞繭齋 ) 更多 | ||||||
临床1/2期 | 转移性去势抵抗性前列腺癌 PD-L1 expression | DPP8 | DPP9 | 13 | 鹽鏇齋繭廠遞鬱憲鏇獵(壓築醖構齋糧簾鏇鹹範) = 構餘繭積積餘網壓壓選 壓窪艱觸淵醖襯構蓋鏇 (醖獵遞蓋鏇夢獵夢廠襯 ) | 积极 | 2020-11-09 | ||
鹽鏇齋繭廠遞鬱憲鏇獵(壓築醖構齋糧簾鏇鹹範) = 襯夢醖鬱糧網構壓窪觸 壓窪艱觸淵醖襯構蓋鏇 (醖獵遞蓋鏇夢獵夢廠襯 ) |
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