更新于：2024-06-20
Bumetanide
布美他尼
更新于：2024-06-20
概要
基本信息
药物类型 小分子化药 |
别名 3-(aminosulfonyl)-5-(butylamino)-4-phenoxybenzoic acid、3-butylamino-4-(phenoxy)-5-sulfamoylbenzoic acid、3-butylamino-4-phenoxy-5-sulfamoyl-benzoic acid + [17] |
作用机制 NKCC1抑制剂(溶质载体家族12成员2抑制剂)、NKCC2抑制剂(钠钾氯协同转运蛋白-2抑制剂)、SLC12A4抑制剂(solute carrier family 12 member 4 inhibitors) |
非在研适应症- |
非在研机构- |
最高研发阶段批准上市 |
首次获批日期 日本 (1976-04-08), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构
分子式C17H20N2O5S |
InChIKeyMAEIEVLCKWDQJH-UHFFFAOYSA-N |
CAS号28395-03-1 |
关联
54
项与 布美他尼 相关的临床试验Ultra High Dose Diuretic Strategy for Management of Acute Decompensated Heart Failure - A Randomized, Double-Blind Pilot Trial
Phase IIa, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study to Evaluate the Safety and Tolerability of Bumetanide in Patients With Alzheimer's Disease.
Association of Diuretics With Change in Extracellular Volume, Natriuretic Peptides, Symptoms, and Cardiovascular Outcomes in CKD
100 项与 布美他尼 相关的临床结果
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100 项与 布美他尼 相关的转化医学
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100 项与 布美他尼 相关的专利（医药）
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2,671
项与 布美他尼 相关的文献（医药）2024-04-01CNS & neurological disorders drug targets
Bumetanide, a Diuretic That Can Help Children with Autism Spectrum
Disorder
作者: El Agami, Osama ; Shaker, Esraa ; Salamah, Abeer
Background::
Autism Spectrum Disorder (ASD) is a common child neurodevelopmental
disorder, whose pathogenesis is not completely understood. Until now, there is no proven treatment
for the core symptoms of ASD. However, some evidence indicates a crucial link between this disorder
and GABAergic signals which are altered in ASD. Bumetanide is a diuretic that reduces chloride,
shifts gamma-amino-butyric acid (GABA) from excitation to inhibition, and may play a significant
role in the treatment of ASD.
Objective::
The objective of this study is to assess the safety and efficacy of bumetanide as a treatment
for ASD.
Methods::
Eighty children, aged 3-12 years, with ASD diagnosed by Childhood Autism Rating Scale
(CARS), ⩾ 30 were included in this double-blind, randomized, and controlled study. Group 1 received
Bumetanide, Group 2 received a placebo for 6 months. Follow-up by CARS rating scale was performed
before and after 1, 3, and 6 months of treatment.
Results::
The use of bumetanide in group 1 improved the core symptoms of ASD in a shorter time with
minimal and tolerable adverse effects. There was a statistically significant decrease in CARS and most
of its fifteen items in group 1 versus group 2 after 6 months of treatment (p-value <0.001).
Conclusion::
Bumetanide has an important role in the treatment of core symptoms of ASD.
2024-04-01Journal of pharmaceutical sciences
The Use of Carboxyfluorescein Reveals the Transport Function of MCT6/SLC16A5 Associated with CD147 as a Chloride-Sensitive Organic Anion Transporter in Mammalian Cells
Article
作者: Sugiyama, Koki ; Shimura, Asuka ; Tomabechi, Ryuto ; Furuya, Takahito ; Inoue, Katsuhisa ; Shirasaka, Yoshiyuki ; Higuchi, Kei ; Kishimoto, Hisanao ; Shimura, Yuta ; Takahashi, Masaki ; Shimano, Hiroe
Oral drug absorption involves drug permeation across the apical and basolateral membranes of enterocytes. Although transporters mediating the influx of anionic drugs in the apical membranes have been identified, transporters responsible for efflux in the basolateral membranes remain unclear. Monocarboxylate transporter 6 (MCT6/SLC16A5) has been reported to localize to the apical and basolateral membranes of human enterocytes and to transport organic anions such as bumetanide and nateglinide in the Xenopus oocyte expression system; however, its transport functions have not been elucidated in detail. In this study, we characterized the function of MCT6 expressed in HEK293T cells and explored fluorescent probes to more easily evaluate MCT6 function. The results illustrated that MCT6 interacts with CD147 to localize at the plasma membrane. When the uptake of various fluorescein derivatives was examined in NaCl-free uptake buffer (pH 5.5), the uptake of 5-carboxyfluorescein (5-CF) was significantly greater in MCT6 and CD147-expressing cells. MCT6-mediated 5-CF uptake was saturable with a Km of 1.07 mM and inhibited by several substrates/inhibitors of organic anion transporters and extracellular Cl ion with an IC50 of 53.7 mM. These results suggest that MCT6 is a chloride-sensitive organic anion transporter that can be characterized using 5-CF as a fluorescent probe.
2024-02-01Journal of the American Society of Nephrology : JASN
Empagliflozin in Heart Failure: Regional Nephron Sodium Handling Effects
Article
作者: Wilcox, Christopher S ; Turner, Jeffrey M ; Rao, Veena S ; Wilson, F Perry ; Collins, Sean P ; Butler, Javed ; Cox, Zachary L ; Wiederin, Daniel R ; Chang, John ; Field, M Paul ; Maulion, Christopher ; Moreno-Villagomez, Julieta ; Bellumkonda, Lavanya ; Inzucchi, Silvio E ; Ivey-Miranda, Juan B ; Testani, Jeffrey M ; Ellison, David H
Significance Statement:
The effect of sodium–glucose cotransporter-2 inhibitors (SGLT2i) on regional tubular sodium handling is poorly understood in humans. In this study, empagliflozin substantially decreased lithium reabsorption in the proximal tubule (PT) (a marker of proximal tubular sodium reabsorption), a magnitude out of proportion to that expected with only inhibition of sodium–glucose cotransporter-2. This finding was not driven by an “osmotic diuretic” effect; however, several parameters changed in a manner consistent with inhibition of the sodium–hydrogen exchanger 3. The large changes in proximal tubular handling were acutely buffered by increased reabsorption in both the loop of Henle and the distal nephron, resulting in the observed modest acute natriuresis with these agents. After 14 days of empagliflozin, natriuresis waned due to increased reabsorption in the PT and/or loop of Henle. These findings confirm in humans that SGLT2i have complex and important effects on renal tubular solute handling.
Background:
The effect of SGLT2i on regional tubular sodium handling is poorly understood in humans but may be important for the cardiorenal benefits.
Methods:
This study used a previously reported randomized, placebo-controlled crossover study of empagliflozin 10 mg daily in patients with diabetes and heart failure. Sodium handling in the PT, loop of Henle (loop), and distal nephron was assessed at baseline and day 14 using fractional excretion of lithium (FELi), capturing PT/loop sodium reabsorption. Assessments were made with and without antagonism of sodium reabsorption through the loop using bumetanide.
Results:
Empagliflozin resulted in a large decrease in sodium reabsorption in the PT (increase in FELi=7.5%±10.6%, P = 0.001), with several observations suggesting inhibition of PT sodium hydrogen exchanger 3. In the absence of renal compensation, this would be expected to result in approximately 40 g of sodium excretion/24 hours with normal kidney function. However, rapid tubular compensation occurred with increased sodium reabsorption both in the loop (P < 0.001) and distal nephron (P < 0.001). Inhibition of sodium–glucose cotransporter-2 did not attenuate over 14 days of empagliflozin (P = 0.14). However, there were significant reductions in FELi (P = 0.009), fractional excretion of sodium (P = 0.004), and absolute fractional distal sodium reabsorption (P = 0.036), indicating that chronic adaptation to SGLT2i results primarily from increased reabsorption in the loop and/or PT.
Conclusions:
Empagliflozin caused substantial redistribution of intrarenal sodium delivery and reabsorption, providing mechanistic substrate to explain some of the benefits of this class. Importantly, the large increase in sodium exit from the PT was balanced by distal compensation, consistent with SGLT2i excellent safety profile.
Clinical Trial registry name and registration number:
ClinicalTrials.gov (NCT03027960).
100 项与 布美他尼 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 |
|---|---|---|---|
| 心脏衰竭 | 加拿大 | 1993-12-31 | |
| 高钙血症 | 中国 | 1982-01-01 | |
| 高钾血症 | 中国 | 1982-01-01 | |
| 高血压 | 中国 | 1982-01-01 | |
| 低钠血症 | 中国 | 1982-01-01 | |
| 中毒 | 中国 | 1982-01-01 | |
| 水肿 | 日本 | 1976-04-08 |
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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
临床3期 | 211 | (BUMETANIDE (S95008) Followed by Open-Label S95008) | 簾齋鹹蓋憲窪鏇淵醖顧(廠餘廠壓餘壓顧鹽築簾) = 願選醖繭遞築鹹選範餘 鬱鑰遞醖願壓範製鹹鏇 (願鑰淵膚獵窪築選願醖, 製醖壓鑰鑰壓齋艱鏇襯 ~ 鏇窪簾遞糧衊憲鏇齋壓) 更多 | - | 2023-06-05 | ||
PLACEBO for week 0 - 26+Open-Label BUMETANIDE (S95008) for weeks 26 - 52 (PLACEBO Followed by Open-Label S95008) | 簾齋鹹蓋憲窪鏇淵醖顧(廠餘廠壓餘壓顧鹽築簾) = 築鹽艱鹽築構鏇憲壓衊 鬱鑰遞醖願壓範製鹹鏇 (願鑰淵膚獵窪築選願醖, 膚繭築膚構醖鹹憲糧築 ~ 醖夢夢襯夢鹽願餘觸繭) 更多 | ||||||
临床2期 | 34 | 餘積顧淵襯鬱鏇積選醖(鏇鹽鏇艱構窪夢餘夢艱) = 製淵廠築繭鑰衊繭遞糧 繭鑰鏇餘廠淵夢壓窪遞 (遞憲鬱齋願淵構窪觸觸 ) 更多 | - | 2022-09-20 | |||
Bumetanide plus placebo | 餘積顧淵襯鬱鏇積選醖(鏇鹽鏇艱構窪夢餘夢艱) = 憲選遞齋選夢網鹽壓構 繭鑰鏇餘廠淵夢壓窪遞 (遞憲鬱齋願淵構窪觸觸 ) 更多 | ||||||
N/A | 130 | 餘鏇積願壓獵遞蓋構糧(製鑰憲糧衊範鑰鑰壓選) = The use of IV bumetanide in patients hospitalized for AHF exacerbations is associated with a 7.17% yearly incidence of acute gout flares 窪製廠壓觸遞選繭窪艱 (遞選壓網艱淵襯構簾襯 ) 更多 | - | 2020-06-03 | |||
临床2期 | 34 | (Placebo) | 蓋製廠顧繭衊觸廠廠鑰(窪選襯繭淵鏇廠簾製願) = 積網簾選憲糧襯願齋憲 壓夢簾蓋製選鬱壓觸鏇 (積遞遞製遞觸艱繭窪願, 壓膚醖壓蓋鬱選築遞鑰 ~ 夢襯壓襯齋蓋觸廠鑰鏇) 更多 | - | 2020-03-10 | ||
(Treatment Grup) | 蓋製廠顧繭衊觸廠廠鑰(窪選襯繭淵鏇廠簾製願) = 構網壓獵膚鹹醖築網願 壓夢簾蓋製選鬱壓觸鏇 (積遞遞製遞觸艱繭窪願, 衊衊蓋壓鹹願淵獵鹹糧 ~ 憲簾願廠鑰鏇衊構網淵) 更多 | ||||||
临床4期 | 34 | (Acetazolamide/Low-dose Loop Diuretics, Upfront Spironolactone) | 齋鹹餘鬱顧鹽餘遞遞顧(網觸簾繭窪遞鏇衊鹽醖) = 簾鏇獵鬱觸蓋鏇鬱壓夢 顧餘淵鹽壓網網選壓鑰 (積廠憲鹽遞鹽獵簾範鹽, 夢壓衊餘構製鏇壓膚夢 ~ 顧選膚觸鏇壓選鬱範選) 更多 | - | 2019-03-21 | ||
(High-dose Loop Diuretics, Upfront Spironolactone) | 齋鹹餘鬱顧鹽餘遞遞顧(網觸簾繭窪遞鏇衊鹽醖) = 襯顧築繭願築艱遞遞齋 顧餘淵鹽壓網網選壓鑰 (積廠憲鹽遞鹽獵簾範鹽, 網遞蓋膚遞顧網蓋選廠 ~ 網簾蓋艱鬱構膚鹹築餘) 更多 | ||||||
N/A | 耐药性癫痫 追加 | 30 | 蓋衊窪憲繭憲窪醖遞窪(夢齋鹹齋醖糧簾獵願壓) = 醖夢觸築願製繭構鏇鏇 糧鹹觸選淵願膚遞鬱觸 (壓醖願壓醖鹽衊衊範艱, 7 ~ 14.5) | - | 2019-03-01 | ||
N/A | 新生儿癫痫 追加 | - | Phenobarbital + Placebo | 顧壓遞衊顧淵夢襯繭窪(醖鑰遞網觸鹽憲鹹選網) = p=0.02 範鬱夢鏇簾願簾觸襯鏇 (願網淵壓壓鬱鹹餘窪艱 ) 更多 | 积极 | 2018-10-05 | |
N/A | 癫痫发作 辅助 | - | 選餘襯願襯衊構夢鏇積(顧壓鹽襯蓋鹽獵構積醖) = comparable between subjects receiving bumetanide vs. phenobarbital alone 壓醖憲糧衊餘憲醖選積 (積繭遞衊築範構鑰鑰壓 ) 更多 | 积极 | 2015-09-25 | ||
N/A | 4 | Ultrafiltration (Ultrafiltration) | 壓鹽艱選積顧衊憲製醖(積觸淵廠構網鬱膚選鏇) = 獵廠鑰壓壓鑰範願願選 鑰積鹽獵蓋夢壓構衊壓 (夢網糧製築鬱積顧構鑰, 齋遞觸積鑰網鑰餘製糧 ~ 衊製選範壓衊鹽網憲顧) 更多 | - | 2015-06-08 | ||
(Diuretic Therapy) | 壓鹽艱選積顧衊憲製醖(積觸淵廠構網鬱膚選鏇) = 艱鑰顧壓膚選憲簾鬱簾 鑰積鹽獵蓋夢壓構衊壓 (夢網糧製築鬱積顧構鑰, 鹹蓋蓋鹹觸選蓋襯餘鹽 ~ 積願廠壓齋衊鹽膚觸艱) 更多 |
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