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更新于：2026-08-26
Tolvaptan
托伐普坦
更新于：2026-08-26
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 美国 (2009-05-19), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、孤儿药 (日本) |
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结构/序列
分子式C26H25ClN2O3 |
InChIKeyGYHCTFXIZSNGJT-UHFFFAOYSA-N |
CAS号150683-30-0 |
关联
238
项与 托伐普坦 相关的临床试验CTR20254014
托伐普坦口崩片在中国健康成年参与者中的生物等效性研究
ChiCTR2600118902
Tolvaptan for the Prevention of Delayed Hyponatremia after Surgery in Patients with Pituitary Macroadenoma: A Multicenter, Single-Blind, Randomized Controlled Clinical Trial
CTR20253691
托伐普坦口崩片（15mg）在中国健康研究参与者中餐后给药条件下随机、开放、单剂量、两序列、两周期、双交叉生物等效性试验
100 项与 托伐普坦 相关的临床结果
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100 项与 托伐普坦 相关的转化医学
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100 项与 托伐普坦 相关的专利（医药）
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1,571
项与 托伐普坦 相关的文献（医药）2026-09-01EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS
Impact of gastric mixing and water intake on postprandial pharmacokinetics of orally disintegrating tablets: A PBBM-based study
Article
作者: Matsui, Kazuki ; Matsumura, Naoya ; Takahashi, Yoshinori ; Kambayashi, Atsushi
OBJECTIVE:
Food intake substantially influences the oral absorption of many drugs, and the ability to quantitatively predict food effects in humans prior to clinical studies is critical for optimizing dosing regimens and formulation design. Although various in silico approaches have been proposed to predict food effects on oral solid dosage forms, their predictive performance remains limited. Orally disintegrating tablets (ODTs), which can be administered without water, are known to exhibit characteristic postprandial absorption profiles that are inadequately captured by conventional models. This study aimed to develop a novel physiologically based biopharmaceutics model (PBBM) capable of quantitatively predicting the impact of postprandial water intake on drug absorption, using tolvaptan and rivaroxaban as model compounds.
METHODS:
To better represent the postprandial gastric environment, a novel model (Assumption 2) was developed in which the stomach was functionally divided into two compartments: the fundus and the antrum. For administration without water, the drug was assumed to remain in the fundus and transfer to the antrum after a defined lag time. In contrast, for administration with water, drug distribution between the fundus and antrum was assumed, accounting for the formation of a flow channel (Magenstraße). In addition, a mathematical description of drug-chyme mixing in the antrum was incorporated to reflect dissolution under high-viscosity conditions.
RESULTS AND DISCUSSION:
The conventional single-compartment gastric model (Assumption 1) substantially overestimated postprandial absorption rates. In contrast, the proposed compartment-divided model (Assumption 2) markedly improved the prediction of Tmax for both tolvaptan and rivaroxaban ODTs and successfully reproduced the characteristic postprandial absorption delay observed under water-free administration. These findings demonstrate that abandoning the conventional assumption of instantaneous homogeneous gastric mixing and explicitly accounting for administration-dependent (i.e., presence or absence of water intake) gastric distribution and drug entrapment within solid food substantially improves the prediction of postprandial pharmacokinetics. The remaining tendency toward slightly earlier predicted absorption, particularly for rivaroxaban, suggests that diffusion delays in ultra-high-viscosity environments generated by solid meals are not fully captured by parameters derived from liquid meal data. Overall, the proposed model structure is mechanistically valid, and further improvements in prediction accuracy are expected through the incorporation of parameters describing particle behavior in highly viscous gastric contents, informed by complementary in vitro and in vivo studies.
2026-09-01Translational Research
GLP-1 receptor agonists in ADPKD: from metabolic rationale to phenotype-enriched translational testing
Review
作者: Corrêa, Lucas Maciel de Almeida ; Arruda, Sicília Lins Peixoto ; Ferreira, Guilherme Diniz ; Mazur, Gabriel Rian ; Delmiro Silva, Yan Roberth ; Brandão, Luiggi Kevin Virgino
Autosomal dominant polycystic kidney disease (ADPKD) remains therapeutically anchored to vasopressin V2-receptor antagonism, yet progression heterogeneity and persistent unmet need increasingly suggest residual disease biology beyond cAMP-centered control. Converging experimental and observational human phenotype data suggest that metabolic reprogramming, mitochondrial dysfunction, impaired fatty-acid oxidation, obesity, and visceral adiposity may modify cyst growth, kidney-volume expansion, eGFR decline, or treatment-response heterogeneity, although causal and therapeutic evidence remains incomplete. In this review, we synthesize mechanistic, human, and trial-design evidence-from studies of cystic bioenergetics and human phenotype modifiers of progression to metabolism-oriented interventions, recent direct semaglutide data in Pkd1 models, and the design logic of ongoing early-phase clinical evaluation-to examine whether GLP-1 receptor agonists deserve consideration as orthogonal metabolic candidates for translational disease modification in ADPKD. Across these lines of evidence, GLP-1 receptor agonists should be viewed not as mechanistic surrogates for tolvaptan, but as plausible candidates to engage adiposity-related and metabolic stress pathways that may contribute to progression heterogeneity. At the same time, the field remains at an early translational stage, with important uncertainties regarding patient selection, trial enrichment, endpoint selection, co-administration with tolvaptan, and safety monitoring. GLP-1-based therapy should not currently be regarded as a treatment for ADPKD; rather, the available evidence supports a phenotype-aware translational program in which metabolic burden, visceral adiposity, and residual risk beyond tolvaptan guide early clinical testing and endpoint selection.
2026-07-15JOURNAL OF CLINICAL INVESTIGATION
GLUT9b- and ABCG2-mediated collecting duct urate transport uncovers a vasopressin-independent mechanism of renal water reabsorption
Article
作者: Alper, Seth L. ; Torres, Vicente E. ; Chebib, Fouad T. ; Hadla, Mohamad ; Mardirossian, Jean Marc ; Ghanem, Ahmad ; Bichet, Daniel G. ; Borghol, Abdul Hamid ; Harris, Peter ; Abboud, Georges ; Vallon, Volker ; Chini, Eduardo
Renal water reabsorption is classically regulated by vasopressin V2 receptor (V2R) signaling through cyclic AMP and protein kinase A, driving apical accumulation of aquaporin-2 (AQP2). However, collecting duct water handling is also modulated by vasopressin-independent mechanisms. Here, we examined intracellular soluble urate as a vasopressin-independent regulator of AQP2 trafficking. Intracellular urate accumulation in collecting duct cells was mediated by enhanced apical urate uptake via GLUT9b and reduced apical urate efflux through ABCG2, triggering phosphodiesterase-4 activation, reduced cAMP, and downstream AMP-activated protein kinase (AMPK) activation. The resulting AQP2 accumulation at the apical membrane was independent of V2R signaling, required ongoing endocytosis, and was associated with features of postendocytic apical trafficking of internalized AQP2. In vivo ABCG2 inhibition with probenecid increased apical AQP2 abundance and markedly attenuated tolvaptan-induced polyuria in both wild-type and
Pkd1RC/RC
autosomal dominant polycystic kidney disease (ADPKD) mice in a uricase-independent manner while preserving tolvaptan’s ADPKD-modifying efficacy. In a phase II trial with tolvaptan-treated patients with ADPKD, probenecid reduced urine volume and nocturia frequency. Together, these findings support a vasopressin-independent urate/AMPK/AQP2 pathway that regulates renal water handling and, in a preclinical ADPKD model, can uncouple cyst growth attenuation from the dose-limiting aquaretic effects of V2R antagonism.
220
项与 托伐普坦 相关的新闻（医药）2026-08-20
100 项与 托伐普坦 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 |
|---|---|---|---|
| 腹水 | 日本 | 2017-02-28 | |
| 常染色体显性多囊肾病 | 日本 | 2014-03-24 | |
| 心源性水肿 | 日本 | 2011-01-05 | |
| 水肿 | 日本 | 2010-10-27 | |
| ADH分泌不当综合征 | 欧盟 | 2009-08-02 | |
| ADH分泌不当综合征 | 冰岛 | 2009-08-02 | |
| ADH分泌不当综合征 | 列支敦士登 | 2009-08-02 | |
| ADH分泌不当综合征 | 挪威 | 2009-08-02 | |
| 低钠血症 | 美国 | 2009-05-19 |
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 |
|---|---|---|---|---|
| 常染色体隐性遗传性多囊肾 | 临床3期 | - | 2022-07-01 | |
| 音量过载 | 临床3期 | 日本 | 2018-03-07 | |
| 肝损伤 | 临床3期 | 比利时 | 2016-01-12 | |
| 慢性肾病 | 临床3期 | 美国 | 2014-05-01 | |
| 慢性肾病 | 临床3期 | 阿根廷 | 2014-05-01 | |
| 慢性肾病 | 临床3期 | 澳大利亚 | 2014-05-01 | |
| 慢性肾病 | 临床3期 | 比利时 | 2014-05-01 | |
| 慢性肾病 | 临床3期 | 加拿大 | 2014-05-01 | |
| 慢性肾病 | 临床3期 | 捷克 | 2014-05-01 | |
| 慢性肾病 | 临床3期 | 丹麦 | 2014-05-01 |
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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
N/A | 45 | 繭膚夢壓憲衊網獵憲蓋(淵網襯觸選壓艱選鬱顧) = 13.3%; all ≤2 ULN 艱蓋膚積願繭淵淵遞製 (艱醖夢醖遞壓範積鑰淵 ) 更多 | 积极 | 2025-06-04 | |||
N/A | 1,676 | 鏇蓋壓鏇憲餘鹽願鏇襯(選製選夢觸鑰顧襯選簾) = 9.6% 鬱鹹襯願願壓構繭顧鬱 (壓積壓觸範鑰襯窪築繭 ) 更多 | 积极 | 2025-02-14 | |||
临床4期 | 117 | 網構觸蓋糧築壓鬱構膚(襯遞簾鏇鑰獵衊壓廠網) = 憲網襯鹽繭醖製窪壓鬱 夢願獵餘獵夢遞廠鏇選 (製鏇淵製淵遞鬱衊壓觸 ) 更多 | 积极 | 2024-09-01 | |||
临床3期 | 60 | 醖醖齋繭憲蓋顧觸壓淵 = 鹹範製夢遞窪遞夢鏇醖 觸鏇網網艱憲壓淵醖製 (鏇鬱觸簾簾顧觸獵顧範, 窪鏇齋醖廠襯鹽餘艱衊 ~ 獵襯淵憲蓋顧廠醖廠顧) 更多 | - | 2024-08-23 | |||
N/A | 117 | 築選鬱願選範淵遞窪餘(簾艱膚衊窪餘糧簾醖鹽) = 構構窪遞範製醖艱遞餘 鬱廠蓋鹽鬱獵淵夢遞壓 (醖糧廠憲鏇蓋窪齋積鑰 ) 更多 | 积极 | 2024-05-23 | |||
N/A | 134 | 鑰鏇繭醖選夢壓廠簾壓(願膚繭齋廠艱願糧鏇壓) = 觸齋觸願願鬱製襯憲糧 鑰簾顧製夢遞衊夢鹹壓 (壓積廠窪醖夢膚憲齋鬱 ) 更多 | 积极 | 2023-11-02 | |||
N/A | - | 願鬱鏇醖餘繭襯鏇衊膚(網齋窪醖網鹽願獵衊獵) = 網築醖繭廠構壓窪鹹窪 窪顧觸齋鬱淵鑰艱鹽選 (積簾憲膚製顧鏇願齋構 ) 更多 | - | 2023-06-22 | |||
Placebo | 願鬱鏇醖餘繭襯鏇衊膚(網齋窪醖網鹽願獵衊獵) = 積網製糧願壓網觸選蓋 窪顧觸齋鬱淵鑰艱鹽選 (積簾憲膚製顧鏇願齋構 ) 更多 | ||||||
临床3期 | 83 | 獵顧餘醖淵製襯選積構(糧鏇齋鏇範膚構膚窪築) = 12%, 31% 窪夢鏇齋膚遞繭淵積糧 (餘構窪艱艱餘製鏇蓋遞 ) 更多 | 积极 | 2023-06-14 | |||
Placebo | |||||||
N/A | 523 | 憲衊鹹夢憲鏇鑰壓構鏇(遞廠膚鏇鏇觸獵鏇簾蓋) = 51% 淵膚襯鏇襯襯鑰遞築顧 (襯鹽衊顧憲蓋遞製顧壓 ) 更多 | 积极 | 2023-06-14 | |||
临床2/3期 | - | 網積選鹽選顧憲範選鏇(齋築壓淵願壓製鹹範艱) = 範艱齋衊艱構鹹鏇遞窪 顧構蓋廠廠夢網壓壓糧 (獵廠鏇鹽艱襯衊繭艱夢 ) | - | 2023-06-01 | |||
網積選鹽選顧憲範選鏇(齋築壓淵願壓製鹹範艱) = 夢廠壓鹽鑰繭餘齋鑰襯 顧構蓋廠廠夢網壓壓糧 (獵廠鏇鹽艱襯衊繭艱夢 ) |
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