预约演示
更新于：2026-05-08
Perindopril Arginine
精氨酸培哚普利
更新于：2026-05-08
概要
基本信息
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- |
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结构/序列
分子式C25H46N6O7 |
InChIKeyRYCSJJXKEWBUTI-YDYAIEMNSA-N |
CAS号612548-45-5 |
关联
10
项与 精氨酸培哚普利 相关的临床试验CTR20240279
精氨酸培哚普利片在中国成年健康受试者中的生物等效性研究
CTR20233406
精氨酸培哚普利片人体生物等效性研究
CTR20230504
一项单中心、随机、开放、单次给药、两制剂、两周期交叉设计研究评价杭州仟源保灵药业有限公司的精氨酸培哚普利片与Les Laboratoires Servier的精氨酸培哚普利片在健康受试者中的空腹和餐后状态下的生物等效性研究
100 项与 精氨酸培哚普利 相关的临床结果
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100 项与 精氨酸培哚普利 相关的转化医学
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100 项与 精氨酸培哚普利 相关的专利（医药）
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2,384
项与 精氨酸培哚普利 相关的文献（医药）2026-06-01Journal of the American Medical Directors Association
Impact of Different Antihypertensive Drug Classes on Incident Dementia in Older Adults: A Systematic Review and Meta-Analysis
Review
作者: Zhu, Xiaojie ; Ding, Lu ; Wu, Huihong ; Zhang, Yuanxi ; Wang, Xiangzhao ; Liu, Ziwang ; Zhang, Meng ; Chen, Zixin
OBJECTIVES:
To evaluate the association between different classes of antihypertensive medications (AHMs) and dementia risk in older adults through systematic review and meta-analysis.
DESIGN:
Systematic review and exploratory network meta-analysis (NMA) following PRISMA-MOOSE guidelines. For traditional meta-analysis, random-effects models (DerSimonian-Laird method) were used for dichotomous outcomes, and fixed-effects models for continuous outcomes. Exploratory NMA employed a frequentist fixed-effects model (Stata 18 network package), as the sparse network precluded Bayesian estimation.
SETTING AND PARTICIPANTS:
Four multicenter randomized controlled trials [Syst-Eur, Perindopril Protection Against Recurrent Stroke Study (PROGRESS), SCOPE, HYVET-COG] comprising 16,823 hypertensive older adults without dementia at baseline, with follow-up durations of 2.0-3.9 years.
METHODS:
Literature searches were conducted in PubMed, Cochrane Library, Web of Science, and Embase from inception to December 31, 2025. Risk of bias was assessed using Cochrane RoB 2, and evidence certainty was evaluated using GRADE. Random-effects models pooled dichotomous outcomes [odds ratios (OR)] and fixed-effects models analyzed continuous outcomes [standardized mean differences (SMDs)].
RESULTS:
Antihypertensive treatment significantly improved cognitive function scores (SMD, 0.06; 95% CI, 0.03-0.09; P < .001, GRADE moderate certainty) and showed a nonsignificant trend toward reduced dementia incidence (OR, 0.89; 95% CI, 0.76-1.05; P = .172, GRADE low certainty). Exploratory NMA suggested calcium channel blockers ranked highest for dementia prevention [surface under the cumulative ranking curve (SUCRA) = 94.7%], while diuretic ± angiotensin-converting enzyme inhibitor combinations ranked highest for cognitive improvement (SUCRA = 95.3%); however, rankings were highly uncertain due to network sparsity (one study per node).
CONCLUSIONS AND IMPLICATIONS:
Antihypertensive therapy significantly improves cognitive function with moderate certainty evidence, supporting its use for cognitive protection in older adults with hypertension. The trend toward dementia risk reduction, although uncertain, suggests potential long-term benefits warranting further investigation.
CLINICAL IMPLICATIONS:
These findings support optimizing antihypertensive regimens for dementia prevention in high-risk populations, with drug class selection informed by specific treatment goals (dementia prevention vs cognitive maintenance).
POLICY AND RESEARCH IMPLICATIONS:
Current evidence is limited by few studies and short follow-up; large-scale randomized controlled trials with dementia as a primary endpoint, head-to-head drug class comparisons, and inclusion of long-term care residents-who bear the highest disease burden yet are underrepresented in trials-are urgently needed to inform precision prescribing guidelines.
2026-03-01BIOMEDICINE & PHARMACOTHERAPY
Dual calcium-ACE inhibition reverses non alcoholic fatty pancreas progression: Mechanistic convergence on miR-762/GPX4 driven NLRP3 inflammasome activation
Article
作者: Khaled, Radwa ; Elanwar, Aly ; Attia, Shimaa S ; Saad, Maha ; Hendawy, Nevien ; Yousef, Tarek M ; Shafei, Marwa ; Matboli, Marwa ; Roushdy, Marian Maher Salib ; Hamam, Ghada Galal ; Tolba, Mohamed Ahmed Mohamed ; Mohamed, Nesma Mohamed
BACKGROUND:
Non-alcoholic fatty pancreas (NAFP) is characterized by abnormal pancreatic fat accumulation and remains poorly understood.
AIM:
This study investigates the therapeutic potential and mechanistic basis of low-dose amlodipine-perindopril combination therapy, hypothesizing dual calcium channel blockade and RAS inhibition synergistically disrupt ferroptotic-inflammatory cascades driving pancreatic lipotoxicity.
METHODS:
The bioinformatics analysis of GEO datasets (GSE40901, GSE101462, and GSE194331) identified differentially expressed genes, which were further validated through molecular docking studies with amlodipine and perindoprilat. Male Wistar rats (n = 30) were randomized into five groups: healthy control, NAFP (high-sugar/high-fat diet), amlodipine-treated, perindopril-treated, and combination therapy. Gene expression of GPX4, ACSL4, NLRP3, and rno-miR-762 was quantified by Real-Time PCR. Metabolic parameters, pancreatic histopathology, and immunohistochemical markers (caspase-1, nuclear factor kappa B (NF-κB)) were assessed.
RESULTS:
Bioinformatics analysis revealed significant alterations in ferroptosis and inflammatory pathways. Molecular docking demonstrated favorable binding affinities between therapeutic compounds and target proteins. NAFP induction resulted in GPX4 downregulation (0.471 ± 0.357 vs. 1.197 ± 0.449, P < 0.05), ACSL4 upregulation (48.633 ± 40.998 vs. 1.197 ± 0.445, p < 0.001), elevated NLRP3 (12.717 ± 7.904 vs. 1.115 ± 0.186, p < 0.001), and increased rno-miR-762 expression. The combination therapy achieved 73 % reduction in pancreatic adipocyte area (vs. 42 % with monotherapies, p < 0.001) through coordinated miR-762 suppression (↓68 %, q=0.003) and GPX4 protein restoration (↑2.1-fold, p = 0.008). NLRP3 inflammasome activity decreased by 89 % (p = 0.004). Crucially, the regimen preserved hemodynamic stability, demonstrating metabolic benefits without cardiovascular compromise.
CONCLUSION:
These findings position miR-762 as a linchpin biomarker connecting metabolic stress to ferroptotic pancreatitis, with clinical translation challenges. This work provides the first evidence that sub-therapeutic calcium-RAS crosstalk modulation can reverse established pancreatic steatosis while outlining a precision medicine framework for NAFP prevention.
2026-02-01Cardiovascular Toxicology
Role of Perindopril in Mitigating Doxorubicin’s Vascular Toxicity in a Rat Model
Article
作者: Šůstková, Lucie ; Hložková, Jana ; Nádeníček, Jaroslav ; Nováková, Marie ; Studenik, Christian ; Smutná, Jindra ; Marhefka, Filip ; Hendrych, Michal ; Scheer, Peter ; Stračina, Tibor ; Marada, Anna ; Paulová, Hana
Abstract:
Doxorubicin (DOX), a widely used anthracycline in cancer therapy, is associated with significant cardiovascular toxicity. While its cardiotoxic effects are well documented, the mechanisms and prevention of DOX-induced vascular toxicity remain insufficiently explored. Angiotensin-converting enzyme inhibitors (ACEIs), such as perindopril (PER), are commonly used in cardiovascular disease management and may offer vascular protection during chemotherapy. Female ovariectomized Wistar rats were treated with
i.v.
DOX and/or
p.o.
PER over five weeks. Cardiac and vascular function were assessed using high-frequency ultrasound and ECG. Vascular reactivity was evaluated in isolated aortal rings using phenylephrine (PE), acetylcholine (ACh), L-N-Nitro arginine methyl ester hydrochloride (L-NAME), and verapamil (VER). Oxidative stress was assessed via plasma 4-hydroxy-2-nonenal (4-HNE) levels, and structural changes were monitored through intima-media thickness (IMT) measurements. DOX administration significantly impaired vascular reactivity, as evidenced by increased contractile responses to PE and reduced endothelium-dependent relaxation. These functional alterations were accompanied by elevated plasma 4-HNE levels, indicating enhanced oxidative stress. Co-treatment with PER preserved vascular responsiveness, reduced contractile tension, and significantly lowered 4-HNE concentrations. Structurally, IMT increased in control and PER-only groups, likely due to post-ovariectomy remodelling, while DOX-treated groups showed no IMT progression. PER co-treatment appeared to stabilize IMT values. PER mitigates DOX-induced vascular toxicity, likely through endothelial protection and reduction of oxidative stress. These findings support the potential use of ACEIs as prophylactic agents in patients undergoing anthracycline-based chemotherapy and highlight the need for further translational studies in cardio-oncology.
Graphical Abstract
100 项与 精氨酸培哚普利 相关的药物交易
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研发状态
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 原发性高血压 | 中国 | 2014-10-17 | |
| 冠状动脉疾病 | 澳大利亚 | 2005-06-08 | |
| 心脏衰竭 | 澳大利亚 | 2005-06-08 | |
| 高血压 | 澳大利亚 | 2005-06-08 |
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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2期 | 224 | (Perindopril) | 遞衊範糧製鏇鹽顧獵壓(選鹽淵鏇糧簾鬱壓製淵) = 夢鑰鹽鬱夢願築繭願鏇 糧艱獵網構觸簾選膚願 (簾糧獵憲繭鹹顧積齋蓋, 0.02) 更多 | - | 2021-01-26 | ||
(Amlodipine) | 遞衊範糧製鏇鹽顧獵壓(選鹽淵鏇糧簾鬱壓製淵) = 鏇膚膚觸夢簾築窪觸蓋 糧艱獵網構觸簾選膚願 (簾糧獵憲繭鹹顧積齋蓋, 0.02) 更多 | ||||||
临床4期 | 291 | 構蓋獵廠齋鏇獵夢網築 = 壓餘觸選夢製壓廠蓋淵 廠淵網繭窪壓簾鑰艱壓 (顧齋簾製鹹構顧網鑰鹽, 願觸憲範憲觸淵艱夢構 ~ 選顧衊淵鹽壓膚顧窪獵) 更多 | - | 2017-12-11 | |||
(ACEI Continuation) | 構蓋獵廠齋鏇獵夢網築 = 願鏇製範醖積餘範糧鑰 廠淵網繭窪壓簾鑰艱壓 (顧齋簾製鹹構顧網鑰鹽, 膚餘鏇繭範網鑰膚夢襯 ~ 簾窪觸築憲衊夢選構糧) 更多 |
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