1. Membrane Transporter/Ion Channel
    Neuronal Signaling
  2. NKCC
    GABA Receptor
  3. Furosemide

Furosemide 

Cat. No.: HY-B0135 Purity: 99.83%
Handling Instructions

Furosemide is a potent and orally active inhibitor of Na+/K+/2Cl- (NKCC) cotransporter, NKCC1 and NKCC2. Furosemide is also a GABAA receptors antagonist and displays 100-fold selectivity for α6-containing receptors than α1-containing receptors. Furosemide acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema.

For research use only. We do not sell to patients.

Furosemide Chemical Structure

Furosemide Chemical Structure

CAS No. : 54-31-9

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5 g USD 180 In-stock
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Based on 1 publication(s) in Google Scholar

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Description

Furosemide is a potent and orally active inhibitor of Na+/K+/2Cl- (NKCC) cotransporter, NKCC1 and NKCC2[1]. Furosemide is also a GABAA receptors antagonist and displays 100-fold selectivity for α6-containing receptors than α1-containing receptors. Furosemide acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema[2].

IC50 & Target

IC50: NKCC1 and NKCC2[1]
IC50: GABAA receptors[2]

In Vitro

Furosemide (500 µM; 72-96 hours) significantly changes the proliferation rates in MKN45 cells (the poorly differentiated human gastric adenocarcinoma cell line). however, it has no effects on MKN28 cells (the moderately differentiated human gastric adenocarcinoma cell line). The growth rate of MKN45 cells is larger than that of MKN28 cells[4].
Furosemide (10 µM, 30 µM, 100 µM; 45 min exposure) significantly decreases cation channel activity and [Ca(2+)](i) in human erythrocytes drawn from healthy individuals. Tert-butylhydroperoxide similarly enhances the non-selective cation channels activity, increases [Ca(2+)](i) and triggered cell membrane scrambling, however, the effects is significantly blunted by furosemide again[5].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Furosemide (intraperitoneal injection; 100 mg/kg; single dose) is injected after kanamycin (KM) (1000 mg/kg) to creat a deaf mouse model in C57BL/6 mouse. After injection, hearing loss and cochlear hair cell damage are evaluated on day 1, day 2 and day 3, respectively. The hearing is markedly deteriorated even from the next day (Day-1 group), OHCs (outer hair cell) morphology of apical, middle and basal turns are disorganized in mice on day3[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial
Molecular Weight

330.74

Formula

C₁₂H₁₁ClN₂O₅S

CAS No.

54-31-9

SMILES

O=C(O)C1=CC(S(=O)(N)=O)=C(Cl)C=C1NCC2=CC=CO2

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

DMSO : ≥ 100 mg/mL (302.35 mM)

H2O : 0.1 mg/mL (0.30 mM; Need ultrasonic)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.0235 mL 15.1176 mL 30.2352 mL
5 mM 0.6047 mL 3.0235 mL 6.0470 mL
10 mM 0.3024 mL 1.5118 mL 3.0235 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (7.56 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (7.56 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
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Keywords:

FurosemideNKCCGABA ReceptorNa-K-Cl cotransporterNa(+)-K(+)-Cl(-) cotransporterNa+-K+-Cl− cotransporter Gamma-aminobutyric acid Receptorγ-Aminobutyric acid Receptorheart failureliver scarringkidney diseasehypertensionedemaInhibitorinhibitorinhibit

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