预约演示
更新于：2026-02-27
Isoprenaline Hydrochloride
盐酸异丙肾上腺素
更新于：2026-02-27
概要
基本信息
权益机构- |
最高研发阶段批准上市 |
首次获批日期 美国 (1956-03-09) |
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C11H18ClNO3 |
InChIKeyIROWCYIEJAOFOW-MERQFXBCSA-N |
CAS号5984-95-2 |
关联
26
项与 盐酸异丙肾上腺素 相关的临床试验NCT06520982
Early Neurovascular Adaptations in Aging Women
NCT06082388
Comparison of the Clinical Utility of Atropine and Isoprenaline in the Invasive Diagnosis of Arrhythmias
NCT05997732
Sympathetic Neurovascular Transduction: Role of Adrenergic Receptors and Sex Differences
100 项与 盐酸异丙肾上腺素 相关的临床结果
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100 项与 盐酸异丙肾上腺素 相关的转化医学
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100 项与 盐酸异丙肾上腺素 相关的专利（医药）
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27,600
项与 盐酸异丙肾上腺素 相关的文献（医药）2026-12-31CLINICAL AND EXPERIMENTAL HYPERTENSION
Glycyrrhetinic acid ameliorates chronic heart failure via the Nrf2 pathway
Article
作者: Li, Xueqi ; Chen, Pengli ; Li, Shiguang ; Xu, Enwen ; Zhang, Ruilei ; Zhang, Hou
OBJECTIVE:
To explore the mechanism by which glycyrrhetinic acid (GA) alleviates chronic heart failure (CHF), focusing on NR3C1-mediated regulation of Nrf2 and oxidative stress.
METHODS:
A CHF rat model was established via transverse aortic constriction and treated with GA or NR3C1 knockdown. Cardiac function, hypertrophy, fibrosis, and oxidative stress markers were evaluated. In vitro, H9c2 cells were treated with isoproterenol to mimic CHF and subjected to GA, Nrf2 inhibitor, or NR3C1 modulation. Gene/protein expression, ROS, GSH, MDA, and mitochondrial membrane potential were assessed. Regulatory interactions between NR3C1 and Nrf2 were examined using luciferase, ChIP-qPCR, and CHX assays.
RESULTS:
GA alleviated myocardial hypertrophy and fibrosis in CHF rat models. GA also suppressed oxidative stress in CHF cell models. GA upregulated Nrf2 and its downstream target HO-1 at the protein level. NR3C1 was identified as a key upstream regulator of Nrf2, promoting its protein stability. NR3C1 knockdown decreased Nrf2 and HO-1 protein expression, disrupted mitochondrial membrane potential, and weakened the protective effects of GA against oxidative stress and cardiac dysfunction both in vitro and in vivo.
CONCLUSION:
GA alleviates CHF by enhancing NR3C1-mediated stabilization of Nrf2 and reducing oxidative stress.
2026-12-31Adipocyte
An acute temperature rise to 40°C inhibits free fatty acid uptake into white adipocytes
Article
作者: Foti, Federica ; Schaepper, Raoul S. ; Konrad, Daniel ; Wueest, Stephan
Fever reflects a physiological rise in body temperature accompanied by elevated production of adrenaline. The increased body temperature in fever is caused by shivering thermogenesis in skeletal muscle and non-shivering thermogenesis in brown adipose tissue (BAT), the latter being mediated by uncoupled oxidation of free fatty acids (FFAs). We hypothesized that an acute temperature rise to 40°C increases adrenalin-induced lipolysis in white adipocytes, thereby potentially providing FFAs as an energy substrate to sustain fever-induced thermogenesis in skeletal muscle and BAT. In 3T3-L1 and primary murine white adipocytes, isoproterenol-induced extracellular FFA accumulation was significantly increased at 40°C compared to 37°C. In contrast, isoproterenol-induced increase in extracellular glycerol concentrations and the protein levels of phosphorylated hormone sensitive lipase were comparable at both temperatures, suggesting a similar degree of lipolysis. Moreover, incubation at 40°C did neither increase isoproterenol-induced oxygen consumption nor intracellular FFA concentrations, indicating that the elevated extracellular FFA accumulation was not due to reduced intracellular consumption. Conversely, isoproterenol blunted FFA uptake into adipocytes to a significantly higher extent at 40°C compared to 37°C. Hence, an acute temperature rise to 40°C reduces FFA uptake into white adipocytes, thereby increasing extracellular FFA availability.
2026-04-01APPETITE
Functional bitter taste signaling and stimulus intensity influence diet-induced salivary protein upregulation
Article
作者: Beede-James, Kimberly F ; Zumpano, Kyle T ; Martin, Laura E ; Torregrossa, Ann-Marie ; Medler, Kathryn F ; Kay, Kristen E ; Gutierrez, Verenice Ascencio
Exposure to tannic acid- and quinine-containing diets upregulates subsets of salivary proteins (SPs), which in turn, results in increased acceptance of the "bitter" diet. However, it is unclear what aspects of the diet consumption influence SP upregulation. It has been thought that taste receptor activation is necessary for upregulation of SPs since sensory stimulation precedes changes in SPs, but no studies have confirmed the contribution of taste to SP upregulation. To test this hypothesis, we used TRPM5 KO and TRPM4/5 DKO mice that have impaired bitter taste signaling. These mice are able to upregulate SPs in response to isoproterenol injections but not when fed a tannic acid diet, which is both bitter and astringent. WT mice upregulate SPs after a tannic acid diet exposure while KO models do not. These data suggest that the mice are able to alter their SP expression but taste signaling is needed to upregulate SPs to diet treatments. The astringency alone from the tannic acid was not able to upregulate SPs. We then asked whether SP upregulation varies with stimulus intensity. Rats were fed quinine or sucrose octaacetate (SOA) at three different concentrations. All rats decrease intake on first day of bitter diet exposure at all three concentrations but increase acceptance of the diet by the fifth day of the quinine. In response to quinine diet, animals show concentration-dependent SP upregulation at the 14 kDa band, other bands were upregulated by diet but were not concentration-dependent. SOA did not alter protein expression at any concentration.
100 项与 盐酸异丙肾上腺素 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 |
|---|---|---|---|
| 心动过缓 | 日本 | 1987-04-16 | |
| 癫痫发作 | 日本 | 1987-04-16 | |
| 眩晕 | 日本 | 1975-12-09 | |
| 阿-斯综合征 | 美国 | 1956-05-25 | |
| 支气管痉挛 | 美国 | 1956-05-25 | |
| 心脏传导阻滞 | 美国 | 1956-05-25 |
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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 | 22,435 | Central neuraxial anesthesia+Dopamine+Glycopyrrolate+Hydroxyethyl starch solutions+Epinephrine+desflurane+Sodium Chloride 0.9%+propofol+Atropine+Ephedrine+Bupivacaine+Isoflurane+Dobutamine+Vasopressin+Isoproterenol+Norepinephrine+Prilocaine+Benzocaine+Procaine+Terlipressin+Tetracaine+ropivacaine+Articaine+Levobupivacaine+Milrinone+Phenylephrine+Sevoflurane+Mepivacaine+Lidocaine+Chloroprocaine (Usual Care Group) | 選廠鬱襯鑰築艱觸鏇鏇 = 繭鹽觸願鏇遞淵窪鹹窪 醖衊齋艱選淵衊膚淵憲 (鑰築夢鑰鏇鏇壓築醖夢, 醖鏇鹽鬱糧網淵獵遞網 ~ 獵衊艱簾廠艱鑰鹽網鹹) 更多 | - | 2019-05-16 | ||
Central neuraxial anesthesia+Dopamine+Glycopyrrolate+Hydroxyethyl starch solutions+Epinephrine+Desflurane+Sodium Chloride 0.9%+propofol+Atropine+Ephedrine+Bupivacaine+Isoflurane+Dobutamine+Vasopressin+Isoproterenol+Norepinephrine+Prilocaine+Benzocaine+Procaine+Terlipressin+Tetracaine+ropivacaine+Articaine+Levobupivacaine+Milrinone+Phenylephrine+Sevoflurane+Mepivacaine+Lidocaine+Chloroprocaine (Hypotension Decision Support) | 選廠鬱襯鑰築艱觸鏇鏇 = 觸願選觸鬱積簾衊鹽壓 醖衊齋艱選淵衊膚淵憲 (鑰築夢鑰鏇鏇壓築醖夢, 襯蓋淵襯獵簾鹹遞鹽壓 ~ 夢壓艱膚鏇窪積鹽餘鹽) 更多 | ||||||
N/A | 40 | (Healthy Seniors) | 鹽衊願夢選鹹襯餘蓋鑰(鬱廠網鏇遞獵憲鬱築獵) = 築艱齋淵壓築壓廠餘壓 鑰鹹艱積鹹繭鑰範膚簾 (醖餘積糧製憲醖壓夢壓, 0.166) 更多 | - | 2019-04-23 | ||
(HFpEF) | 鹽衊願夢選鹹襯餘蓋鑰(鬱廠網鏇遞獵憲鬱築獵) = 膚齋築餘壓鏇繭觸膚選 鑰鹹艱積鹹繭鑰範膚簾 (醖餘積糧製憲醖壓夢壓, 0.133) 更多 | ||||||
临床2期 | 131 | (Adenosine and Isoproterenol) | 繭艱齋憲膚膚憲簾壓夢 = 積簾膚糧遞鑰鏇膚醖範 淵鹽餘餘鑰壓顧淵積鏇 (獵築鏇製憲獵蓋積襯選, 淵獵構鹹顧築壓築廠廠 ~ 鏇鬱糧選夢選繭築簾製) 更多 | - | 2017-12-13 | ||
(Isoproterenol) | 繭艱齋憲膚膚憲簾壓夢 = 鬱餘膚窪襯憲鬱遞簾淵 淵鹽餘餘鑰壓顧淵積鏇 (獵築鏇製憲獵蓋積襯選, 憲範夢壓鬱鑰鹽鬱遞蓋 ~ 築構願簾襯鬱憲繭觸鏇) 更多 | ||||||
N/A | 20 | 範壓憲範鏇顧餘鏇鹹壓 = 糧蓋網襯餘蓋餘蓋蓋鹹 鬱糧糧蓋製壓獵廠衊鹽 (憲觸觸淵鏇糧製襯餘壓, 願衊簾廠夢獵選網餘鑰 ~ 鹹衊糧襯壓醖艱淵製願) 更多 | - | 2015-02-23 | |||
临床1/2期 | 10 | Prednisolone+Isoproteronol | 製膚窪繭齋繭獵蓋選簾(構膚淵蓋積構遞範衊選) = 夢鏇餘淵鏇遞衊網鹹衊 蓋壓鹹襯鹹餘簾蓋衊鹹 (膚艱鏇膚積壓選廠憲鏇, 願簾衊廠構構鑰構齋窪 ~ 齋網艱窪築築觸鏇遞選) 更多 | - | 2012-06-22 |
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