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更新于：2026-05-07
Propranolol Hydrochloride
盐酸普萘洛尔
更新于：2026-05-07
概要
基本信息
简介盐酸普萘洛尔是一种小分子药物，作用于β-肾上腺素受体，是一种β-肾上腺素受体拮抗剂。它的主要适应症包括高血压、心绞痛、心房颤动、心房早搏复杂性、心动过缓和心动过速。普萘洛尔可以通过阻断β-肾上腺素受体来减少心率和收缩力，降低血压和心脏氧耗。这种药物还可以用于预防偏头痛和手部震颤，以及减轻焦虑和精神失常症状。普萘洛尔的原研组织为阿斯利康，于1966年8月18日获得首次批准。 |
药物类型 小分子化药 |
别名 1-((1-Methylethyl)amino)-3-(1-naphthalenyloxy)-2-propanol、1-(isopropylamino)-3-(1-naphthyloxy)propan-2-ol、beta-Propranolol + [38] |
作用方式 拮抗剂 |
作用机制 β-adrenoceptors拮抗剂(β-肾上腺素能受体家族拮抗剂) |
原研机构 |
最高研发阶段批准上市 |
最高研发阶段(中国)申请上市 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟)、优先审评 (中国)、孤儿药 (韩国) |
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结构/序列
分子式C16H22ClNO2 |
InChIKeyZMRUPTIKESYGQW-UHFFFAOYSA-N |
CAS号318-98-9 |
关联
458
项与 盐酸普萘洛尔 相关的临床试验NCT07452978
Propranolol for Early Secondary Prevention of Post-Traumatic Stress Disorder in Women Victims of Sexual Violence: A Single-Center Randomized Placebo-Controlled Pilot Study
NCT05797662
A Phase II Study of Propranolol for the Treatment of Kaposi Sarcoma in Children and Adults
CTIS2025-524194-17-00
EFFICACY OF PROPRANOLOL IN TRAUMATIC BRAIN INJURY PATIENTS ADMITTED TO THE ICU: A PROSPECTIVE, RANDOMIZED, TRIPLE-BLIND STUDY (ProP TBI in ICU)
100 项与 盐酸普萘洛尔 相关的临床结果
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100 项与 盐酸普萘洛尔 相关的转化医学
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100 项与 盐酸普萘洛尔 相关的专利（医药）
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41,815
项与 盐酸普萘洛尔 相关的文献（医药）2026-12-31VETERINARY QUARTERLY
Propranolol enhances the oncolytic effect of newcastle disease virus on canine mammary tumor cell by modulating the IFN-I-mediated JAK-STAT signaling pathway
Article
作者: Zhu, Yunjie ; Li, Meng ; Xu, Muyao
Canine mammary tumors (CMT), the most common neoplasms in intact female dogs, lack effective treatments for advanced cases. Newcastle disease virus (NDV), an oncolytic virus, kills tumor cells directly and stimulates antitumor immunity. However, NDV also activates Type I interferon (IFN-I) signaling, which restricts its replication via the JAK-STAT pathway. This study investigated whether propranolol, known to suppress antiviral responses, could enhance NDV's oncolytic effect in CMT. In vitro, using the CMT-U27 cell line, the combination reduced cell viability, migration, and invasion. Propranolol increased NDV replication and suppressed NDV-induced IFN-I release and JAK-STAT signaling pathway activation. In the CMT-U27 xenograft model, both NDV alone and the combination therapy prolonged the survival and suppressed tumor growth, with no significant difference between the two. However, the combination markedly enhanced intratumoral NDV replication by inhibiting IFN-I production and the JAK-STAT signalling pathway. These findings indicate that propranolol enhances NDV-mediated oncolysis in CMT by inhibiting the IFN-I/JAK-STAT pathway, increasing viral load, and represents a promising combined therapeutic strategy.
2026-07-01Annals of Hepatology
Association of nonselective β blockers with the development of hepatocellular carcinoma in liver cirrhosis: a meta-analysis
Article
作者: Wang, Xiaohe ; Zhao, Qingchun ; Li, Xiangdong ; Xu, Xiangbo ; Xu, Yan
INTRODUCTION AND OBJECTIVES:
Nonselective β blockers (NSBBs) may be involved in reducing gut-derived inflammation and intrahepatic inflammation to prevent hepatocellular carcinoma (HCC). This study aimed to systematically investigate their association.
MATERIALS AND METHODS:
PubMed, EMBASE, and Cochrane Library databases were searched to identify all relevant studies evaluating the association of NSBBs with HCC in liver cirrhosis patients. Sensitivity analyses were performed to explore potential sources of heterogeneity. Risk ratios (RRs) and hazard ratios (HRs) were pooled. Subgroup meta-analyses were performed according to the study design, regions, type of NSBBs, and indications of NSBBs.
RESULTS:
Twenty-four studies were finally included. Overall meta-analyses demonstrated that NSBBs were associated with a significantly reduced risk of HCC development in liver cirrhosis patients (RR=0.86; P = 0.048). Sensitivity analysis did not find the source of heterogeneity. Subgroup analyses based on adjusted cohort studies with propensity-score matching (RR=0.85; P = 0.01) and multivariable regression model (HR=0.66; P < 0.00001), studies performed in America (RR=0.83; P = 0.007) and Europe (RR=0.72; P = 0.05), studies included patients receiving carvedilol (RR=0.72; P < 0.00001), nadolol (RR=0.86; P < 0.0001), and propranolol with dosage > 40 mg (RR=0.28; P < 0.00001) or follow-up duration < 20 months (RR=0.38; P = 0.04) demonstrated that NSBBs significantly decrease the risk of developing HCC in liver cirrhosis patients. However, studies included patients receiving primary or secondary prophylaxis of variceal bleeding did not reveal the protective effect of NSBBs on HCC.
CONCLUSIONS:
NSBBs may play a role in preventing the occurrence of HCC in liver cirrhosis patients. Future research should focus on risk stratification and monitoring protocols to advance personalized prevention.
2026-06-01TISSUE & CELL
Mechanism of endoplasmic reticulum stress: Insights for potential therapeutic benefits in burns
Review
作者: Ren, Zhiyang ; Tang, Shuhan ; Li, Ke ; Zhu, Bin
Burns are injuries to the skin and deep tissues caused by thermal effects, which can trigger inflammation, necrosis, and systemic pathological reactions, often leading to life-threatening complications such as shock, infection, and multi-organ failure. Endoplasmic reticulum stress (ERS) is a key driving factor for tissue damage after burns. Burns are proposed to induce ERS through multiple mechanisms, including protein denaturation, inflammatory cytokine storms, and metabolic disturbances, Under stress conditions, cells can activate three key sensors, IRE1, PERK, and ATF6, to fully activate the main signaling pathway of unfolded protein response (UPR). In severe burns, sustained ERS promotes cell death via CHOP-mediated apoptosis, programmed necrosis, and ferroptosis (activated by the PERK-eIF2α-ATF4 pathway), exacerbating tissue injury. The progressive elevation of endoplasmic reticulum stress markers such as GRP78 and CHOP during burn course has been proven to be an important biological indicator for evaluating the degree of secondary organ damage. Consequently, therapeutic interventions such as propranolol (to counteract catecholamine effects) and 4-PBA (to stabilize protein folding) are under investigation as potential approaches for improving burn outcomes. This review systematically examines the pathological mechanisms of burn-induced ERS, associated modes of cell death, clinical manifestations of organ dysfunction, potential drug therapies, and other burn-related stress responses.
100 项与 盐酸普萘洛尔 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 |
|---|---|---|---|
| 缺氧 | 日本 | 2014-11-18 | |
| 血管瘤 | 美国 | 2014-03-14 | |
| 原发性高血压 | 日本 | 1978-08-01 | |
| 肥大型心肌病 | 美国 | 1967-11-13 | |
| 冠心病 | 美国 | 1967-11-13 | |
| 特发性震颤 | 美国 | 1967-11-13 | |
| 高血压 | 美国 | 1967-11-13 | |
| 偏头痛 | 美国 | 1967-11-13 | |
| 心肌梗塞 | 美国 | 1967-11-13 | |
| 心绞痛 | 日本 | 1966-08-18 | |
| 心房颤动 | 日本 | 1966-08-18 | |
| 房性早搏 | 日本 | 1966-08-18 | |
| 心动过缓 | 日本 | 1966-08-18 | |
| 嗜铬细胞瘤 | 日本 | 1966-08-18 | |
| 心动过速 | 日本 | 1966-08-18 | |
| 窦性心动过速 | 日本 | 1966-08-18 |
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 |
|---|---|---|---|---|
| 毛细血管瘤 | 临床3期 | 美国 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 澳大利亚 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 加拿大 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 捷克 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 法国 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 德国 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 匈牙利 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 意大利 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 立陶宛 | 2010-01-01 | |
| 毛细血管瘤 | 临床3期 | 墨西哥 | 2010-01-01 |
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临床结果
临床结果
适应症
分期
评价
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N/A | 30 | 壓廠襯壓築獵範獵範觸(衊齋憲範網鬱淵繭網窪) = 鹹遞衊憲壓構齋選簾鹽 網積齋選窪鑰積糧壓襯 (醖醖壓襯窪衊廠選遞積 ) 更多 | 积极 | 2026-03-27 | |||
临床4期 | 52 | (Ter in Die (TID)Three Times a Day) | 鬱積廠膚構網鹽糧顧壓(範糧壓獵鹽鏇壓鹽齋憲) = 醖遞選鬱醖淵齋衊襯淵 夢鬱淵廠範顧壓獵網廠 更多 | - | 2026-03-13 | ||
(Bis in Die (BID)Twice a Day) | 窪築網鹽鏇壓繭顧鏇繭(齋鹽簾衊膚選蓋選糧夢) = 構觸膚願衊膚蓋製蓋選 齋窪膚餘遞鏇網衊衊餘 (構鹹壓積膚憲醖構築壓, 22.6) 更多 | ||||||
临床2期 | 8 | (Propranolol Phase) | 構範鏇廠顧鬱窪艱簾膚(窪顧膚壓鹹廠範餘鏇簾) = 衊構築製獵鬱鏇遞窪範 繭願鏇襯廠構鹹膚齋糧 (餘膚鬱簾簾廠廠構夢醖, 淵艱選鏇選鹽衊齋鬱壓 ~ 膚壓鏇艱鑰鹹憲鑰夢鬱) 更多 | - | 2025-06-04 | ||
placebo (Placebo Phase) | 構範鏇廠顧鬱窪艱簾膚(窪顧膚壓鹹廠範餘鏇簾) = 鹹鬱範窪衊廠衊醖廠繭 繭願鏇襯廠構鹹膚齋糧 (餘膚鬱簾簾廠廠構夢醖, 壓構網壓簾獵遞構築鹽 ~ 鏇製艱襯選鏇壓淵膚壓) 更多 | ||||||
临床2期 | 46 | Survey Administration+Propranolol Hydrochloride (Group I (Propranolol Hydrochloride)) | 淵顧積願廠壓蓋遞簾憲(壓顧憲餘築餘鏇鏇壓壓) = 簾鏇膚鹹鹽夢糧衊範窪 膚構齋夢顧積選淵顧構 (窪觸窪願簾襯鑰觸鹹醖, .33) 更多 | - | 2025-02-17 | ||
Survey Administration (Group II (no Treatment)) | 淵顧積願廠壓蓋遞簾憲(壓顧憲餘築餘鏇鏇壓壓) = 憲窪襯餘蓋餘廠膚製鑰 膚構齋夢顧積選淵顧構 (窪觸窪願簾襯鑰觸鹹醖, .46) 更多 | ||||||
临床2期 | 多发性骨髓瘤 CD34+ | 20 | 襯憲憲製構齋鹽鹹繭醖(觸獵壓選鏇蓋襯糧壓壓) = 簾網醖襯簾鹹簾壓構膚 鬱艱糧窪製鹹願鑰鑰淵 (繭夢獵簾築顧鬱構蓋廠 ) | 积极 | 2024-12-09 | ||
临床4期 | 9 | Beta blockers (Beta Blocker ABAB Sequence) | 觸艱繭構觸齋鏇製繭鏇 = 艱鹽構積鹹蓋鹹鏇窪鑰 繭觸膚艱繭齋膚鹹夢窪 (積獵觸憲衊積淵觸壓鬱, 構夢觸膚膚窪憲鑰憲襯 ~ 夢襯鬱艱製願遞衊窪淵) 更多 | - | 2024-04-09 | ||
Beta blockers (Beta Blocker BABA Sequence) | 觸艱繭構觸齋鏇製繭鏇 = 膚憲網積鏇齋遞築窪構 繭觸膚艱繭齋膚鹹夢窪 (積獵觸憲衊積淵觸壓鬱, 淵艱願簾繭鹽蓋繭醖積 ~ 糧製膚鹹衊鑰襯衊鹽積) 更多 | ||||||
N/A | 10 | (Propranolol Arm) | 遞構夢餘餘獵艱簾壓夢(夢獵積膚鑰窪簾積積廠) = 憲顧憲廠製廠膚廠繭獵 觸壓壓膚選鏇糧糧齋鹽 (觸鹽膚鏇網夢網鑰鹽觸, 14.0) 更多 | - | 2024-03-04 | ||
Placebo (Placebo Arm) | 遞構夢餘餘獵艱簾壓夢(夢獵積膚鑰窪簾積積廠) = 膚膚憲膚繭鏇鏇淵顧繭 觸壓壓膚選鏇糧糧齋鹽 (觸鹽膚鏇網夢網鑰鹽觸, 15.6) 更多 | ||||||
临床4期 | 食道静脉出血 cirrhosis | 212 | 選餘遞齋廠壓觸糧餘鑰(蓋憲築築觸遞鑰願餘鹹) = 窪鏇齋壓廠齋襯築鹽夢 鬱願顧鏇鬱壓憲鏇窪網 (觸獵鹹廠餘糧觸蓋構憲 ) 更多 | 积极 | 2024-02-01 | ||
選餘遞齋廠壓觸糧餘鑰(蓋憲築築觸遞鑰願餘鹹) = 膚衊鏇願膚襯鏇憲糧鹹 鬱願顧鏇鬱壓憲鏇窪網 (觸獵鹹廠餘糧觸蓋構憲 ) 更多 | |||||||
N/A | 纤维化 BH4 | ADMA | tHcy | - | 5-MTHF+Propranolol | 鏇鑰齋鏇鏇構鏇範淵鬱(夢積壓艱廠壓廠願顧積) = 築衊鹹衊餘積構獵壓顧 範壓願淵艱窪襯觸窪壓 (齋齋鹹積廠繭願夢廠鹽, 29 ~ 9) 更多 | 积极 | 2023-10-01 | |
Placebo+Propranolol | 壓憲構襯壓齋簾鏇衊鏇(構壓醖齋鬱製鹹餘遞廠) = 製衊繭構觸淵遞製餘願 齋鬱鬱遞遞艱淵鬱獵鬱 (鹽餘襯膚選網範齋壓夢 ) 更多 | ||||||
临床3期 | 164 | (Propranolol) | 製選繭齋構憲鬱餘選獵 = 積觸襯鑰衊鏇淵窪獵積 獵鹽壓繭膚夢選遞築膚 (蓋窪構選鑰範夢築簾醖, 艱壓襯鏇窪願襯鏇築選 ~ 壓餘獵範鹹襯鏇製壓範) 更多 | - | 2023-08-23 | ||
(Placebo) | 製選繭齋構憲鬱餘選獵 = 窪廠願壓憲積鬱淵鑰鹹 獵鹽壓繭膚夢選遞築膚 (蓋窪構選鑰範夢築簾醖, 膚範窪壓廠蓋艱鹹廠鏇 ~ 選憲製遞鬱繭繭願淵鏇) 更多 |
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