预约演示
更新于：2026-07-17
Perindopril Arginine
精氨酸培哚普利
更新于：2026-07-17
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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2,467
项与 精氨酸培哚普利 相关的文献（医药）2026-11-01JOURNAL OF ETHNOPHARMACOLOGY
Yiqi Huoxue formula promotes post-myocardial infarction angiogenesis by modulating mitochondria-associated membranes (MAMs) and calcium homeostasis via the cGMP/PKG signaling pathway
Article
作者: Guo, Shuwen ; Du, Tianhui ; Liang, Caiyu ; Zhang, Yunshu ; Zheng, Chenglong ; Xie, Weibin ; Guo, Jingyun ; Wang, Hui
ETHNOPHARMACOLOGICAL RELEVANCE:
Therapeutic angiogenesis represents a promising strategy for recovery following myocardial infarction (MI). Yiqi Huoxue Formula (YQHX), a well-known traditional Chinese medicinal prescription, is widely utilized in clinical practice to treat myocardial ischemia and enhance cardiac performance in patients with MI. This study aims to elucidate the regulatory role of YQHX on mitochondria-associated membranes (MAMs) via the cGMP/PKG signaling pathway in promoting post-MI angiogenesis and restoring cardiac function.
MATERIALS AND METHODS:
An in vivo MI model was established via left anterior descending (LAD) coronary artery ligation in rats, and an in vitro model was developed using hypoxia-induced injury in human umbilical vein endothelial cells (HUVECs). The effects of YQHX on cardiac function and HUVEC behaviors (proliferation, migration, and tube formation) were evaluated. Myocardial histopathology and endothelial damage were assessed using HE/Masson staining and biochemical assays. Angiogenesis in the infarct border zone was visualized by platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) immunofluorescence. Ultrastructural changes in MAMs, the endoplasmic reticulum (ER), and mitochondria were observed via transmission electron microscopy (TEM). Intracellular reactive oxygen species (ROS) and calcium (Ca 2+) levels were detected using fluorescent probes. Transcriptomic sequencing was performed to identify key therapeutic pathways, followed by validation of the cGMP/PKG axis and MAMs-associated proteins (including cGMP, PKG, IP3R2, GRP75, FUNDC1, VDAC1, CYPD, and MCU) using ELISA, Western blotting, and immunofluorescence.
RESULTS:
Echocardiography and biochemical analysis demonstrated that high-dose YQHX demonstrated comparable efficacy to the first-line clinical drug Perindopril in preserving cardiac function and mitigating myocardial injury. Immunofluorescence revealed that while the infarct border zone in the MI group exhibited disordered and dysfunctional capillary proliferation, YQHX treatment promoted the formation of organized and functional microvessels. TEM revealed significant disruption of MAMs ultrastructure post-MI. Furthermore, the colocalization of IP3R2 and VDAC1 was markedly reduced in MI tissues and hypoxic HUVECs, an effect that was reversed by YQHX. Transcriptomic analysis identified the cGMP/PKG pathway as a pivotal mechanism. Activation of this pathway by YQHX restored MAMs structural integrity and rescued impaired cytosolic Ca2+ signaling, as confirmed by TEM, Western blotting, triple-labeling immunofluorescence, and calcium assays. Consequently, YQHX-mediated MAMs repair enhanced HUVEC proliferation, migration, and angiogenic capacity.
CONCLUSION:
This study demonstrates that MI/hypoxia impairs endothelial function by disrupting the structural and functional integrity of MAMs. YQHX effectively preserves MAMs architecture and restores intracellular Ca2+ signaling via the cGMP/PKG signaling axis, thereby promoting post-MI angiogenesis and improving cardiac performance. These findings identify a novel therapeutic target for MI and highlight the unique advantages of traditional Chinese medicine formulas in modulating subcellular organelle interactions. However, given the inherent variability of botanical materials, these mechanistic findings are based on a single validated batch, and future multi-batch standardizations are warranted.
2026-09-01ARCHIVES OF ORAL BIOLOGY
Facilitatory effects of LY404187, a positive allosteric modulator of AMPA receptors, on swallowing initiation in anesthetized male rats
Article
作者: Magara, Jin ; Tsujimura, Takanori ; Inoue, Makoto ; Norimine, Yoshihiko ; Hamashima, Hokuto ; Suzuki, Taku ; Pan, Charng-Rong ; Yoshihara, Midori ; Shirato, Manabu ; Ono, Mizuki
OBJECTIVE:
The present study aimed to investigate the effects of the systemic administration of LY404187, a positive allosteric modulator of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), on swallowing function.
DESIGN:
Experiments were conducted on 78 male Sprague-Dawley rats anesthetized with urethane. Upper airway distention with continuous airflow and the topical laryngeal application of distilled water or capsaicin were used to induce swallowing, which was identified by electromyographic activity recordings from the mylohyoid and thyrohyoid muscles. We investigated the effects of systemic administration of LY404187 (0.25-5.0 mg/kg), an angiotensin-converting enzyme inhibitor (perindopril), a dopamine agonist (amantadine), or a benzodiazepine inverse agonist (S-8510) on swallowing initiation.
RESULTS:
An optimal concentration of LY404187 (1.0 mg/kg) significantly increased the number of airflow-induced swallows compared with before administration. However, LY404187 did not modulate the initiation of chemically induced swallows. The pre-administration of talampanel, an AMPAR antagonist, diminished facilitatory effects of LY404187 on airflow-induced swallows. Perindopril, amantadine, and S-8510 did not facilitate both mechanically and chemically induced swallows.
CONCLUSION:
These results suggest that LY404187 facilitates the initiation of mechanically induced swallows via AMPAR activation.
2026-08-01LIFE SCIENCES
Serelaxin has greater anti-fibrotic potential than perindopril but maintains its anti-fibrotic efficacy in the presence of perindopril in normotensive mouse models of heart disease
Article
作者: Wang, Chao ; Ferens, Dorota ; Salimova, Ekaterina ; Samuel, Chrishan S ; Widdop, Robert E ; Gaspari, Tracey A ; She, Gang ; Wang, Ziqiao
AIMS:
Serelaxin (RLX), the drug form of human gene-2 relaxin, has potent anti-fibrotic properties that are currently being clinically-evaluated for the treatment of heart failure (HF). Whilst these effects can potentially be antagonised by angiotensin receptor blocker co-administration, this study determined if RLX was a suitable adjunct therapy to angiotensin converting enzyme inhibitor (ACEi) treatment. In particular, the anti-fibrotic effects of RLX were compared to or combined with the clinically-used ACEi, perindopril, in murine models of isoprenaline (ISO)-induced cardiomyopathy and surgically-induced myocardial infarction (MI).
METHODS:
The dose-response effects of perindopril (1, 2 or 4 mg/kg/day) on systolic blood pressure (SBP) and left ventricular (LV) fibrosis were first assessed in ISO-injured mice, after 7- or 14-days of treatment. The therapeutic effects of RLX (0.5 mg/kg/day) on SBP, LV fibrosis and LV functional parameters (ejection fraction, fractional shortening, stroke volume, cardiac output) were then compared to or combined with perindopril (2 mg/kg/day) pre-treatment (7-days prior) or co-administration (over 7-days) in ISO-injured mice; or perindopril co-administration (over 21-days) in MI-injured mice.
KEY FINDINGS:
Perindopril attenuated the ISO-induced LV fibrosis at 2 or 4 mg/kg/day, but induced significant hypotension at 4 mg/kg/day. RLX reduced the ISO- or MI-induced LV fibrosis, and restored measures of LV dysfunction, to a greater extent than perindopril (2 mg/kg/day), in the absence of BP regulation. These effects were maintained in the presence of perindopril pre-treatment or co-administration.
SIGNIFICANCE:
These findings confirmed that RLX had greater anti-fibrotic potential than perindopril, but could be applied as a rapidly-acting adjunct therapy to ACEi.
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) | 夢願齋繭糧餘遞夢簾糧(壓構窪網網鹽窪齋築觸) = 鏇鑰鑰範壓蓋遞餘醖膚 壓構遞醖襯淵鏇襯齋築 (遞顧積壓構醖憲蓋壓鹹, 0.02) 更多 | - | 2021-01-26 | ||
(Amlodipine) | 夢願齋繭糧餘遞夢簾糧(壓構窪網網鹽窪齋築觸) = 繭築鏇壓廠齋製構淵醖 壓構遞醖襯淵鏇襯齋築 (遞顧積壓構醖憲蓋壓鹹, 0.02) 更多 | ||||||
临床4期 | 291 | 蓋艱壓蓋窪選選蓋衊襯 = 糧夢繭蓋襯窪繭餘艱廠 鏇繭鑰鹹範齋網獵壓鬱 (廠廠襯艱鹽獵艱窪餘範, 鑰衊遞鹹鹽觸壓鹹餘構 ~ 憲鏇構襯遞淵積築鹽窪) 更多 | - | 2017-12-11 | |||
(ACEI Continuation) | 蓋艱壓蓋窪選選蓋衊襯 = 製築鹽積鏇糧醖夢糧觸 鏇繭鑰鹹範齋網獵壓鬱 (廠廠襯艱鹽獵艱窪餘範, 鹽顧簾鹹鹹顧餘繭積獵 ~ 艱網餘製夢鑰鬱窪艱鏇) 更多 |
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