Referencia número: HY-B0135

Furosemide

Name: Furosemide
Brand: MedChemExpress
SKU: HY-B0135
Price: 55.00 USD
Availability: InStock
Rating: 5 (10 reviews)

10 Cited Publications

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Based on 10 publication(s) in Google Scholar

Furosemide is an orally active GABAA receptor antagonist. Furosemide inhibits carbonic anhydrase, the sodium-chloride cotransporter, sodium reabsorption, tubuloglomerular feedback, and GABA-induced chloride flux. Furosemide can be used as a diuretic reagent. Furosemide is applied in the research of hepatic necrosis, sepsis-associated acute kidney injury, hypoalbuminemia-related fluid retention, and congestive heart failure.

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Pureza : 99.83%
No. CAS: 54-31-9
Fòrmula: C₁₂H₁₁ClN₂O₅S
Peso molecular:330.74

Almacenamiento:

4°C, protect from light

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

Furosemide Chemical Structure

No. CAS: 54-31-9

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

Actividad biológica
- Descripciòn
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (10)
Solvente y solubilidad
- In Vitro
- In Vivo
Protocolo (3)
Pureza y Documentación
Referencias
Help & FAQs
Classifications
Bioz

Actividad biológica

Descripciòn

Cellular Effect

Cell Line	Type	Value	Description	References
CHO	EC₅₀	11.2 μM Compound: 7	Agonist activity at C-terminal beta-galactosidase tagged human recombinant GPR35 expressed in CHO cells after 90 mins by beta-arrestin recruitment assay Agonist activity at C-terminal beta-galactosidase tagged human recombinant GPR35 expressed in CHO cells after 90 mins by beta-arrestin recruitment assay	[PMID: 23888932]
HEK293	IC₅₀	3.76 μM Compound: 2	Inhibition of human 11beta-HSD1 expressed in HEK293 cells assessed as conversion of [3H]cortisone to [3H]cortisol by scintillation proximity assay in presence of NADPH Inhibition of human 11beta-HSD1 expressed in HEK293 cells assessed as conversion of [3H]cortisone to [3H]cortisol by scintillation proximity assay in presence of NADPH	[PMID: 18653260]
HEK293	IC₅₀	3.76 μM Compound: 2	Inhibition of mouse 11beta-HSD1 expressed in HEK293 cells assessed as conversion of [3H]cortisone to [3H]cortisol by scintillation proximity assay in presence of NADPH Inhibition of mouse 11beta-HSD1 expressed in HEK293 cells assessed as conversion of [3H]cortisone to [3H]cortisol by scintillation proximity assay in presence of NADPH	[PMID: 18653260]
HEK293	IC₅₀	>500 μM Compound: furosemide	Inhibition of human MATE1-mediated ASP+ uptake expressed in HEK293 cells after 1.5 mins by fluorescence assay Inhibition of human MATE1-mediated ASP+ uptake expressed in HEK293 cells after 1.5 mins by fluorescence assay	[PMID: 23241029]
HeLa	IC₅₀	15 μM Compound: Furosemide	TP_TRANSPORTER: inhibition of Taurocholate uptake in NTCP-expressing HeLa cells TP_TRANSPORTER: inhibition of Taurocholate uptake in NTCP-expressing HeLa cells	[PMID: 10565843]
Sf21	IC₅₀	>1000 μM Compound: Furosemide	Inhibition of human BSEP expressed in plasma membrane vesicles of Sf21 cells assessed as inhibition of ATP-dependent [3H]taurocholate uptake Inhibition of human BSEP expressed in plasma membrane vesicles of Sf21 cells assessed as inhibition of ATP-dependent [3H]taurocholate uptake	[PMID: 21965623]
Sf21	IC₅₀	>1000 μM Compound: Furosemide	Inhibition of Sprague-Dawley rat Bsep expressed in plasma membrane vesicles of Sf21 cells assessed as inhibition of ATP-dependent [3H]taurocholate uptake Inhibition of Sprague-Dawley rat Bsep expressed in plasma membrane vesicles of Sf21 cells assessed as inhibition of ATP-dependent [3H]taurocholate uptake	[PMID: 21965623]

In Vitro

Furosemide cytochrome P-450-dependent metabolic activation of the furan ring produces an arylating metabolite that covalently binds to hepatic microsomal protein in mouse and human hepatic microsomes^[2].
Furosemide (300 μM; 90 min) enhances basal [³⁵S]-TBPS binding in rat cerebellar membranes (an effect blocked by SR 95531 (Gabazine) (HY-103533) and Ro 5-4864 (4'-Chlorodiazepam) (HY-124268)) and exhibits additive GABA antagonism with SR 95531, while having no such effects in rat cerebrocortical membranes; it also decreases [³H]-Ro 5-4864 binding in both membrane types at concentrations above 30 μM^[7].
Furosemide (0.1-1000 μM; 90 min) antagonizes GABA-induced inhibition of [³⁵S]-TBPS binding in human cerebellar cortical membranes, but does not enhance basal binding in the absence of GABA^[7].
Furosemide (300 μM; 90 min) reverses GABA-induced inhibition of [³⁵S]-TBPS binding in recombinant GABA_A receptors (dependent only on α6 and β3 subunits), but enhances basal binding exclusively in α6β3γ2 receptors^[7].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

In Vivo

Furosemide (4 mg/kg; i.v.; bolus followed by continuous infusion) inhibits tubuloglomerular feedback activity in healthy male Munich-Wistar rats, with no change in whole-kidney GFR or SNGFR when volume status is maintained, and a decrease in GFR and SNGFR when 3% volume depletion occurs; absolute proximal reabsorption remains unchanged with volume replacement despite increased interstitial hydrostatic pressure, and decreases only with volume depletion due to reduced SNGFR^[1].
Furosemide (4 mg/kg; i.v.; bolus followed by continuous infusion) reduces renal interstitial protein concentration and oncotic pressure in healthy male Munich-Wistar rats when volume status is maintained^[1].
Furosemide (4 mg/kg; i.v.; bolus followed by continuous infusion) increases renal interstitial volume index in healthy male Munich-Wistar rats when volume status is maintained^[1].
Furosemide (0.5-2 mg/kg; i.v., i.m.; single dose) alone induces robust diuresis and natriuresis in normal rats but not in analbuminemic rats, while co-administration with equimolar albumin restores diuretic efficacy in analbuminemic rats by increasing urinary Furosemide recovery to 18% of the administered dose^[5].
Furosemide (100-500 mg/kg; i.p.; single dose) induces dose-dependent hepatic necrosis in male Swiss albino mice via cytochrome P-450-mediated formation of a reactive arylating metabolite that covalently binds to hepatic macromolecules, with 92% of mice developing necrosis (ranging from slight to massive) at a 400 mg/kg single intraperitoneal dose^[2].
Furosemide (1 mg/kg; i.m.; daily) accelerates the development of tachycardia-induced left ventricular systolic dysfunction in Yorkshire pigs to a mean time of 21.4 days, while increasing serum aldosterone levels, reducing serum sodium levels, elevating basal NCX currents, and blunting NCX responsiveness to isoproterenol^[6].
Furosemide (5 mg/kg; i.v.; prime followed by 5 mg/kg/hr continuous infusion) acutely abolishes renal blood flow autoregulation and increases renal blood flow by up to 56% above control at 15 minutes post-administration, with these effects resolving and renal function returning to control levels by 60 minutes, while sustained natriuresis is maintained^[9].
Furosemide (5 mg/kg; i.v.; prime followed by 5 mg/kg/hr continuous infusion) acutely abolishes renal blood flow autoregulation and increases renal blood flow even in the presence of prostaglandin synthesis inhibition, demonstrating prostaglandins do not mediate these effects^[9].

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.

Chemical Information

No. CAS 54-31-9
Appearance Solid
Peso molecular 330.74
Fòrmula C₁₂H₁₁ClN₂O₅S
Color White to off-white
SMILES

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

Room temperature in continental US; may vary elsewhere.
Almacenamiento

4°C, protect from light

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

Publications (10)

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 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 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 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).
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 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 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 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 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 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

Solvente y solubilidad

In Vitro:

DMSO : ≥ 100 mg/mL (302.35 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

H₂O : < 0.1 mg/mL (insoluble)

* "≥" 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

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. 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, 1 year; -20°C, 6 months (protect from light). When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Calculadora de molaridad

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

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Molecular Weight Molecular Weight

Calculadora de dilución

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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 (7.56 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% Corn Oil

Solubility: ≥ 2.5 mg/mL (7.56 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.

In Vivo Dissolution Calculator

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The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Protocolo

All Animals and Diseases Signal Pathway Related

Nephrotoxicity Study
This protocol assesses nephrotoxicity by combining functional kidney injury readouts, urinary/tissue injury biomarkers, and renal histopathology. Serum creatinine and BUN reflect impaired kidney function, while KIM-1, NGAL, clusterin, osteopontin, IL-18, cystatin C, nephrin, Oat5, urinary protein, glucose, and alkaline phosphatase have been used to detect tubular injury in cisplatin-, gentamicin-, and acetaminophen-induced nephrotoxicity models.
LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.

Pureza y Documentación

Select Batch:

Pureza: 99.98%

Assay: 99.98%

ee.: 99.98%

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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)
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OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Instrucciones de manejo (2659 KB)

Referencias

[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]

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
DMSO	1 mM	3.0235 mL	15.1176 mL	30.2352 mL	75.5881 mL
	5 mM	0.6047 mL	3.0235 mL	6.0470 mL	15.1176 mL
	10 mM	0.3024 mL	1.5118 mL	3.0235 mL	7.5588 mL
	15 mM	0.2016 mL	1.0078 mL	2.0157 mL	5.0392 mL
	20 mM	0.1512 mL	0.7559 mL	1.5118 mL	3.7794 mL
	25 mM	0.1209 mL	0.6047 mL	1.2094 mL	3.0235 mL
	30 mM	0.1008 mL	0.5039 mL	1.0078 mL	2.5196 mL
	40 mM	0.0756 mL	0.3779 mL	0.7559 mL	1.8897 mL
	50 mM	0.0605 mL	0.3024 mL	0.6047 mL	1.5118 mL
	60 mM	0.0504 mL	0.2520 mL	0.5039 mL	1.2598 mL
	80 mM	0.0378 mL	0.1890 mL	0.3779 mL	0.9449 mL
	100 mM	0.0302 mL	0.1512 mL	0.3024 mL	0.7559 mL

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Furosemide

Publications Citing Use of MedChemExpress (MCE) Furosemide