Cat. No.: HY-B0135A

Furosemide sodium

Name: Furosemide sodium
Brand: MedChemExpress
SKU: HY-B0135A
Price: 90.00 USD
Availability: InStock
Rating: 5 (11 reviews)

11 Cited Publications

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Based on 11 publication(s) in Google Scholar

Furosemide sodium is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide sodium inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide sodium selectively antagonizes GABA_A receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide sodium penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide sodium can be used in research on congestive heart failure, hypertension, and edema.

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

Purity : 99.87%
CAS No.: 41733-55-5
Formula: C₁₂H₁₀ClN₂NaO₅S
Molecular Weight:352.73

Storage:

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Furosemide sodium Chemical Structure

CAS No.: 41733-55-5

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Publications (11)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]

NKCC1

NKCC2

KCC2

KCC3

KCC4

GABAAR

In Vitro

Renal RegulationOthers

Renal Regulation

Furosemide sodium inhibits NKCC1 and NKCC2 in SLC12 cotransporter profiling, with IC₅₀ values of 10-50 mM and 15-60 mM, respectively^[10].

Others

Furosemide sodium undergoes cytochrome P-450-dependent metabolic activation of the furan ring to generate an arylated metabolite that covalently binds to liver microsomal proteins in mouse and human liver microsomes^[2].
Furosemide (300 μM; 90 min) sodium enhances basal [³⁵S]-TBPS binding activity in rat cerebellar cell membranes (this effect is blocked by SR 95531 (Gabazine) (HY-103533) and Ro 5-4864 (4'-Chlorodiazepam) (HY-124268)), and exhibits additive GABA antagonism with SR 95531, but has no such effect in rat cerebral cortex cell membranes; at concentrations above 30 μM, it also reduces [³H]-Ro 5-4864 binding activity in both cell membranes^[7].
Furosemide (0.1-1000 μM; 90 min) sodium antagonizes GABA-induced inhibition of [³⁵S]-TBPS binding in human cerebellar cortex membranes, but does not enhance basal binding in the absence of GABA^[7].
Furosemide (300 μM; 90 min) sodium reverses the inhibitory effect of GABA on [³⁵S]-TBPS binding in recombinant GABA_A receptors (dependent only on α6 and β3 subunits), but only enhances basal binding in α6β3γ2 receptors^[7].

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

In Vivo

Regulation of Cardiac Pump FunctionCardiovascular RegulationRenal RegulationLocal Vascular RegulationOthers

Regulation of Cardiac Pump Function

Cardiovascular Regulation

Renal Regulation

Furosemide (1 mg/kg; intramuscular injection; daily) sodium accelerates the onset of tachycardia-induced left ventricular systolic dysfunction in Yorkshire pigs, shortening the mean onset time to 21.4 days, while also increasing serum aldosterone levels, decreasing serum sodium levels, enhancing basal NCX current, and attenuating the responsiveness of NCX to isoproterenol^[6].

Renal Regulation

Furosemide (4 mg/kg; intravenous injection; bolus followed by continuous infusion) sodium inhibits tubuloglomerular feedback activity in healthy male Munich-Wistar rats; whole-kidney GFR and SNGFR remain unchanged under euvolemic conditions, whereas GFR and SNGFR decrease under 3% volume depletion; absolute proximal reabsorption remains unchanged under volume-repleted conditions even when interstitial hydrostatic pressure increases, and decreases only under volume depletion resulting from reduced SNGFR^[1].
Furosemide (4 mg/kg; intravenous injection; bolus followed by continuous infusion) sodium reduces renal interstitial protein concentration and colloid osmotic pressure in healthy male Munich-Wistar rats while maintaining volume status^[1].
Furosemide (4 mg/kg; intravenous injection; bolus followed by continuous infusion) sodium increases the renal interstitial volume index in healthy male Munich-Wistar rats while maintaining volume status^[1].
Furosemide (0.5-2 mg/kg; intravenous injection, intramuscular injection; single administration) sodium alone induces significant diuresis and natriuresis in normal rats, but not in analbuminemic rats; however, when co-administered with an equimolar amount of albumin, it restores its diuretic efficacy in analbuminemic rats by increasing the urinary recovery of Furosemide to 18% of the administered dose^[5].

Renal Regulation

Local Vascular Regulation

Furosemide (5 mg/kg; intravenous injection; a loading dose is administered first, followed by continuous infusion at 5 mg/kg/hr) sodium rapidly eliminates the autoregulation of renal blood flow, increasing renal blood flow by up to 56% compared with the control group at 15 minutes after administration; this effect gradually subsides, renal function returns to the control group level at 60 minutes, while the sustained natriuretic effect is maintained^[9].
Furosemide (5 mg/kg; intravenous injection; loading dose administered first, followed by continuous infusion at 5 mg/kg/hr) sodium acutely abolishes renal blood flow autoregulation and increases renal blood flow even when prostaglandin synthesis is inhibited, indicating that prostaglandins do not mediate these effects^[9].

Others

Furosemide (100-500 mg/kg; intraperitoneal injection; single administration) sodium induces dose-dependent hepatic necrosis in male Swiss albino mice through the formation of cytochrome P-450-mediated reactive arylation metabolites, which can covalently bind to hepatic macromolecules; at a single intraperitoneal dose of 400 mg/kg, 92% of mice develop necrosis (ranging from mild to severe)^[2].

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

Animal Model:

Munich-Wistar (male, 215-295 g)^[1]
Dosage:

4 mg/kg (bolus); 4 mg/kg per hour (continuous infusion)
Administration:

i.v.; bolus followed by continuous infusion
Result:

Decreased whole-kidney glomerular filtration rate from 0.97 to 0.66 mL/min in 3% volume depletion group.
Decreased single nephron filtration rate from 28 to 20 nl/min in 3% volume depletion group.
Decreased mean arterial pressure from 118 to 100 mmHg in 3% volume depletion group.
Increased hematocrit from 56 to 59% in 3% volume depletion group.
Increased urinary sodium excretion from 0.06 to 2.1 μEq/min in 3% volume depletion group.
Increased urinary potassium excretion from 0.3 to 1.0 μEq/min in 3% volume depletion group.
Decreased absolute proximal reabsorption from 13 to 10 nl/min in 3% volume depletion group.
Decreased absolute loop-of-Henle reabsorption from 9 to 5 nl/min in 3% volume depletion group.
Eliminated proximal-distal single nephron filtration rate difference in both groups.
Maintained whole-kidney glomerular filtration rate at 1.1 mL/min in volume replacement group.
Maintained single nephron filtration rate at 31 nl/min (distal collection) and 33 nl/min (late proximal collection) in volume replacement group.
Increased urine flow from 2 to 84 μl/min in volume replacement group.
Decreased mean arterial pressure from 114 to 106 mmHg in volume replacement group.
Maintained hematocrit at 55% in volume replacement group.
Increased urinary sodium excretion from 0.09 to 15.2 μEq/min in volume replacement group.
Increased urinary potassium excretion from 0.4 to 2.7 μEq/min in volume replacement group.
Maintained absolute proximal reabsorption at 13 nl/min in volume replacement group.
Decreased absolute loop-of-Henle reabsorption from 10 to 8 nl/min in volume replacement group.
Increased distal tubular flow rate from 5 to 10 nl/min in volume replacement group.
Increased interstitial hydrostatic pressure from 4 to 11 mmHg in volume replacement group.
Decreased interstitial oncotic pressure from 4.6 to 2.0 mmHg in volume replacement group.
Decreased afferent arteriolar resistance from 29 to 22×10⁹ dynes·sec·cm^-5 in volume replacement group.
Increased renal interstitial volume index from 12.1 to 19.6% of wet renal cortical tissue weight in volume replacement group.

Animal Model:

Munich-Wistar (male)^[1]
Dosage:

4 mg/kg (bolus); 4 mg/kg per hour (continuous infusion)
Administration:

i.v.; bolus followed by continuous infusion
Result:

Decreased interstitial protein concentration from 1.7 to 0.8 g/dl.
Maintained systemic plasma protein concentration at 5.6 g/dl (control) and 5.3 g/dl (post-furosemide).
Increased ratio of plasma albumin to interstitial albumin concentration from 2.5:1 to 4.9:1.
Decreased interstitial oncotic pressure from 4.6 to 2.0 mmHg.

Animal Model:

Munich-Wistar (male, 227-235 g)^[1]
Dosage:

4 mg/kg (bolus); 4 mg/kg per hour (continuous infusion)
Administration:

i.v.; bolus followed by continuous infusion
Result:

Maintained blood volume at 11.4 mL (control) and 11.2 mL (post-furosemide).
Maintained hematocrit at 56% (control) and 57% (post-furosemide).
Increased renal interstitial volume index from 12.1 to 19.6% of wet renal cortical tissue weight.

Animal Model:

Swiss albino (male, 20-25 g, National Institutes of Health stock)^[2]
Dosage:

100 mg/kg; 200 mg/kg; 300 mg/kg; 400 mg/kg; 500 mg/kg
Administration:

i.p.; single dose
Result:

Exhibited 0% mortality and 100% no hepatic necrosis at 100 mg/kg.
Exhibited 0% mortality, 16% slight necrosis, and 84% no necrosis at 200 mg/kg.
Exhibited 2% mortality, 4% necrosis affecting 26-50% of hepatocytes, 16% necrosis affecting 6-25% of hepatocytes, 48% slight necrosis, and 32% no necrosis at 300 mg/kg.
Exhibited 4% mortality, 6% necrosis affecting >50% of hepatocytes, 18% necrosis affecting 26-50% of hepatocytes, 36% necrosis affecting 6-25% of hepatocytes, 32% slight necrosis, and 8% no necrosis at 400 mg/kg; nucleolar changes and single cell necrosis appeared within 3 hours, midzonal and centrilobular necrosis by 6 hours, massive confluent necrosis by 12 hours, necrosis peaked at 24-48 hours, and regeneration started by 48-72 hours.
Exhibited 20% mortality, 20% necrosis affecting >50% of hepatocytes, 35% necrosis affecting 26-50% of hepatocytes, 40% necrosis affecting 6-25% of hepatocytes, and 5% slight necrosis at 500 mg/kg.
Reached ~1.5 nmol/mg protein of in vivo covalent binding to hepatic protein, occurring a few hours before histological necrosis.
Abolished both covalent binding and hepatic necrosis following pretreatment with cytochrome P-450 inhibitors.
Showed no prevention of liver damage with fluid resuscitation using Ringer's lactate in 5% glucose.

Animal Model:

Analbuminemic mutant rats (NAR, fed ad libitum, no fasting); normal rats (fed ad libitum, no fasting)^[5]
Dosage:

0.5 mg/kg (normal rat i.v. diuresis; NAR albumin co-administration); 2 mg/kg (NAR plasma clearance); 0.5-2 mg/kg (i.m. dose-response)
Administration:

i.v.; single dose over 10 seconds; i.m.; single dose
Result:

Rapidly and sustainably increased urine volume and sodium excretion in normal rats following 0.5 mg/kg i.v. dose.
Failed to enhance diuresis in NAR following 0.5 mg/kg i.v. dose.
Dose-dependently increased urine volume and sodium excretion in normal rats via i.m. administration, with responses significantly less pronounced in NAR.
Reduced urinary recovery of furosemide to about three times lower in NAR than in normal rats across tested i.m. doses.
Produced total plasma clearance of 24.4 mL/min×kg and distribution volume of 545.5 mL/kg in NAR, compared to 9.4 mL/min×kg and 59.6 mL/kg in normal rats following 2 mg/kg i.v. dose.
Resulted in urinary recovery of furosemide of 7% of the dose in NAR versus 26% in normal rats following 2 mg/kg i.v. dose.
Increased urine volume in NAR to a peak at 10 minutes post-administration, and raised urinary recovery of furosemide in NAR to 18% of the dose when administered at 0.5 mg/kg i.v. mixed with equimolar albumin.

Animal Model:

Yorkshire pigs (male and female, 7 to 10 weeks of age, tachycardia-induced congestive heart failure via permanent transvenous pacemaker implantation set to 200 beats/min after 48-hour recovery)^[6]
Dosage:

1 mg/kg
Administration:

i.m.; daily
Result:

Shortened mean time to development of significant left ventricular systolic dysfunction to 21.4 days.
Raised serum aldosterone levels to 43.0 ng/dL at day 14 of pacing.
Reduced serum sodium levels to 133.0 mmol/L at day 14 of pacing.
Significantly increased basal sodium-calcium exchanger (NCX) peak outward currents compared with placebo-treated failing animals.
Significantly reduced responsiveness of NCX currents to isoproterenol stimulation compared with placebo-treated failing animals.

Animal Model:

Either sex, weighing 20 kg (range 15-25 kg; sodium pentobarbital-anesthetized, unilateral renal artery constriction)^[9]
Dosage:

5 mg/kg (prime); 5 mg/kg/hr (continuous infusion)
Administration:

i.v.; prime followed by continuous infusion
Result:

Abolished RBF autoregulation above 80 mmHg RPP at 15 minutes, with RBF changing proportionally to RPP.
Reduced renal vascular resistance by 39% and 29% below control at 140 and 120 mmHg RPP, respectively, at 15 minutes.
Increased renin secretory rate from 7.8 ng/min·g to 14.6 ng/min·g at 15 minutes.
Increased fractional excretion of sodium from 0.9% to 18.2% at 15 minutes.
Restored RBF and RBF autoregulatory capability to control values by 60 minutes.
Maintained GFR autoregulation throughout infusion, averaging 0.49 mL/min·g at 15 minutes and 0.57 mL/min·g at 60 minutes.
Returned renin secretory rate to control levels (6.5 ng/min·g) by 60 minutes.
Sustained elevated fractional excretion of sodium at 20.3% at 60 minutes.

Animal Model:

Either sex, weighing 20 kg (range 15-25 kg; sodium pentobarbital-anesthetized, pretreated with indomethacin or RO 20-5720, unilateral renal artery constriction)^[9]
Dosage:

5 mg/kg (prime); 5 mg/kg/hr (continuous infusion)
Administration:

i.v.; prime followed by continuous infusion
Result:

Abolished RBF autoregulation 15 minutes after initiation, with RBF changing proportionally to RPP.
Increased RBF from 2.59 mL/min·g to 4.05 mL/min·g at 140 mmHg RPP, and from 2.59 mL/min·g to 3.56 mL/min·g at 120 mmHg RPP.
Reduced renal vascular resistance to a nadir that remained unchanged across all RPP values examined.

Related Protocols :

Research Protocol for Cardiovascular Diseases

Chemical Information

CAS No. 41733-55-5
Appearance Solid
Molecular Weight 352.73
Formula C₁₂H₁₀ClN₂NaO₅S
Color White to off-white
SMILES

O=C(C1=CC(S(=O)(N)=O)=C(C=C1NCC2=CC=CO2)Cl)O[Na]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Publications (11)

All Bio/Physico-chemical AssayCell Proliferation/Viability AssayELISAIn Vivo Efficacy StudyIHC

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Journal Impact Factor

Nat Aging

mRNA metabolism regulator human antigen R (HuR) regulates age-related hearing loss in aged mice. [Abstract]

2025 May;5(5):848-867. PMID: 40394214
Sci Adv

3D bioprinted human-scale intestine models for physiological and microbial insights through fluid-driven heterogeneity. [Abstract]

2025 Nov 21;11(47):eady6562. PMID: 41270182
EMBO J

Structural basis for human NKCC1 inhibition by loop diuretic drugs. [Abstract]

2025 Mar;44(5):1540-1562. PMID: 39875725
Emerg Contam

2026 Feb 23.
Eur J Pharmacol

Loop diuretics mitigate juvenile immobilization treatment-induced hippocampal dysfunction. [Abstract]

2025 Jun 5:996:177447. PMID: 40023355

Furosemide sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Jun 5:996:177447. [Abstract]

Suprafusion of bumetanide and Furosemide (50 μM ; 65 min) inhibited LTP formation in the hippocampus, with typical traces in the right panels. Points a and b represent high-frequency stimulation (HFS) for 5 min before induction and 40 min after induction, respectively.

Furosemide sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Jun 5:996:177447. [Abstract]

At the 40-min time point (b), hippocampal LTP was measured with suprafusion of 5 μM bumetanide or 50 μM Furosemide.

Furosemide sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Jun 5:996:177447. [Abstract]

In the inhibitory avoidance test, each group received intraperitoneal injections of either a vehicle, 15.2 mg/kg bumetanide, or 152 mg/kg Furosemide (dissolved in 1.1% DMSO in PBS) 30 min prior to the extinction phase (n = 9 per group).
Mol Nutr Food Res

2026 Aug;70(15):e70571. PMID: 42533546
iScience

Heart failure pleural fluid impairs endothelial barrier through miR 501-3p mediated ZO 1 remodeling. [Abstract]

2026 Apr 2;29(5):115549. PMID: 42058897
iScience

Impact of endogenous sonosensation on in vivo sonogenetics. [Abstract]

2025 Nov 12;28(12):114030. PMID: 41377656
J Orthop Surg Res

Several first-line anti-hypertensives act on fibrosarcoma progression and PD1ab blockade therapy. [Abstract]

2024 Feb 19;19(1):147. PMID: 38373964

Furosemide sodium purchased from MedChemExpress. Usage Cited in: J Orthop Surg Res. 2024 Feb 19;19(1):147. [Abstract]

Furosemide (10 μM; 1-6 days) had no effect on MCA-205 growth. CCK8 experiment was used to detect the proliferation ability of MCA-205 after Furosemide treatment.

Furosemide sodium purchased from MedChemExpress. Usage Cited in: J Orthop Surg Res. 2024 Feb 19;19(1):147. [Abstract]

Furosemide (10 μM; 24 h) did not significantly alter the level of VEGF produced by MCA-205. Elisa kit was used to detect the VEGF production after furosemide treatment.

Furosemide sodium purchased from MedChemExpress. Usage Cited in: J Orthop Surg Res. 2024 Feb 19;19(1):147. [Abstract]

Furosemide (200 mg/kg; ip; every other day) did not inhibit MCA-205 fibrosarcoma growth.

Furosemide sodium purchased from MedChemExpress. Usage Cited in: J Orthop Surg Res. 2024 Feb 19;19(1):147. [Abstract]

Furosemide (200 mg/kg; ip; every other day) combination of PD1ab (250 µg/mice; ip; every other day, 4 times) displayed a weaker therapeutic impact on tumor growth when compared with PD1ab single therapy.

Furosemide sodium purchased from MedChemExpress. Usage Cited in: J Orthop Surg Res. 2024 Feb 19;19(1):147. [Abstract]

Furosemide (200 mg/kg; ip; every other day) combination with PD1ab (250 µg/mice; ip; every other day, 4 times) showed no impact on the level of infiltrating CD8+ T cells compared with control. Compared with PD1ab treatment alone, the combination of both agents showed a decreasing impact on the level of infiltrating CD8+ T cells.
Nanotoxicology

Polystyrene nanoplastics promote tumor lung metastasis by inducing sodium overload in macrophages in an NMDAR-dependent way. [Abstract]

2026 May 19:1-18. PMID: 42154607
J Pharm Biomed Anal

Screening method of mildronate and over 300 doping agents by reversed-phase liquid chromatography-high resolution mass spectrometry. [Abstract]

2021 Feb 20:195:113870. PMID: 33453569

Solvent & Solubility

In Vitro:

DMSO : ≥ 150 mg/mL (425.25 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

H₂O : 100 mg/mL (283.50 mM; Need ultrasonic)

* "≥" means soluble, but saturation unknown.

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.8350 mL

14.1751 mL

28.3503 mL

5 mM

0.5670 mL

2.8350 mL

5.6701 mL

10 mM

0.2835 mL

1.4175 mL

2.8350 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

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

Solubility: ≥ 2.5 mg/mL (7.09 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (7.09 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (7.09 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

Working Solution

For the following dissolution methods, please prepare the working solution directly:

It is recommended to prepare fresh solutions and use them promptly within a short period of time.

The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: PBS

Solubility: 100 mg/mL (283.50 mM); Clear solution; Need ultrasonic

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Working solution concentration: 0.22 mg/mL

This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact

MedChemExpress (MCE) .

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (316 KB)
SDS (419 KB)
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COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Tucker BJ, et al. Effect of furosemide administration on glomerular and tubular dynamics in the rat. Kidney international. 1984 Aug;26(2):112-21.

[2]. Mitchell JR, et al. Hepatic necrosis caused by furosemide. Nature. 1974 Oct 11;251(5475):508-11.

[3]. Das PK, et al. Furosemide Stress Test and Renal Resistive Index for Prediction of Severity of Acute Kidney Injury in Sepsis. Cureus. 2023 Aug;15(8):e44408.

[4]. Kelly MR, et al. Pharmacokinetics of orally administered furosemide. Clin Pharmacol Ther. 1974 Feb;15(2):178-86.

[5]. Inoue M, et al. Mechanism of furosemide resistance in analbuminemic rats and hypoalbuminemic patients. Kidney international. 1987 Aug;32(2):198-203.

[6]. McCurley JM, et al. Furosemide and the progression of left ventricular dysfunction in experimental heart failure. Journal of the American College of Cardiology. 2004 Sep 15;44(6):1301-7.

[7]. Korpi ER, et al. Furosemide interactions with brain GABAA receptors. British journal of pharmacology. 1997 Mar;120(5):741-8.

[8]. Cataliotti A, et al. Brain natriuretic peptide enhances renal actions of furosemide and suppresses furosemide-induced aldosterone activation in experimental heart failure. Circulation. 2004 Apr 06;109(13):1680-5.

[9]. Duchin KL, et al. Effect of furosemide on renal autoregulation. Kidney Int. 1977 Dec;12(6):379-86. [Content Brief]

[10]. Orlov SN, et al. NKCC1 and NKCC2: The pathogenetic role of cation-chloride cotransporters in hypertension. Genes & diseases. 2015 Jun;2(2):186-196.

[11]. Limmer F, et al. Regulation of the Na(+)-K(+)-2Cl(-) cotransporter by cGMP/cGMP-dependent protein kinase I after furosemide administration. The FEBS journal. 2015 Oct;282(19):3786-98.

[12]. Suki WN, et al. Acute treatment of hypercalcemia with furosemide. N Engl J Med. 1970;283(16):836-840.

[13]. Osmanovic E, et al. The Effect of Furosemide on Arterial Blood Pressure, Blood Glucose Levels and Incidence of Heart Arrhythmias. American Journal of Internal Medicine. 2017;5(3):41-45.

[14]. Tenzing D, et al. Effect of furosemide in the treatment of high-altitude pulmonary edema. BMC Pulm Med. 2024 Mar 4;24(1):109.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
H₂O / DMSO	1 mM	2.8350 mL	14.1751 mL	28.3503 mL	70.8757 mL
	5 mM	0.5670 mL	2.8350 mL	5.6701 mL	14.1751 mL
	10 mM	0.2835 mL	1.4175 mL	2.8350 mL	7.0876 mL
	15 mM	0.1890 mL	0.9450 mL	1.8900 mL	4.7250 mL
	20 mM	0.1418 mL	0.7088 mL	1.4175 mL	3.5438 mL
	25 mM	0.1134 mL	0.5670 mL	1.1340 mL	2.8350 mL
	30 mM	0.0945 mL	0.4725 mL	0.9450 mL	2.3625 mL
	40 mM	0.0709 mL	0.3544 mL	0.7088 mL	1.7719 mL
	50 mM	0.0567 mL	0.2835 mL	0.5670 mL	1.4175 mL
	60 mM	0.0473 mL	0.2363 mL	0.4725 mL	1.1813 mL
	80 mM	0.0354 mL	0.1772 mL	0.3544 mL	0.8859 mL
	100 mM	0.0284 mL	0.1418 mL	0.2835 mL	0.7088 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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Furosemide sodium

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