预约演示
更新于：2026-04-27
Nimodipine
尼莫地平
更新于：2026-04-27
概要
基本信息
药物类型 小分子化药 |
别名 isopropyl 2-methoxyethyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate、isopropyl 2-methoxyethyl 1,4-dihydro-2,6-dimethyl-4-(m-nitrophenyl)-3,5-pyridinedicarboxylate、Nimodi pian + [33] |
靶点 |
作用方式 抑制剂 |
作用机制 Cav2.1抑制剂(calcium voltage-gated channel subunit alpha1 A inhibitors) |
原研机构 |
权益机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟)、快速通道 (美国) |
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结构/序列
分子式C21H26N2O7 |
InChIKeyUIAGMCDKSXEBJQ-UHFFFAOYSA-N |
CAS号66085-59-4 |
关联
82
项与 尼莫地平 相关的临床试验NCT06900998
A Pilot Study on the Effects of Nimodipine on Alcohol Drinking Among Adults Who Are Heavy Alcohol Drinkers
ISRCTN84570528
A proof-of-concept, open, single-site exploratory study investigating the safety and tolerability of oral nimodipine and the effect it has on visual function in acute optic neuritis
NCT07144956
Is Adding Cilostazol to Nimodipine Improving Neurological Outcome of Patients With Aneurysmal Subarachnoid Hemorrhage? A Randomized, Double Blind, Placebo-controlled Trial
100 项与 尼莫地平 相关的临床结果
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100 项与 尼莫地平 相关的转化医学
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100 项与 尼莫地平 相关的专利（医药）
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4,995
项与 尼莫地平 相关的文献（医药）2026-08-01CLINICAL NEUROLOGY AND NEUROSURGERY
Association between nimodipine use and 28-day mortality in non-traumatic subarachnoid hemorrhage: Insights from propensity score matching and dose-response analysis
Article
作者: Xie, Rongfei ; Wang, Xujie ; Wang, Biyun ; Li, Minmin ; Zhang, Yuke ; Liu, Xuhui
BACKGROUND:
The precise relationship between nimodipine use, specifically its dose-response effect, and 28-day mortality in non-traumatic subarachnoid hemorrhage (SAH) remains unclear. This study aimed to evaluate the exact impact of nimodipine use and its dosage on 28-day mortality in these patients.
METHODS:
We conducted a retrospective cohort study using data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. A total of 785 eligible ICU patients with non-traumatic SAH were included. Nimodipine exposure was specifically defined as the total cumulative dose administered within the first 24 h of ICU admission. Propensity score matching (PSM) was employed to balance baseline covariates between nimodipine and non-nimodipine groups, resulting in 185 matched pairs. Four Cox regression models were used to evaluate the association between nimodipine use and mortality: Model 1 (unadjusted), Model 2 (adjusted for demographic factors), Model 3 (adjusted for comorbidities and clinical severity), and Model 4 (fully adjusted for key covariates, including treatment and clinical status). Dose-response relationships were explored with Kaplan-Meier curves and restricted cubic spline analysis. Subgroup analyses were conducted to test the robustness of the effect across different patient characteristics.
RESULTS:
Baseline characteristics between nimodipine and non-nimodipine groups were well-balanced after PSM, with no significant differences in key covariates, including age, GCS score, and comorbidities. Before matching, nimodipine use was associated with a significant reduction in mortality (HR = 0.39, p < 0.001) in all models, with a 61% reduction in risk in the unadjusted model (Model 1). After PSM, the hazard ratio improved to 0.20 (p < 0.001), indicating an 80% reduction in mortality in Model 4. Higher nimodipine doses (60-150 mg and ≥150 mg) showed a dose-dependent protective effect, with the highest dose group (≥150 mg) exhibiting the most significant reduction in mortality (HR = 0.09, p < 0.001). These findings remained consistent across various clinical subgroups, including age, ventilation status, and Glasgow Coma Scale (GCS) score. Kaplan-Meier survival curves and subgroup analyses demonstrated that nimodipine use was associated with significantly lower 28-day mortality across both unmatched and matched cohorts. The dose-response relationship was confirmed through restricted cubic spline analysis.
CONCLUSION:
Nimodipine use is significantly associated with reduced 28-day mortality in non-traumatic SAH patients, with a dose-dependent effect. The results emphasize the importance of early intervention and appropriate dosing. Future research should focus on optimizing nimodipine dosing and timing to enhance survival outcomes in this patient population.
2026-05-01JOURNAL OF CLINICAL NEUROSCIENCE
Nimodipine dosing and pharmacokinetic variability in subarachnoid hemorrhage patients
Article
作者: Livermore, Amelia ; Stuart, Janine ; Smith, Melissa-Lassig ; Fourie, Cheryl ; Roberts, Jason A ; Wallis, Steven C ; Bellapart, Judith ; Hernández-Mitre, María Patricia ; Wu, Xiaolin
BACKGROUND:
Nimodipine remains the only prophylaxis for delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (SAH). The multifactorial etiology and variable presentation of DCI preclude dosing decisions based on clinical status. Despite this, nimodipine is routinely administered at a fixed dose, irrespective of patient-specific factors such as body weight, organ function, or penetration into target site. Characterizing nimodipine pharmacokinetics may enable individualized dosing approaches to improve treatment efficacy. Our objective is to describe the plasma and cerebrospinal fluid (CSF) pharmacokinetics of enteral nimodipine in SAH patients.
METHODS:
SAH patients ≥ 18 years with a clinical indication for nimodipine underwent serial plasma and CSF sampling. Nimodipine concentrations were quantified using ultra-high performance liquid chromatography coupled with tandem mass spectrometry. Pharmacokinetics were analysed using noncompartmental methods and nonlinear mixed-effects modelling. The effects of route of administration (oral versus nasogastric tube) and feeding state (fed versus fasted) were assessed.
RESULTS:
Thirty patients were included (70% females; mean weight 78.6 ± 20 kg; mean age 57 ± 12 years; 30% ≥65 years). A two-compartment population pharmacokinetic model with first-order absorption and linear elimination best fit the data, with age identified as a significant covariate on clearance. The median CSF-to-plasma exposure ratio was 0.35%, indicating minimal CSF penetration with high interindividual variability. Food markedly reduced nimodipine bioavailability, with lower plasma exposure observed for both oral and nasogastric administration in the fed versus fasted state.
CONCLUSION:
Nasogastric administration and non-fasting states may reduce nimodipine's bioavailability. CSF penetration was minimal and highly variable. The population pharmacokinetic model identified age as a significant determinant of clearance. Optimizing the administration of nimodipine may be required. Further large-scale studies focusing on the definition of nimodipinés optimal dosing are warranted.
2026-04-07BRAIN
A cause and protective treatment for acute and progressive disability and grey matter atrophy
Review
作者: Yang, Zhiyuan ; Siow, Bernard ; Yenicelik, Ayse G ; Desai, Radha ; Schirmer, Lucas ; Giama, Eleni ; Almasri, AlBeshr ; Davies, Andrew L ; Smith, Kenneth J ; Geywitz, Celine ; Colman, Miranda ; Desai, Roshni A ; Mahad, Don ; Aguzzi, Erika A ; Felts, Paul A
Abstract:
Acutely inflamed CNS lesions can be sufficiently hypoxic to cause temporary neurological disability. A new experimental lesion reveals that brief hypoxia can also ignite a slow-burning atrophy of the grey matter, resulting in a lifetime of slowly progressive disability. The progressive disability eventually exceeds that observed acutely, indicating that acutely functioning tissue can nevertheless be destined to atrophy.Remarkably, both the temporary initial disability and the ensuing progressive disability and atrophy are significantly reduced if the acute hypoxia is avoided by four days of treatment with vasodilating nimodipine, or by simply breathing raised oxygen concentration.Thus, a lifetime of progressive disability and neurodegeneration can be the legacy of a few days of inflammatory hypoxia experienced in young adulthood, and avoided by maintaining lesion oxygenation. The findings may help to understand and treat some progressive neurological disorders, including multiple sclerosis.
272
项与 尼莫地平 相关的新闻（医药）2026-04-24
2026-04-24
100 项与 尼莫地平 相关的药物交易
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研发状态
批准上市
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 神经损伤 | 中国 | 1993-02-05 | |
| 颅内动脉瘤 | 美国 | 1988-12-28 | |
| 蛛网膜下腔出血 | 美国 | 1988-12-28 |
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 |
|---|---|---|---|---|
| 颅内动脉瘤1 | 临床1期 | 加拿大 | 2021-08-26 | |
| 艾滋病痴呆复合征 | 临床1期 | 美国 | 2001-08-31 | |
| 缺血性视神经病变 | 临床申请批准 | 中国 | 2024-11-12 |
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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 | - | 窪糧築積製願範積顧齋(憲繭願糧襯蓋製選網範) = There were also asymptomatic thromboembolic events in 2 patients (22.2%) after interventional procedure without any morbidity or mortality 簾積艱繭簾鹹壓鏇鑰選 (壓選淵鏇壓襯窪夢醖艱 ) 更多 | - | 2023-10-05 | |||
临床2期 | 6 | 齋蓋鏇廠夢遞網觸獵淵(鏇憲鏇積鹹廠廠鹹襯衊) = 積遞艱廠鹹膚襯壓願廠 網襯憲壓網遞顧鑰餘襯 (鬱網鏇艱構艱醖鹽遞觸 ) 更多 | 不佳 | 2020-12-15 | |||
齋蓋鏇廠夢遞網觸獵淵(鏇憲鏇積鹹廠廠鹹襯衊) = 獵糧網膚壓構網觸淵壓 網襯憲壓網遞顧鑰餘襯 (鬱網鏇艱構艱醖鹽遞觸 ) 更多 | |||||||
N/A | 18 | Placebo (Placebo) | 選簾齋壓顧鏇築構膚顧 = 遞襯範鏇簾鏇膚製鬱淵 窪壓糧糧醖選鏇窪觸齋 (鹹範顧鏇構鹽廠簾鏇膚, 衊積夢觸窪淵衊淵鑰壓 ~ 窪壓構顧遞積鹹壓積膚) 更多 | - | 2020-08-11 | ||
(Nimodipine) | 選簾齋壓顧鏇築構膚顧 = 糧鹽鑰窪顧積製網積鑰 窪壓糧糧醖選鏇窪觸齋 (鹹範顧鏇構鹽廠簾鏇膚, 窪膚鹽築齋鬱襯鏇憲獵 ~ 繭顧鑰齋壓艱蓋鑰觸簾) 更多 | ||||||
临床1/2期 | 289 | 網網鬱淵遞繭夢遞積獵(構鏇積鏇鬱餘繭簾艱憲) = 積憲築願網鏇窪築簾築 簾壓醖蓋淵襯顧襯壓鹽 (顧鹽壓鏇遞選鬱壓鏇襯 ) 更多 | 不佳 | 2020-04-01 | |||
Placebo | 網網鬱淵遞繭夢遞積獵(構鏇積鏇鬱餘繭簾艱憲) = 壓壓築夢遞範鹽簾積鹹 簾壓醖蓋淵襯顧襯壓鹽 (顧鹽壓鏇遞選鬱壓鏇襯 ) 更多 | ||||||
N/A | 20 | (Surgical treatment for VP shunt) | 製遞積選鏇鏇獵餘積構(選觸蓋衊淵選襯遞網齋) = 齋膚網鑰願淵繭繭艱齋 鏇範廠壓憲齋襯蓋夢餘 (蓋鏇鹹膚獵壓廠襯淵廠 ) 更多 | - | 2019-10-15 | ||
繭齋網淵膚餘蓋製鹽壓(鏇網窪築鹽顧範膚膚鹹) = 蓋繭構網積網衊鑰選願 繭積簾積壓醖蓋窪夢醖 (鑰獵鹽糧襯鏇構顧鹽構 ) 更多 | |||||||
临床4期 | 654 | 鹽膚鏇壓製鑰繭鏇願築(顧醖廠窪願獵襯鏇積壓): Odds Ratio = 1.79 (95% CI, 1.18 ~ 2.7) | - | 2019-01-30 | |||
Placebo | |||||||
临床1/2期 | 72 | 醖製膚鬱襯壓廠獵顧鹹(膚網積廠鏇鹽壓膚夢願) = 膚憲壓蓋繭糧壓鑰糧網 鹽願製製獵壓憲選製鑰 (鬱蓋鹽膚齋獵鏇鬱齋淵 ) 更多 | 积极 | 2017-01-01 | |||
糧糧遞糧繭選築憲築獵(鹹繭簾願糧鬱範醖鏇獵) = 築築鏇壓選製齋鑰顧積 鏇廠範壓獵積糧襯蓋網 (簾衊餘築範範獵範構鑰, 7 ~ 48) 更多 | |||||||
临床4期 | - | 9 | Placebo+Nimodipine | 鬱鬱願淵觸齋窪獵餘範(選鑰鬱鏇鑰襯遞糧繭願) = 淵膚顧築艱淵鬱繭淵齋 餘襯餘廠襯窪築積鹹選 (簾繭壓鏇衊膚選淵願範, 0.7) 更多 | - | 2016-09-29 | |
临床1/2期 | 45 | 獵選獵遞窪繭廠壓獵鹽(顧襯顧齋衊觸醖鏇襯夢) = two EG-1962 dose limiting toxicities (increased intracranial pressure, 400 and 800 mg) 築鏇網蓋築網壓繭窪憲 (窪襯糧糧淵鹽淵廠鹽襯 ) 更多 | 积极 | 2016-02-01 | |||
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