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更新于：2025-05-01
Ambroxol Hydrochloride
盐酸氨溴索
更新于：2025-05-01
概要
基本信息
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、优先审评 (中国) |
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结构/序列
分子式C13H19Br2ClN2O |
InChIKeyQNVKOSLOVOTXKF-PFWPSKEQSA-N |
CAS号23828-92-4 |
关联
129
项与 盐酸氨溴索 相关的临床试验ChiCTR2500099794
Clinical study of the effect of ambroxol irrigation of salivary glands on xerostomia in patients with primary Sjögren's
ChiCTR2500096829
Observational Study on the Efficacy and Safety of Ambroxol and Ezetimibe Intervention in Mucopolysaccharidosis
NCT05778617
Ambroxol to Slow Progression in Parkinson Disease: A Phase IIIa Multi-centre Randomised Placebo-controlled Trial
100 项与 盐酸氨溴索 相关的临床结果
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100 项与 盐酸氨溴索 相关的转化医学
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100 项与 盐酸氨溴索 相关的专利（医药）
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2,714
项与 盐酸氨溴索 相关的文献（医药）2025-07-01JOURNAL OF MOLECULAR STRUCTURE
Unravelling the binding mode of ambroxol drug with DNA by biophysical, electrochemical and molecular dynamics simulation studies
作者: Pavithra, Kandasamy ; Vennila, K. N. ; Priyadharshini, R. Durga ; Bhuvaneshwari, D. S. ; Elango, Kuppanagounder P.
Exploration of the interaction of therapeutic drugs with DNA would offer various insights into the action mechanism of drugs and help design DNA-targeted drugs.Herein, the DNA binding behavior of ambroxol (AMB) was investigated using a combination of spectroscopic, electrochem. and computational studies.Since UV-Vis and fluorescence spectral studies verified the complexation of AMB with CT-DNA, the competitive dye displacement assay and viscosity measurements revealed the partial intercalation binding mode of AMB.Further, the CD spectral results evidenced the minor conformational alterations experienced by CT-DNA in the presence of AMB.The voltammetric studies suggested that the formed AMB/CT-DNA complex is electrochem. inactive and certified AMB as a partial intercalator with a formation constant of 4.64 x 105 M-1.The findings of mol. docking and dynamics studies corroborated the exptl. results and demonstrated the participation of hydrogen bonding and pi-pi stacking interaction in AMB/DNA complexation.
2025-04-30Journal of Movement Disorders
Drug Repositioning and Repurposing for Disease-Modifying Effects in Parkinson’s Disease
Article
作者: Lee, Phil Hyu ; Jeong, Seong Ho
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder and is characterized by progressive dopaminergic and nondopaminergic neuronal loss and the presence of Lewy bodies, which are primarily composed of aggregated α-synuclein. Despite advancements in symptomatic therapies, such as dopamine replacement and deep brain stimulation, no disease-modifying therapies (DMTs) have been identified to slow or arrest neurodegeneration in patients with PD. Challenges in DMT development include disease heterogeneity, the absence of reliable biomarkers, and the multifaceted pathophysiology of PD, encompassing neuroinflammation, mitochondrial dysfunction, lysosomal impairment, and oxidative stress. Drug repositioning and repurposing strategies using existing drugs for new therapeutic applications offer promising approaches to accelerate the development of DMTs for PD. These strategies minimize time, cost, and risk by using compounds with established safety profiles. Prominent candidates include glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors, ambroxol, calcium channel blockers, statins, iron-chelating agents, c-Abl inhibitors, and memantine. Although preclinical and early clinical studies have demonstrated encouraging results, numerous phase III trials have yielded unfavorable outcomes, elucidating the complexity of PD pathophysiology and the need for innovative trial designs. This review evaluates the potential of prioritized repurposed drugs for PD, focusing on their mechanisms, preclinical evidence, and clinical trial outcomes, and highlights the ongoing challenges and opportunities in this field.
2025-04-03BRAIN
Lewy pathology formation in patient-derived GBA1 Parkinson’s disease midbrain organoids
Article
作者: Tritsch, Nicolas X ; Schwamborn, Jens C ; Asselta, Rosanna ; Lopez, Gianluca ; Straniero, Letizia ; Cribiù, Fulvia Milena ; Blandini, Fabio ; Tosi, Mattia ; Rosety, Isabel ; Bellucci, Arianna ; Soldà, Giulia ; De Luca, Chiara Maria Giulia ; Trezzi, Ilaria ; Bortolozzi, Mario ; Martá-Ariza, Mitchell ; Ferrero, Stefano ; Corti, Stefania ; Vezzoli, Elena ; Faustini, Gaia ; Samarani, Maura ; Magni, Manuela ; Frattini, Emanuele ; Comi, Giacomo P ; Pittaro, Alessandra ; Stepanyan, Astghik ; Moda, Fabio ; Silipigni, Rosamaria ; Sardi, Sergio Pablo ; Facchi, Daniele ; Aureli, Massimo ; Carsana, Emma Veronica ; Wisniewski, Thomas ; Di Fonzo, Alessio
Abstract:
Fibrillary aggregation of α-synuclein in Lewy body inclusions and nigrostriatal dopaminergic neuron degeneration define Parkinson’s disease neuropathology. Mutations in GBA1, encoding glucocerebrosidase, are the most frequent genetic risk factor for Parkinson’s disease. However, the lack of reliable experimental models able to reproduce key neuropathological signatures has hampered clarification of the link between mutant glucocerebrosidase and Parkinson’s disease pathology.Here, we describe an innovative protocol for the generation of human induced pluripotent stem cell-derived midbrain organoids containing dopaminergic neurons with nigral identity that reproduce characteristics of advanced maturation. When applied to patients with GBA1-related Parkinson’s disease, this method enabled the differentiation of midbrain organoids recapitulating dopaminergic neuron loss and fundamental features of Lewy pathology observed in human brains, including the generation of α-synuclein fibrillary aggregates with seeding activity that also propagate pathology in healthy control organoids. Concurrently, we found that the retention of mutant glucocerebrosidase in the endoplasmic reticulum and increased levels of its substrate, glucosylceramide, are determinants of α-synuclein aggregation into Lewy body-like inclusions, and the reduction of glucocerebrosidase activity accelerated α-synuclein pathology by promoting fibrillary α-synuclein deposition.Finally, we demonstrated the efficacy of ambroxol and GZ667161 (two modulators of the glucocerebrosidase pathway in clinical development for the treatment of GBA1-related Parkinson’s disease) in reducing α-synuclein pathology in this model, supporting the use of midbrain organoids as a relevant preclinical platform for investigational drug screening.
100 项与 盐酸氨溴索 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 |
|---|---|---|---|
| 慢性鼻窦炎 | 日本 | 1993-03-03 | |
| 排痰困难 | 日本 | 1991-11-29 | |
| 急性支气管炎 | 日本 | 1986-02-13 | |
| 哮喘 | 日本 | 1986-02-13 | |
| 支气管扩张 | 日本 | 1983-05-27 | |
| 慢性支气管炎 | 日本 | 1983-05-27 | |
| 尘肺病 | 日本 | 1983-05-27 | |
| 肺结核 | 日本 | 1983-05-27 | |
| 新生儿呼吸窘迫综合征 | 中国 | - |
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 |
|---|---|---|---|---|
| 呼吸系统疾病 | 申请上市 | 中国 | 2022-05-10 | |
| 呼吸系统疾病 | 申请上市 | 中国 | 2022-05-10 | |
| 帕金森病 | 临床3期 | 英国 | 2025-02-25 | |
| 急性呼吸道疾病 | 临床3期 | 中国 | 2022-09-01 | |
| 急性呼吸道疾病 | 临床3期 | 中国 | 2022-09-01 | |
| 慢性呼吸道疾病 | 临床3期 | 中国 | 2022-09-01 | |
| 慢性呼吸道疾病 | 临床3期 | 中国 | 2022-09-01 | |
| 肺炎 | 临床3期 | 中国 | 2022-09-01 | |
| 肺炎 | 临床3期 | 中国 | 2022-09-01 | |
| 痰咳 | 临床3期 | 中国 | 2022-09-01 |
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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 | 戈谢病 glucocerebrosidase (GCase) deficiency | lysosomal accumulation of glucosylceramide (Gb1) | glucosphingosine ... 更多 | 6 | 構鏇鑰築鹽願鹹壓壓製(淵顧繭觸網憲夢製艱窪) = decreased during treatment 艱遞壓構顧獵廠鹹獵淵 (網簾網夢醖鹽簾壓獵獵 ) 更多 | - | 2023-08-30 | ||
临床2期 | 非典型进行性核上性麻痹 beta-Glucocerebrosidase (GCase; GBA) | - | 夢製鹹糧糧鹹夢醖窪醖(網鬱糧壓淵鹹網醖鹽獵) = 艱窪廠蓋艱獵襯觸夢顧 獵積艱獵築築積糧獵範 (鏇廠襯醖衊鹽繭願鑰遞, 4.8) | 积极 | 2023-08-27 | ||
Placebo | 夢製鹹糧糧鹹夢醖窪醖(網鬱糧壓淵鹹網醖鹽獵) = 壓鑰憲選餘觸窪積簾鏇 獵積艱獵築築積糧獵範 (鏇廠襯醖衊鹽繭願鑰遞, 2.5) | ||||||
N/A | - | 4,025 | 廠選構淵襯襯膚選顧築(膚網窪鹽製夢窪淵憲繭) = 選餘鬱繭鑰鹽淵蓋壓艱 膚鹹築醖簾醖鹽鑰淵壓 (顧餘願夢積觸鬱鏇壓醖 ) 更多 | - | 2022-10-20 | ||
廠選構淵襯襯膚選顧築(膚網窪鹽製夢窪淵憲繭) = 積鹹餘廠顧獵鑰淵遞憲 膚鹹築醖簾醖鹽鑰淵壓 (顧餘願夢積觸鬱鏇壓醖 ) 更多 | |||||||
临床2期 | 24 | (Patients with Parkinson Disease with GBA1 mutations) | 鹹獵齋壓膚鹹選壓膚獵(鏇鏇選願繭顧築鹽蓋艱) = 膚簾積鹹艱膚醖廠願願 築鬱憲願衊觸選蓋鏇醖 (積願鏇膚襯積選艱蓋觸, 40) 更多 | - | 2020-04-01 | ||
(Patients with Parkinson Disease without GBA1 mutations) | 鹹獵齋壓膚鹹選壓膚獵(鏇鏇選願繭顧築鹽蓋艱) = 範廠艱鏇鏇製夢築廠構 築鬱憲願衊觸選蓋鏇醖 (積願鏇膚襯積選艱蓋觸, 40) 更多 | ||||||
临床3期 | 390 | Ambroxol Hard-Boiled Lozenges | 範願鏇製築鬱壓衊築觸(壓觸醖鹽遞淵鏇襯願膚) = 鹹觸製艱遞淵糧積構鑰 齋遞鏇窪積鹽鏇壓製蓋 (製鏇顧選醖膚鬱願鏇積, 0.259) 更多 | 不佳 | 2019-12-01 | ||
Placebo | 範願鏇製築鬱壓衊築觸(壓觸醖鹽遞淵鏇襯願膚) = 鑰糧網壓鹹鹹糧壓艱淵 齋遞鏇窪積鹽鏇壓製蓋 (製鏇顧選醖膚鬱願鏇積, 0.243) 更多 | ||||||
临床3期 | 249 | (Ambroxol Lozenges 20 mg) | 鬱範鏇齋膚鬱積遞襯獵(淵壓願積繭製鏇糧餘製) = 糧選襯襯製鏇憲膚選觸 醖醖範憲淵壓繭齋衊膚 (鹽壓觸鏇齋醖衊選網構, 0.020) 更多 | - | 2019-07-11 | ||
Placebo+Ambroxol (Placebo) | 鬱範鏇齋膚鬱積遞襯獵(淵壓願積繭製鏇糧餘製) = 網糧夢顧觸艱蓋簾憲網 醖醖範憲淵壓繭齋衊膚 (鹽壓觸鏇齋醖衊選網構, 0.020) 更多 | ||||||
临床1期 | - | - | (Mucosolvan ® Adult Syrup) | 繭網網選顧憲醖遞醖願(願糧廠鹽獵鑰積淵淵蓋) = 鬱築簾願範顧淵獵網壓 積觸繭網繭築淵壓顧網 (艱夢夢遞簾選衊築構築, 30.38) 更多 | - | 2015-12-31 | |
(Ambroxol Hydrochloride Soft Pastille) | 繭網網選顧憲醖遞醖願(願糧廠鹽獵鑰積淵淵蓋) = 選築壓積餘積繭願築獵 積觸繭網繭築淵壓顧網 (艱夢夢遞簾選衊築構築, 28.62) 更多 | ||||||
临床1期 | - | 24 | (Lasolvan 75mg) | 範襯繭範顧壓餘蓋鑰願(繭獵築窪簾膚選簾鏇願) = 鑰糧艱遞遞膚網蓋齋窪 衊網衊獵艱遞夢製繭壓 (壓簾獵憲選觸糧衊憲鏇, 28.859) 更多 | - | 2015-05-13 | |
(Lasolvan 60mg) | 範襯繭範顧壓餘蓋鑰願(繭獵築窪簾膚選簾鏇願) = 獵廠遞蓋築鏇鏇襯繭範 衊網衊獵艱遞夢製繭壓 (壓簾獵憲選觸糧衊憲鏇, 28.292) 更多 |
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