Furosemide

製品コードS1603 バッチS160303

化学情報

	Synonyms	NSC 269420	Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent
	化学式	C₁₂H₁₁ClN₂O₅S
	分子量	330.74	CAS No.	54-31-9
Solubility (25°C)*	体外	DMSO	66 mg/mL (199.55 mM)
		Ethanol	20 mg/mL (60.47 mM)
		Water	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Furosemide is a potent NKCC2 (Na-K-2Cl symporter) inhibitor, used in the treatment of congestive heart failure and edema.
in vitro	Furosemide reversibly alters the responses to tones and clicks of the chinchilla basilar membrane in hair cells, causing response-magnitude reductions that are largest (up to 61 dB, averaging 25-30 dB) at low stimulus intensities at the characteristic frequency (CF) and small or nonexistent at high intensities and at frequencies far removed from CF. Furosemide also induces response-phase lags that are largest at low stimulus intensities (averaging 77 degrees) and are confined to frequencies close to CF. ^[1] Furosemide concentration- and time-dependently increases the formation of nitric oxide andprostacyclin. Furosemide leads to an enhanced release of kinins into the supernatant of the cells. ^[2] Furosemide reversibly suppresses low Ca2+-induced epileptiform activity in hippocampus proper and blocks or significantly reduces different types of epileptiform discharges in the low Mg2+ model and the 4-aminopyridine model. ^[3] Furosemide significantly inhibits cell growth in MKN45 cells, but not in MKN28 cells. Furosemide diminishes cell growth by delaying the G(1)-S phase progression in poorly differentiated gastric adenocarcinoma cells, which show high expression and activity of NKCC, but not in moderately differentiated gastric adenocarcinoma cells with low expression and NKCC activity. ^[4]
in vivo	Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduces right atrial pressure (RAP) and pulmonary arterial pressure (PAP) during exercise in dose-dependent manner in horse. ^[5]

製品説明

Furosemide is a potent NKCC2 (Na-K-2Cl symporter) inhibitor, used in the treatment of congestive heart failure and edema.

in vitro

Furosemide reversibly alters the responses to tones and clicks of the chinchilla basilar membrane in hair cells, causing response-magnitude reductions that are largest (up to 61 dB, averaging 25-30 dB) at low stimulus intensities at the characteristic frequency (CF) and small or nonexistent at high intensities and at frequencies far removed from CF. Furosemide also induces response-phase lags that are largest at low stimulus intensities (averaging 77 degrees) and are confined to frequencies close to CF. ^[1]

Furosemide concentration- and time-dependently increases the formation of nitric oxide andprostacyclin. Furosemide leads to an enhanced release of kinins into the supernatant of the cells. ^[2]

Furosemide reversibly suppresses low Ca2+-induced epileptiform activity in hippocampus proper and blocks or significantly reduces different types of epileptiform discharges in the low Mg2+ model and the 4-aminopyridine model. ^[3]

Furosemide significantly inhibits cell growth in MKN45 cells, but not in MKN28 cells. Furosemide diminishes cell growth by delaying the G(1)-S phase progression in poorly differentiated gastric adenocarcinoma cells, which show high expression and activity of NKCC, but not in moderately differentiated gastric adenocarcinoma cells with low expression and NKCC activity. ^[4]

in vivo

Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduces right atrial pressure (RAP) and pulmonary arterial pressure (PAP) during exercise in dose-dependent manner in horse. ^[5]

プロトコル(参考用のみ)

細胞アッセイ	細胞株	Erythrocytes
	濃度	10, 30 and 100 µM
	反応時間	45 minutes
	実験の流れ	Cells were treated with indicated concentrations of drug for 45 minutes.
動物実験	動物モデル	CD-1 male mice
	投薬量	3 mg/kg
	投与方法

参考

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A novel contrast-induced acute kidney injury mouse model based on low-osmolar contrast medium [ Ren Fail, 2022, 44(1):1345-1355]	PubMed: 35938700
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Inhibition of class IIa histone deacetylase activity by gallic acid, sulforaphane, TMP269, and panobinostat [Choi SY, et al. Biomed Pharmacother, 2018, 101:145-154]	PubMed: 29482060
Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure [Jin L, et al. Sci Rep, 2018, 8(1):9302]	PubMed: 29915390
Gallic acid attenuates pulmonary fibrosis in a mouse model of transverse aortic contraction-induced heart failure [Jin L, et al. Vascul Pharmacol, 2017, 99:74-82]	PubMed: 29097327

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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