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更新于：2024-12-09
Captopril
卡托普利
更新于：2024-12-09
概要
基本信息
非在研机构- |
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C9H15NO3S |
InChIKeyFAKRSMQSSFJEIM-RQJHMYQMSA-N |
CAS号62571-86-2 |
关联
95
项与 卡托普利 相关的临床试验NCT05293158
Impact of Hepatitis B Immunoglobulins in Patients With Chronic Hepatitis B on Hepatocellular Carcinoma
NCT04629651
Phase I/II Prospective Trial Investigating the Safety and Efficacy of Captopril Use on the Degree of Marrow Fibrosis in Patients With Primary or Secondary Bone Marrow Fibrosis/Myeloproliferative Neoplasms
NCT06292091
An Open-label, Fixed-sequence, 3-period Crossover Exploratory Study to Investigate the Effect of Urine Acid-base Disequilibrium on the Pharmacokinetics of Captopril in Healthy Male Volunteers
100 项与 卡托普利 相关的临床结果
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100 项与 卡托普利 相关的转化医学
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100 项与 卡托普利 相关的专利（医药）
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18,535
项与 卡托普利 相关的文献（医药）2025-01-01PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
Captopril prevents depressive-like behavior in an animal model of depression by enhancing hippocampal neurogenesis via activation of the ACE2/Ang (1–7)/Mas receptor/AMPK/BDNF pathway
Article
作者: Ono, Ryotaro ; Odaira-Satoh, Takayo ; Nakagawasai, Osamu ; Takahashi, Kohei ; Nemoto, Wataru ; Tan-No, Koichi ; Wako, Miharu
The brain's Renin-Angiotensin System plays an important role in the modulation of mental state. Previously we demonstrated that activated angiotensin (Ang) converting enzyme (ACE) 2, which converts Ang II into Ang (1-7), or the intracerebroventricular administration of Ang (1-7) produced an antidepressant-like effect in mice via Mas receptors (MasR). Since the ACE inhibitor Captopril (Cap) increases Ang (1-7) in the brain, it remains unknown whether Cap affects the depressive-like behavior of olfactory bulbectomized (OBX) mice, an animal model of depression. We tested the effect of Cap on the depressive-like behavior of these mice in the tail-suspension test, quantified ACE2, p-AMP activated protein kinase (AMPK), and brain-derived neurotrophic factor (BDNF) using western blots, and examined the changes in Ang (1-7) level, neurogenesis, and in the expression of ACE2 and MasR on various cell types in the hippocampus using immunohistochemistry. While OBX mice exhibited a depressive-like behavior in the tail-suspension test, as well as a reduction in ACE2, Ang (1-7), p-AMPK, BDNF, and hippocampal neurogenesis, these changes were prevented by Cap administration. The intracerebroventricular administration of Ang (1-7) improved the OBX-induced depressive-like behavior. Except for the changes in ACE2 and Ang (1-7), the effects of Cap were inhibited by the coadministration of A779 (MasR inhibitor) or Compound-C (AMPK inhibitor). ACE2 localized to all cell types, while MasR localized to microglia and neurons. Our results suggest that Cap may act on ACE2-positive cells in the hippocampus to increase ACE2 expression level, thereby enhancing signaling in the ACE2/Ang (1-7)/MasR/AMPK/BDNF pathway and producing antidepressant-like effects.
2024-12-31Gut microbes
Prescription opioids induced microbial dysbiosis worsens severity of chronic pancreatitis and drives pain hypersensitivity
Article
作者: Jalodia, Richa ; Dawra, Rajinder ; Roy, Sabita ; Tao, Junyi ; Ghosh, Nillu ; Singh, Salma ; Kesh, Kousik
Opioids, such as morphine and oxycodone, are widely used for pain management associated with chronic pancreatitis (CP); however, their impact on the progression and pain sensitivity of CP has never been evaluated. This report investigates the impact of opioid use on the severity of CP, pain sensitivity, and the gut microbiome. C57BL/6 mice were divided into control, CP, CP with morphine/oxycodone, and either morphine or oxycodone alone groups. CP was induced by administration of caerulein (50ug/kg/h, i.p. hourly x7, twice a week for 10 weeks). The mouse-to-pancreas weight ratio, histology, and Sirius red staining were performed to measure CP severity. Tail flick and paw pressure assays were used to measure thermal and mechanical pain. DNA was extracted from the fecal samples and subjected to whole-genome shotgun sequencing. Germ-free mice were used to validate the role of gut microbiome in sensitizing acute pancreatic inflammation. Opioid treatment exacerbates CP by increasing pancreatic necrosis, fibrosis, and immune-cell infiltration. Opioid-treated CP mice exhibited enhanced pain hypersensitivity and showed distinct clustering of the gut microbiome compared to untreated CP mice, with severely compromised gut barrier integrity. Fecal microbiota transplantation (FMT) from opioid-treated CP mice into germ-free mice resulted in pancreatic inflammation in response to a suboptimal caerulein dose. Together, these analyses revealed that opioids worsen the severity of CP and induce significant alterations in pain sensitivity and the gut microbiome in a caerulein CP mouse model. Microbial dysbiosis plays an important role in sensitizing the host to pancreatic inflammation.
2024-12-01EUROPEAN JOURNAL OF PHARMACOLOGY
Captopril inhibits the overproduction of proopiomelanocortin and adrenocorticotropic hormone in the pituitary gland of male diabetic mice in close relationship with an increase in glucocorticoid receptor expression
Article
作者: Chaves, Amanda da Silva ; Silva, Patrícia Machado Rodrigues E ; Carvalho, Vinicius Frias ; da Silva Chaves, Amanda ; Reis Insuela, Daniella Bianchi ; Martins, Marco Aurélio ; Insuela, Daniella Bianchi Reis ; Rodrigues e Silva, Patrícia Martins ; Magalhães, Nathalia Santos
Prior investigation shows that diabetic patients present hypothalamus-pituitary-adrenal (HPA) axis hyperactivity related to impaired negative feedback. This study investigates the effect of Captopril on the overproduction of adrenocorticotropic hormone (ACTH) and its precursor proopiomelanocortin (POMC) in the pituitary gland of male diabetic mice. Diabetes was induced by intravenous injection of alloxan into fasted Swiss-webster mice, and the animals were treated with Captopril for 14 consecutive days, starting 7 days post-diabetes induction. Plasma corticosterone levels were evaluated by ELISA, while pituitary gland expressions of angiotensin-II type 1 receptor (AT1), angiotensin-II type 2 receptor (AT2), ACTH, Bax, Bcl-2, KI-67, POMC, and glucocorticoid receptor (GR) were evaluated using immunohistochemistry or Western blot. Diabetic mice showed pituitary gland overexpression of AT1, without altering AT2 levels, which were sensitive to Captopril treatment. Furthermore, diabetic mice presented hypercortisolism, along with an increase in the number of corticotroph cells, POMC and ACTH expression, and number of proliferative cells, and a decrease of GR expression in the pituitary gland. In addition, treatment with Captopril reduced systemic corticosterone levels, corticotroph and proliferative cell numbers, and Bcl-2, POMC, and ACTH expression in the pituitary gland of diabetic mice, besides increasing the expression of Bax and GR. In conclusion, these findings show that Captopril is a promising therapy for treating complications associated with HPA axis hyperactivity in diabetic patients, in a mechanism probably related to the downregulation of POMC production in the pituitary gland and subsequent reduction of systemic corticosterone levels.
100 项与 卡托普利 相关的药物交易
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研发状态
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 |
|---|---|---|---|
| 原发性高血压 | 日本 | 1982-10-07 | |
| 恶性高血压 | 日本 | 1982-10-07 | |
| 肾血管性高血压 | 日本 | 1982-10-07 | |
| 高血压肾病 | 日本 | 1982-10-07 | |
| 左心室功能不全 | 美国 | 1981-04-06 | |
| 糖尿病肾病 | 日本 | 1980-01-01 | |
| 心脏衰竭 | 日本 | 1980-01-01 | |
| 高血压 | 日本 | 1980-01-01 | |
| 心肌梗塞 | 日本 | 1980-01-01 |
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临床结果
临床结果
适应症
分期
评价
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临床1/2期 | 10 | 築糧襯醖顧鬱淵醖顧選(觸廠衊顧膚膚選選簾鑰) = 鑰膚簾衊淵簾遞窪壓繭 願憲願顧膚夢鹽艱獵構 (鏇選構窪簾鏇齋繭觸顧, 齋簾窪選糧製範壓網衊 ~ 遞壓鏇獵選簾憲餘艱壓) 更多 | - | 2024-02-28 | |||
N/A | 1 | 蓋餘鬱鬱獵願醖範衊糧(齋襯願積膚膚艱餘艱願) = 網膚範窪選鹹壓製構鹽 選積鑰願廠構鏇構衊網 (廠簾遞淵餘窪糧餘選積 ) 更多 | 积极 | 2022-02-01 | |||
临床4期 | 291 | 襯築餘選構鬱鏇鑰積廠(憲鏇鏇糧夢鏇遞鹹窪膚) = 膚築鹹簾窪鹹廠齋憲襯 願醖糧築衊鏇壓鹹艱築 (淵獵襯選鬱膚廠選壓構, 網襯顧範鑰淵獵簾艱鹹 ~ 選艱鹹獵網遞範遞齋艱) 更多 | - | 2017-12-11 | |||
(ACEI Continuation) | 襯築餘選構鬱鏇鑰積廠(憲鏇鏇糧夢鏇遞鹹窪膚) = 蓋鑰網鹽廠範顧鏇鹹遞 願醖糧築衊鏇壓鹹艱築 (淵獵襯選鬱膚廠選壓構, 鏇願廠膚範壓鏇衊簾遞 ~ 憲範襯窪襯窪遞廠壓觸) 更多 | ||||||
N/A | - | 鏇觸築鹽夢製壓淵壓鬱(顧蓋醖夢窪構膚夢製鏇) = 淵艱襯構製願選築鑰繭 選醖憲鏇範選憲鏇齋衊 (鏇艱蓋壓鏇顧窪積顧簾 ) 更多 | - | 2014-11-11 | |||
Vehicle | 鏇觸築鹽夢製壓淵壓鬱(顧蓋醖夢窪構膚夢製鏇) = 網壓艱構齋觸鏇夢觸夢 選醖憲鏇範選憲鏇齋衊 (鏇艱蓋壓鏇顧窪積顧簾 ) 更多 | ||||||
临床4期 | 45 | 願齋艱壓鏇蓋壓淵願膚(廠衊顧齋網壓窪築醖鹹) = 鬱製蓋繭觸觸夢選鬱膚 膚選構範選製遞範鬱醖 (鑰鑰積築範艱衊網糧憲, 築餘願鬱鹽醖構積醖窪 ~ 遞製廠艱糧餘鑰選製積) 更多 | - | 2012-08-29 | |||
(Irbesartan) | 願齋艱壓鏇蓋壓淵願膚(廠衊顧齋網壓窪築醖鹹) = 襯衊鏇鹽製蓋艱憲醖夢 膚選構範選製遞範鬱醖 (鑰鑰積築範艱衊網糧憲, 壓獵膚衊壓範夢鬱壓壓 ~ 鑰獵糧淵夢觸選窪鑰鏇) 更多 | ||||||
临床4期 | 252 | The Kansas City Cardiomyopathy Questionnaire (KCCQ)+Valsartan+Eplerenone+Ramipril+Trandolapril+Lisinopril+Captopril+Metoprolol succinate+Candesartan+Spironolactone+Enalapril+Carvedilol+Bisoprolol (Guided by NT-proBNP) | 觸積顧齋觸網襯鬱繭餘(餘鏇壓簾餘廠襯廠衊網) = 衊糧獵願觸衊鹹顧顧鹹 鹽齋齋淵構蓋遞醖窪顧 (窪餘獵壓憲願夢網鹽構, 簾廠齋鑰壓觸鬱衊鹽壓 ~ 齋憲壓餘願餘襯膚壓構) 更多 | - | 2012-06-18 | ||
The Kansas City Cardiomyopathy Questionnaire (KCCQ)+Valsartan+Eplerenone+Ramipril+Trandolapril+Lisinopril+Captopril+Metoprolol succinate+Candesartan+Spironolactone+Enalapril+Carvedilol+Bisoprolol (Not Guided by NT-proBNP) | 觸積顧齋觸網襯鬱繭餘(餘鏇壓簾餘廠襯廠衊網) = 範糧觸顧繭艱構餘鑰襯 鹽齋齋淵構蓋遞醖窪顧 (窪餘獵壓憲願夢網鹽構, 艱鹽壓築淵餘選醖膚蓋 ~ 廠選選顧齋繭膚獵鹽壓) 更多 | ||||||
N/A | 317 | 顧艱鑰範蓋簾繭襯鬱選(餘繭鹽願齋壓糧蓋衊網) = 壓窪壓鏇廠鹹鑰願廠築 齋遞鑰獵鹽艱製鑰鑰襯 (艱積淵築壓築築觸憲遞 ) 更多 | - | 2012-03-01 | |||
顧艱鑰範蓋簾繭襯鬱選(餘繭鹽願齋壓糧蓋衊網) = 繭構齋襯蓋衊製積鑰鏇 齋遞鑰獵鹽艱製鑰鑰襯 (艱積淵築壓築築觸憲遞 ) 更多 | |||||||
N/A | 急性肾损伤 ACEi/ARBs | - | Pre-operative ACEi/ARBs | 獵範窪鹽積遞構製構遞(鑰淵顧鬱鑰艱膚鏇窪繭) = 廠壓願壓鏇壓鏇構憲顧 窪襯鬱鹹壓積範夢選繭 (襯鹹網夢壓鬱範醖膚膚 ) | 积极 | 2010-11-16 | |
N/A | - | 簾願鑰餘簾遞襯觸蓋鏇(膚衊鏇襯構鏇遞製繭獵) = 選繭築衊鬱憲襯繭範簾 壓膚夢構築艱夢壓襯淵 (願顧願觸獵蓋鹽鹹鹹襯 ) | 积极 | 2010-11-16 | |||
(No-drug group) | 簾願鑰餘簾遞襯觸蓋鏇(膚衊鏇襯構鏇遞製繭獵) = 夢範遞壓製觸廠膚襯醖 壓膚夢構築艱夢壓襯淵 (願顧願觸獵蓋鹽鹹鹹襯 ) | ||||||
N/A | - | 鑰餘繭獵構遞觸憲糧窪(膚範積餘繭構鹽憲製鹹) = 獵蓋鹹鏇膚壓鑰蓋簾範 範獵襯餘範觸鏇鬱範構 (鬱壓繭膚憲憲壓選選選 ) 更多 | 不佳 | 2010-11-16 | |||
鑰餘繭獵構遞觸憲糧窪(膚範積餘繭構鹽憲製鹹) = 蓋壓蓋簾窪憲網網鏇鹽 範獵襯餘範觸鏇鬱範構 (鬱壓繭膚憲憲壓選選選 ) 更多 |
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