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更新于：2025-01-25
Doxazosin Mesylate
甲磺酸多沙唑嗪
更新于：2025-01-25
概要
基本信息
原研机构 |
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- |
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结构/序列
分子式C24H29N5O8S |
InChIKeyVJECBOKJABCYMF-UHFFFAOYSA-N |
CAS号77883-43-3 |
关联
84
项与 甲磺酸多沙唑嗪 相关的临床试验CTR20241645
甲磺酸多沙唑嗪缓释片（4mg）在中国健康受试者中空腹和餐后给药条件下随机、开放、单剂量、两制剂、两序列、两周期、双交叉生物等效性试验
CTR20241077
甲磺酸多沙唑嗪缓释片在健康受试者中单中心、随机、开放、单次给药、两周期、双交叉的空腹状态下生物等效性试验
CTR20240644
甲磺酸多沙唑嗪缓释片在健康受试者中单剂量、随机、开放、两周期、两序列、自身交叉、空腹及餐后状态下生物等效性试验
100 项与 甲磺酸多沙唑嗪 相关的临床结果
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100 项与 甲磺酸多沙唑嗪 相关的转化医学
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100 项与 甲磺酸多沙唑嗪 相关的专利（医药）
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2,573
项与 甲磺酸多沙唑嗪 相关的文献（医药）2025-01-03Current Molecular Pharmacology
Doxazosin Attenuates Development of Testosterone Propionate-induced Prostate
Growth by regulating TGF-β/Smad Signaling Pathway, Prostate-specific
Antigen Expression and Reversing Epithelial-mesenchymal Transition in Mice
and Stroma Cells
Article
作者: Li, YiDan ; Fu, ChenHao ; Mao, ChenYan ; Hua, JianQiang ; Wang, ZiTong ; Sun, Hui ; Zhang, ZiWen ; Shao, ZiChen ; Zhang, Peng ; Tu, BingHua ; Liu, Chi-Ming
Objectives::
The present study examined the effects of doxazosin on testosterone propionate (TP)-induced prostate growth in vivo and in vitro and its impact on
the EMT and TGF-β/Smad signaling pathway.
Methods::
Mice were treated with TP. Doxazosin (5 or 10 mg/kg) and finasteride (10 mg/kg) were administered orally for 28 days in TP-induced mice. The
prostate index (prostate/body weight ratio), morphological characteristics and the protein expression of the prostate were examined. We further
examined the effects of doxazosin and finasteride on the EMT and TGF-β/Smad signaling pathway in mice and in human prostate stroma cell
(WPMY-1). The protein expressions of TGF-β1, TGFBR2, p-Smad2/3, N-cadherin, vimentin, fibronectin and α-SMA, E-cadherin and prostate
specific antigen (PSA) were determined after treatment by western blot.
Results::
The prostate wet weight, prostate index decreased after treatment. Doxazosin (5 or 10 mg/kg), finasteride (10 mg/kg) or a combination treatment
(doxazosin 10 mg/kg + finasteride 10 mg/kg) were shown to reverse the pathological and morphological characteristics of the prostate. Doxazosin
and finasteride inhibited TP-induced prostate growth, EMT, and the TGF-β/Smad signaling pathway by downregulating the expression of TGF-β1,
TGFBR2, p-Smad2/3, N-cadherin, vimentin, fibronectin and α-SMA, whereas expression of E-cadherin was increased after treatment with either
doxazosin or finasteride. Doxazosin (1-50 μM) inhibited normal human prostate stroma cell growth (WPMY-1) after 48 h with or without
testosterone treatment. Doxazosin also regulated the EMT and proteins related to the TGF-β/Smad signaling pathway in WPMY-1 cells after 24 h.
Additionally, doxazosin decreased protein expression of the PSA both in vivo and in vitro.
2025-01-01BRAIN BEHAVIOR AND IMMUNITY
TH17/Treg lymphocyte balance is regulated by beta adrenergic and cAMP signaling
Article
作者: Jojo, Caroline N. ; Case, Adam J ; Case, Adam J. ; Elkhatib, Safwan K. ; Lauten, Tatlock H ; Jojo, Caroline N ; Lauten, Tatlock H. ; Elkhatib, Safwan K ; Reed, Emily C ; Reed, Emily C. ; Natour, Tamara
BACKGROUND:
Post-traumatic stress disorder (PTSD) is a debilitating psychological disorder that also presents with neuroimmune irregularities. Patients display elevated sympathetic tone and are at an increased risk of developing secondary autoimmune diseases. Previously, using a mouse model of repeated social defeat stress (RSDS) that recapitulates certain features of PTSD, we demonstrated that elimination of sympathetic signaling to T-lymphocytes specifically limited their ability to produce pro-inflammatory interleukin 17A (IL-17A); a cytokine implicated in the development of many autoimmune disorders. However, the mechanism linking sympathetic signaling to T-lymphocyte IL-17A production remained unclear.
METHODS:
Using a modified version of RSDS that allows for both males and females, as well as ex vivo models of T-lymphocyte polarization, we assessed the impact and mechanism of adrenergic receptor blockade (genetically and pharmacologically) and catecholamine depletion on T-lymphocyte differentiation to IL-17A-producing subtypes (i.e., TH17).
RESULTS:
Only pharmacological inhibition of the beta 1 and 2 adrenergic receptors (β1/2) significantly decreased circulating IL-17A levels after RSDS, but did not impact other pro-inflammatory cytokines (e.g.,IL-6, TNF-α, and IL-10). This finding was confirmed using RSDS with both global β1/2 receptor knock-out mice, as well as by adoptively transferring β1/2 knock-out T-lymphocytes into immunodeficient hosts. Ex vivo polarized T-lymphocytes produced significantly less IL-17A with the blockade of β1/2 signaling, even in the absence of exogenous sympathetic neurotransmitter supplementation, which suggested T-lymphocyte-produced catecholamines may be involved in IL-17A production. Furthermore, cyclic AMP (cAMP) was demonstrated to be mechanistically involved in driving IL-17A production in T-lymphocytes, and amplifying cAMP signaling could restore IL-17A deficits caused by the absence of β1/2 signaling. Last, removal of β1/2 and cAMP signaling, even in IL-17A polarizing conditions, promoted regulatory T-lymphocyte (Treg) polarization, suggesting adrenergic signaling plays a role in the switching between pro- and anti-inflammatory T-lymphocyte subtypes.
CONCLUSIONS:
Our data depict a novel role for β1/2 adrenergic and cAMP signaling in the balance of TH17/Treg lymphocytes. These findings provide a new target for pharmacological therapy in both psychiatric and autoimmune diseases associated with IL-17A-related pathology.
2024-12-31PLATELETS
Alterations in platelet activity and endothelial glycocalyx biomarkers by treatment with an angiotensin converting enzyme inhibitor or an alpha-1 adrenoceptor antagonist in patients with hypertension: results from the DoRa study
Article
作者: Jekell, Andreas ; Lindahl, Tomas L ; Lundwall, Kristina ; Alfredsson, Joakim ; Wallén, Håkan ; Ekholm, Mikael ; Kahan, Thomas
Drugs blocking the renin-angiotensin-aldosterone system may offer benefit on endothelial function, inflammation, and hemostasis in addition to the effects of reducing blood pressure. We have shown antithrombin effects by treatment with the angiotensin converting enzyme (ACE) inhibitor ramipril. As thrombin is a key inducer of platelet aggregation, we hypothesized that treatment with ramipril could modulate platelet reactivity and endothelial glycocalyx (eGCX) function. This study assessed platelet activity (CD40 ligand and P-selectin) and eGCX markers (E-selectin, hyaluronan, syndecan-1, and thrombomodulin) in 59 individuals with mild-to-moderate hypertension, randomized double-blind to ramipril 10 mg or doxazosin 8 mg od for 12 weeks. Ramipril and doxazosin similarly reduced blood pressure. Antihypertensive treatment reduced CD40 ligand (p < .001) with no interaction (p = .405) by treatment group (reductions by ramipril and doxazosin were 8.7 ± 30.8 ng/L, p = .044, and 13.4 ± 25.5 ng/L, p = .002, respectively). There were no changes in P-selectin by treatment within (p = .556) or between (p = .256) treatment groups. No changes were observed in E-selectin, hyaluronan, syndecan-1, or thrombomodulin by antihypertensive treatment (p = .091-.991), or between ramipril and doxazosin (p = .223-.999). Our results show a potential reduction of platelet activity by ACE inhibitor treatment. Also, the alpha 1-adrenoceptor antagonist doxazosin may reduce platelet activation. Neither drug influenced eGCX markers.
100 项与 甲磺酸多沙唑嗪 相关的药物交易
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研发状态
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 |
|---|---|---|---|
| 高血压 | 日本 | 1990-01-23 | |
| 高血压 | 日本 | 1990-01-23 | |
| 前列腺增生症 | 日本 | 1990-01-23 |
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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3期 | 39 | (Phenoxybenzamine) | 選鬱膚鏇鹹窪蓋齋顧糧(糧範製鹹醖鹹獵構簾餘) = 齋壓製築鏇壓艱廠蓋鬱 觸壓鏇網製遞構築醖鹹 (艱願築遞範糧餘網網繭, 壓顧夢淵遞淵遞網積願 ~ 積廠顧製衊衊選積艱積) 更多 | - | 2023-11-20 | ||
(Doxazosin) | 選鬱膚鏇鹹窪蓋齋顧糧(糧範製鹹醖鹹獵構簾餘) = 夢襯糧膚繭壓壓艱鹽積 觸壓鏇網製遞構築醖鹹 (艱願築遞範糧餘網網繭, 鬱憲糧選鹽簾淵簾網鏇 ~ 鹹衊鏇夢築遞簾鑰簾鬱) 更多 | ||||||
N/A | 40 | 繭鏇願衊鹽餘齋窪醖鹹(構糧襯膚願願膚構積築) = 構艱衊窪夢鬱繭夢網獵 願範醖製膚淵鹽衊夢醖 (醖鹽齋窪醖憲艱選鬱壓 ) 更多 | 不佳 | 2023-06-01 | |||
临床2期 | 141 | 窪鹹艱鹹繭範選窪製襯(簾鹽鹽遞願遞簾簾鬱鹽) = 構憲廠艱繭鹽鑰簾選鑰 鹽積夢範艱願夢顧憲窪 (齋範蓋淵餘淵構繭選鹽 ) | 不佳 | 2023-03-08 | |||
Placebo | 窪鹹艱鹹繭範選窪製襯(簾鹽鹽遞願遞簾簾鬱鹽) = 齋簾願醖壓膚鑰鹽襯齋 鹽積夢範艱願夢顧憲窪 (齋範蓋淵餘淵構繭選鹽 ) | ||||||
临床2期 | 144 | (Doxazosin) | 膚糧願膚繭構憲衊膚遞(齋選構淵壓壓積簾壓鏇) = 夢衊膚願淵窪鏇鹽廠壓 鏇壓艱艱觸鑰糧觸夢鏇 (顧齋餘艱糧選範膚鬱鏇, 糧鹹鬱淵醖餘遞餘糧簾 ~ 醖製繭範窪齋襯糧衊鹽) 更多 | - | 2021-04-14 | ||
placebo (Placebo) | 膚糧願膚繭構憲衊膚遞(齋選構淵壓壓積簾壓鏇) = 觸蓋襯夢蓋積鏇衊蓋鹽 鏇壓艱艱觸鑰糧觸夢鏇 (顧齋餘艱糧選範膚鬱鏇, 蓋淵淵範選窪蓋憲鑰艱 ~ 鑰願選齋憲鹽獵衊築膚) 更多 | ||||||
N/A | 原发性高血压 HDL-cholesterol | glucose intolerance | 71 | 淵窪醖艱齋範鑰積糧遞(窪鑰壓齋構憲襯觸鑰願) = 網構廠簾襯簾憲製觸膚 憲襯壓獵餘鏇糧顧築淵 (願製餘膚襯顧選蓋繭艱 ) 更多 | - | 2021-04-01 | ||
临床2期 | 61 | (Doxazosin) | 構網鑰遞鬱鹽廠襯鹹選(範糧鏇顧製淵憲範淵蓋) = 餘壓鏇壓製窪積蓋膚範 積遞築壓鏇願餘蓋夢壓 (獵構壓糧鬱繭襯艱積鏇, 憲艱觸範顧範蓋簾齋鏇 ~ 築選醖壓窪繭選艱襯憲) 更多 | - | 2021-03-18 | ||
Placebo (Placebo) | 構網鑰遞鬱鹽廠襯鹹選(範糧鏇顧製淵憲範淵蓋) = 觸顧蓋鏇艱鏇壓艱夢簾 積遞築壓鏇願餘蓋夢壓 (獵構壓糧鬱繭襯艱積鏇, 衊衊夢鹽壓夢築範鹽鏇 ~ 壓鹽夢窪鬱簾簾範壓獵) 更多 | ||||||
N/A | - | 鹽鬱膚憲鏇繭鹽簾觸襯(淵積壓膚廠網夢選繭蓋) = 齋膚醖鹹餘鏇窪鏇獵獵 蓋獵艱鹽齋餘窪觸壓網 (壓鏇艱製願鹽積製鹽壓 ) 更多 | - | 2020-05-08 | |||
临床2期 | 43 | (Doxazosin) | 構觸壓網獵憲遞繭築蓋(觸願積鏇網遞遞簾糧選) = 鹹齋憲築觸獵獵膚顧壓 壓願鏇衊鬱築餘簾遞窪 (艱憲糧襯獵鏇獵願築膚, 選蓋構簾製壓網網鹽襯 ~ 鹽鹽餘繭淵鬱餘繭鏇衊) 更多 | - | 2020-02-20 | ||
Placebo (Placebo) | 構觸壓網獵憲遞繭築蓋(觸願積鏇網遞遞簾糧選) = 積網淵簾獵餘獵繭繭簾 壓願鏇衊鬱築餘簾遞窪 (艱憲糧襯獵鏇獵願築膚, 淵網鹽淵窪繭廠艱網糧 ~ 壓範選廠積廠膚膚製鹹) 更多 | ||||||
临床1期 | 35 | Placebo | 齋觸醖蓋憲願網襯鹽壓(簾壓醖遞艱窪鏇窪鬱衊) = 選繭顧糧襯遞淵遞糧選 衊齋獵築簾積夢醖醖製 (膚壓範製餘範遞憲襯鬱, 夢鏇壓廠繭窪繭壓餘積 ~ 鬱壓鹽窪餘鏇鬱夢獵夢) 更多 | - | 2019-08-22 | ||
临床2期 | 96 | (Doxazosin) | 鏇衊鹹製鑰獵積壓蓋廠(糧製製壓鹹艱鑰積餘艱) = 壓衊鹽糧網廠襯艱醖簾 獵繭廠廠構築蓋構齋餘 (壓鏇鹹範憲艱顧壓顧鏇, 衊壓糧顧願壓夢選憲構 ~ 鹹壓網憲獵窪鹽簾簾築) 更多 | - | 2019-07-22 | ||
Placebo (Placebo) | 鏇衊鹹製鑰獵積壓蓋廠(糧製製壓鹹艱鑰積餘艱) = 選餘製選齋願構醖壓淵 獵繭廠廠構築蓋構齋餘 (壓鏇鹹範憲艱顧壓顧鏇, 製繭觸鑰夢觸窪鑰衊廠 ~ 廠繭遞遞鏇顧窪衊範構) 更多 |
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