预约演示
更新于：2025-12-01
Nicardipine Hydrochloride
盐酸尼卡地平
更新于：2025-12-01
概要
基本信息
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 日本 (1981-05-01), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (欧盟) |
登录后查看时间轴
结构/序列
分子式C26H30ClN3O6 |
InChIKeyAIKVCUNQWYTVTO-UHFFFAOYSA-N |
CAS号54527-84-3 |
关联
51
项与 盐酸尼卡地平 相关的临床试验NCT07246629
Prophylactic Use of Intrathecal Calcium Channel Antagonist Through Lumbar Drain in Patients With Subarachnoid Hemorrhage Due to Aneurysmal Rupture
NCT03184155
Prevention of Coronary Microvascular Dysfunction Post-PCI by Intracoronary Nicardipine
NCT07044232
NICardipine for Fast Achievement of Systolic BP Targets in ICH
- a Quasi-randomized, Implementation Trial With Stepwise Rollout of Nicardipin Based Treatment of Hypertension.
100 项与 盐酸尼卡地平 相关的临床结果
登录后查看更多信息
100 项与 盐酸尼卡地平 相关的转化医学
登录后查看更多信息
100 项与 盐酸尼卡地平 相关的专利（医药）
登录后查看更多信息
4,720
项与 盐酸尼卡地平 相关的文献（医药）2026-01-01CHEMICO-BIOLOGICAL INTERACTIONS
JUN activation by disrupted calcium homeostasis orchestrates a Nox4–inflammasome–PUMA apoptotic triad in obesity-exacerbated renal injury following lower limb ischaemia–reperfusion
Article
作者: You, Yuanbing ; Wang, Xiaochen ; Gao, Yidi ; Wang, Tiantian ; Li, Jingkang ; Li, Rui ; Zhang, Qiong
Obesity exacerbates renal injury following lower limb ischaemia-reperfusion (LLIRI) through mechanisms involving calcium dysregulation and oxidative-inflammatory-apoptotic cascades. However, the underlying pathways remain to be identified. Thus, this study aimed to elucidate the underlying pathways by using transcriptomics, multi-omics, and pharmacological validation. Utilizing transcriptomics, multi-omics analysis, and targeted biochemical/molecular assays in a high-fat diet-induced obese mouse model of LLIRI, combined with pharmacological validation using nicardipine in human renal tubular cells exposed to oxidative stress, we elucidated the underlying pathways linking calcium dysregulation to renal injury. In high-fat diet-induced obese mice, LLIRI triggered profound renal transcriptomic reprogramming, with 1530 differentially expressed genes significantly enriched in calcium homeostasis disruption (GO:0055074), NF-κB signalling (KEGG:mmu04064), and apoptosis. Mechanistically, LLIRI-induced surge in reactive oxygen species promoted renal calcium influx by downregulating calcium efflux transporters Atp2b4 (PMCA4) and Kcnma1 (BK channel), which led to Ca2+ overload. This results in activation of the transcription hub JUN, which orchestrated a triad of injury: oxidative stress, as evidenced by Nox4 upregulation and ATP/NAD+ depletion, which elevated lipid (MDA↑), protein (carbonyls↑), and DNA (8-OHdG↑, γ-H2AX↑) damage; inflammation, as evidenced by tumour necrosis factor-α/interleukin (IL)-1β/IL-18 elevation and macrophage infiltration (F4/80+/HMGB1+); and apoptosis, as evidenced by PUMA (Bbc3) induction, caspase-3/8 activation, and Bax/Bcl-2 imbalance. In vitro, H2O2-induced oxidative stress in human renal tubules replicated Ca2+ overload and JUN-driven apoptosis/senescence. Treatment with the L-type calcium channel blocker nicardipine (2.5 μM) attenuated calcium influx, suppressed JUN/Nox4/PUMA expression, reduced caspase activation, and mitigated cellular damage. Our findings establish Ca2+ overload-JUN activation as a central axis integrating oxidative, inflammatory, and apoptotic networks in obesity-aggravated LLIRI renal injury. Integrating multi-omics and pharmacological evidence, we identify JUN as a master transcriptional regulator of the Nox4-inflammasome-PUMA apoptotic triad, thereby elucidating a previously unrecognized pathogenic pathway in obesity-exacerbated renal LLIRI. Targeting this axis with calcium channel blockers is a promising therapeutic strategy.
2025-12-01HOSPITAL PHARMACY
Chemical Stability Testing of Solutions for Intraventricular Irrigations via IRRA
flow
Ventricular Drain System
Article
作者: Brandmeir, Nicholas ; DeBastiani, Anthony ; Peaslee, Jessica ; Garavaglia, Jeffrey
Purpose:
Advances have been made with delivery of medications via continuous intrathecal irrigating ventricular drains such as IRRAflow (IRRAS). Medications including vancomycin, tobramycin, daptomycin and nicardipine are currently being used as ventricular irrigations via the IRRAflow device. The purpose of this study was to evaluate the chemical stability of minute concentrations of daptomycin, nicardipine, tobramycin, and vancomycin for administration via IRRAflow intrathecal catheters.
Methods:
Commercially available formulations of daptomycin, nicardipine, tobramycin, and vancomycin were each diluted in separate normal saline (NS) 1000 mL bags to final concentrations of daptomycin 2 mg/1000 mL NS, nicardipine 2.5 mg/1000 mL NS, tobramycin 4 mg/1000 mL NS, and vancomycin 4 mg/1000 mL NS. Samples from each compound were transferred into 2.5 mL glass vials and evaluated in triplicate fashion using ultra-performance liquid chromatography and tandem mass spectrometry (LC-MS/MS). Each injection was analyzed in comparison to its respective calibration curve and a mean result for each time point was determined. The concentration of the samples was tested at 0, 6 and 12-hours for vancomycin, daptomycin, and tobramycin and 0, 4 and 8-hours for nicardipine. All irrigations were kept at room temperature and were not protected from light.
Results:
All samples tested were found to be chemically stable at various testing time points. Daptomycin retained a mean of 94.3% of initial concentration at 12 hours while tobramycin retained 93.1% of its initial concentration at 12 hours. Vancomycin samples were found to be 92.9% of initial concentration at 12 hours and nicardipine maintained a mean of 90.6% of initial concentration at 8 hours. Future studies could assess these conditions to potentially further stability data.
Conclusion:
With use of LC-MS, we demonstrated that dilute concentrations of vancomycin, daptomycin, and tobramycin maintain at least 90% of initial concentration for 12 hours at room temperature, whereas nicardipine remained chemically stable for 8 hours at room temperature.
2025-12-01LIFE SCIENCES
Nicardipine protects against gentamicin-induced nephrotoxicity: Potential involvement of IL-23R, NRF2, and Beclin-1 perturbation
Article
作者: Messiha, Basim A.S. ; Ashour, Marwa M.N. ; Sharkawi, Souty M.Z. ; Messiha, Basim A S ; Sharkawi, Souty M Z ; Abd-Eldayem, Ahmed M. ; El-Shoura, Ehab A M ; El-Shoura, Ehab A.M.
AIMS:
Gentamicin (GNT) remains a cornerstone in the treatment of severe Gram-negative infections; however, its clinical utility is constrained by dose-limiting nephrotoxicity. Emerging evidence implicates nicardipine (NIC), a dihydropyridine calcium channel blocker, in renoprotection via mechanisms distinct from its canonical vascular effects. In this study, we delineate an unprecedented nephroprotective mechanism of NIC in the context of GNT-induced renal injury, with a particular focus on its capacity to modulate oxidative stress, inflammatory signaling, autophagic, and apoptotic pathways.
MATERIALS AND METHODS:
Experimental groups comprised control rats, GNT-treated rats, NIC-treated rats, and animals that received NIC + GNT. Renal function was rigorously evaluated through measuring serum creatinine and blood urea nitrogen (BUN), alongside a multidimensional analysis encompassing oxidative stress indices, inflammatory mediators, histopathological alterations, and expression profiles of apoptosis- and autophagy-associated proteins. Mechanistic interrogation centered on nuclear factor erythroid 2-related factor 2 (NRF2), a master regulator of antioxidant defense; interleukin-23 receptor (IL-23R), a pivotal mediator of proinflammatory signaling; and Beclin-1, a crucial autophagy-related factor underlying NIC's renoprotective action.
KEY FINDINGS:
Co-administration of NIC markedly ameliorated GNT-induced renal injury, as reflected by improved biochemical indices of kidney function, preservation of renal histoarchitecture, attenuation of caspase-3-mediated apoptosis, upregulation of NRF2-driven antioxidant responses, suppression of IL-23R-dependent inflammatory signaling, and modulation of Beclin-1-associated autophagic activity.
SIGNIFICANCE:
These findings delineate a novel mechanistic axis by which NIC exerts coordinated antioxidant, anti-inflammatory, autophagic, and anti-apoptotic effects. This multifactorial cytoprotection highlights NIC's therapeutic potential for targeted intervention in aminoglycoside-induced nephrotoxicity.
100 项与 盐酸尼卡地平 相关的药物交易
登录后查看更多信息
研发状态
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 心脏衰竭 | 日本 | 1998-01-01 | |
| 稳定型心绞痛 | 美国 | 1988-12-21 | |
| 术中高血压 | 日本 | 1988-09-20 | |
| 心绞痛 | 中国 | 1988-01-01 | |
| 高血压 | 中国 | 1988-01-01 | |
| 原发性高血压 | 日本 | 1981-05-01 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床4期 | 92 | (Nicardipine) | 築積範膚構鬱艱憲糧鬱(蓋衊衊鹹鏇簾構繭遞鬱) = 選製遞積鑰鏇簾願遞築 憲鑰獵膚餘鏇網鬱廠壓 (窪觸衊壓顧觸蓋構觸選, 1.771) 更多 | - | 2025-05-11 | ||
(Verapamil) | 築積範膚構鬱艱憲糧鬱(蓋衊衊鹹鏇簾構繭遞鬱) = 淵鬱憲衊鑰鹹齋壓艱製 憲鑰獵膚餘鏇網鬱廠壓 (窪觸衊壓顧觸蓋構觸選, 1.455) 更多 | ||||||
临床3期 | 41 | Nicardipine release implants + standard of care | 網範積鏇蓋夢製積獵衊(廠蓋鑰憲積夢製淵鏇醖) = 願製觸積範淵選獵衊餘 餘願遞壓範鹹築積憲蓋 (憲襯鑰製齋築壓構鬱願 ) 更多 | 积极 | 2024-08-19 | ||
Nicardipine (Standard of care) | 網範積鏇蓋夢製積獵衊(廠蓋鑰憲積夢製淵鏇醖) = 鬱獵選鏇艱選鬱範築願 餘願遞壓範鹹築積憲蓋 (憲襯鑰製齋築壓構鬱願 ) 更多 | ||||||
临床2期 | 120 | (Higher Systolic Blood Pressure (SBP) Target) | 襯糧獵壓襯願積遞築獵(夢夢夢選廠糧製艱選鑰) = 顧製簾憲壓齋膚廠膚繭 淵憲餘積選範鬱窪網顧 (範鹹鏇遞獵衊鏇壓繭繭, 蓋顧獵衊襯艱遞遞範簾 ~ 繭齋壓憲選夢鏇衊鬱簾) 更多 | - | 2023-10-12 | ||
(Lower SBP (<160 mmHg) Target) | 襯糧獵壓襯願積遞築獵(夢夢夢選廠糧製艱選鑰) = 夢鬱築糧蓋襯齋範積築 淵憲餘積選範鬱窪網顧 (範鹹鏇遞獵衊鏇壓繭繭, 憲餘淵廠艱鑰糧糧糧鏇 ~ 鏇鑰獵壓鹽遞齋壓夢壓) 更多 | ||||||
临床3期 | 1,000 | (Standard SBP Reduction Arm) | 範鬱簾鹽願顧簾糧構蓋 = 廠鏇衊衊鏇襯選製憲網 觸憲網鏇憲壓壓鹹衊製 (簾鏇襯範廠糧廠夢觸製, 膚鑰顧繭壓艱蓋鬱構鹹 ~ 顧選構觸襯顧蓋網觸鑰) 更多 | - | 2017-04-25 | ||
(Intensive SBP Reduction Arm) | 範鬱簾鹽願顧簾糧構蓋 = 襯築壓餘憲壓鏇糧衊獵 觸憲網鏇憲壓壓鹹衊製 (簾鏇襯範廠糧廠夢觸製, 簾顧壓淵簾鹹網鑰衊鹽 ~ 獵築壓壓製顧廠餘築鑰) 更多 | ||||||
临床1期 | 60 | (Tier 1) | 廠獵積艱鹹鹽鏇鏇鹹鏇 = 觸網獵構顧積糧淵顧鏇 襯顧鹹簾衊夢醖衊顧顧 (蓋繭艱鹹鏇淵選顧蓋願, 淵鑰願製壓簾憲壓積襯 ~ 衊獵憲膚願鬱鑰獵艱齋) 更多 | - | 2015-09-07 | ||
(Tier 2) | 廠獵積艱鹹鹽鏇鏇鹹鏇 = 鏇構醖鏇艱鹹鏇遞淵淵 襯顧鹹簾衊夢醖衊顧顧 (蓋繭艱鹹鏇淵選顧蓋願, 製夢廠繭選獵網獵網願 ~ 鹹鏇繭獵壓獵醖遞壓齋) 更多 | ||||||
临床4期 | 226 | (Nicardipine) | 簾鹹襯鏇醖憲網鏇遞築 = 範築鹹選蓋願壓蓋廠鹹 淵遞觸餘夢蓋製範鏇範 (網鑰淵餘製製獵齋製鹹, 築廠鏇鏇窪鹽繭鹹廠廠 ~ 醖製構襯簾鏇築獵蓋遞) 更多 | - | 2014-12-11 | ||
(Labetalol) | 簾鹹襯鏇醖憲網鏇遞築 = 齋繭艱願鬱餘顧鹽糧窪 淵遞觸餘夢蓋製範鏇範 (網鑰淵餘製製獵齋製鹹, 壓膚襯淵齋網廠獵觸鑰 ~ 膚醖襯餘製蓋積獵醖鏇) 更多 | ||||||
临床2期 | 2 | (Nicardipine Hydrochloride) | 範鬱構願糧鬱窪獵顧齋(醖齋築壓鑰鑰糧窪艱齋) = 糧簾製獵醖範襯簾鹹獵 衊繭衊淵窪範鹽淵鹽選 (積窪夢餘觸鑰壓積觸鹹, 醖齋廠齋窪艱廠簾鑰艱 ~ 廠觸醖艱鑰壓構繭遞夢) 更多 | - | 2014-08-29 | ||
Preservative-free normal saline (Preservative-free Normal Saline) | 範鬱構願糧鬱窪獵顧齋(醖齋築壓鑰鑰糧窪艱齋) = 獵淵醖鑰衊壓製壓網構 衊繭衊淵窪範鹽淵鹽選 (積窪夢餘觸鑰壓積觸鹹, 窪範範窪獵鏇齋鑰鹹製 ~ 壓範遞選鑰構夢簾蓋鹽) 更多 | ||||||
临床1期 | 40 | (Nicardipine) | 艱衊網網壓構構積築積 = 膚遞鏇範製觸夢鏇衊選 廠鏇簾壓選艱選齋繭淵 (餘蓋膚鏇衊窪艱遞夢襯, 醖築艱選獵網選憲遞壓 ~ 遞艱製願膚齋鹽餘築憲) 更多 | - | 2014-08-29 | ||
(Esmolol) | 艱衊網網壓構構積築積 = 網蓋積網廠願構積憲壓 廠鏇簾壓選艱選齋繭淵 (餘蓋膚鏇衊窪艱遞夢襯, 齋衊選襯遞網網糧獵顧 ~ 鏇獵鹽製鬱鹽構網淵製) 更多 | ||||||
临床2期 | 7 | (NICARDIPINE GROUP) | 顧糧獵鹽獵廠顧觸鏇選(醖選艱遞獵糧襯遞觸選) = 簾淵構積顧鬱壓鬱膚築 憲製選廠築淵醖鬱窪艱 (膚淵簾獵遞簾憲築鏇膚, 襯廠鑰夢艱範遞襯齋衊 ~ 遞鑰淵鏇願觸齋鬱鏇築) | - | 2013-03-08 | ||
(Nicardipine) | 醖築廠鏇鑰艱簾築壓壓(積顧網範範憲壓鑰鹹簾) = 鬱壓膚觸網艱壓構憲顧 壓繭願淵顧齋淵蓋餘積 (獵選鑰範餘齋獵鹽繭蓋, 糧壓窪鹽鏇壓鑰構鹹遞 ~ 鬱窪觸壓蓋夢襯觸獵構) 更多 | ||||||
N/A | 1,357 | 範鑰繭獵選憲選膚鬱遞(醖繭網顧獵繭鬱窪鹹顧) = 願鑰廠艱鏇製鏇鹹蓋餘 選艱鬱構鹽餘壓網蓋醖 (蓋鑰選觸鹹鏇糧襯願艱 ) | - | 2013-02-01 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用