What do you know about Furosemide?


Pharmacopoeia Information

This product is 2- [(2-furomethyl) amino] -5- (sulfamoyl) -4-chlorobenzoic acid. Calculated as dry product, the content of C12H11ClN2O5S should not be less than 99.0%.


This product is a white or almost white crystalline powder, odorless.

This product is soluble in acetone, slightly soluble in ethanol, and insoluble in water.

absorption coefficient

Take this product, weigh it precisely, add 0.4% sodium hydroxide solution to dissolve it and dilute it quantitatively to make it contain about 10% in every 1mL μ G solution, according to Ultraviolet–visible spectroscopy (general rule 0401), measure the absorbance at the wavelength of 271nm, and the absorption coefficient (E1% 1cm) is 565~595.


1. Take about 25mg of this product, add 5mL of water, drop sodium hydroxide test solution to dissolve it properly, and add 1-2 drops of Copper(II) sulfate test solution to generate green sediment.

2. Take 25mg of this product, put it in a test tube, add 2.5mL of ethanol to dissolve it, drop 2mL of p-dimethylamino Benzaldehyde test solution along the tube wall, and it will turn green and gradually turn dark red.

3. Take this product and add 0.4% sodium hydroxide solution to make it contain about 5% per 1mL μ G solution, according to Ultraviolet–visible spectroscopy (general rule 0401), there is maximum absorption at the wavelength of 228nm, 271nm and 333nm.

4. The infrared absorption spectrum of this product should be consistent with the reference spectrum (Spectrum Collection 184).


Clarity and color of alkaline solutions

Take 0.50g of this product, add 5mL of sodium hydroxide test solution to dissolve it, and then add 5mL of water. The solution should be clear and colorless. If it appears turbid, it should not be thicker than No. 2 turbidity standard solution (General Rule 0902 Method 1). If it appears color, it should not be deeper than No. 3 yellow standard solution (General Rule 0901 Method 1).


Take 2.0g of this product, add 100mL of water, shake thoroughly, filter, take 25mL of filtrate, and check according to the law (general rule 0801). Compared with the control solution made of 7.0mL of standard sodium chloride solution, it should not be more concentrated (0.014%).


Take 25mL of the remaining filtrate under the above chloride item, and check according to the law (general rule 0801). Compared with the control solution made of 2.0mL of standard Potassium sulfate solution, it should not be more concentrated (0.04%).

Related substances

Determine according to High-performance liquid chromatography (general rule 0512), and operate in dark.

Mixed solvent: Take 22mL of glacial acetic acid, add acetonitrile water (1:1) to 1000mL, and mix well.

Test solution: Take this product, dissolve it in a mixed solvent, and dilute it to make a solution containing approximately 1mg per 1mL.

Reference solution: Accurately measure an appropriate amount of the test sample solution and dilute it with a mixed solvent to produce a solution containing 10% per 1mL μ G solution.

Chromatographic conditions: octadecyl silane bonded silica gel is used as the filler, water tetrahydrofuran glacial acetic acid (70:30:1) is used as the mobile phase, the detection wavelength is 272nm, and the injection volume is 20 μ L.

System applicability requirements: the number of theoretical plates shall not be less than 4000 based on Furosemide peak.

Determination method: Accurately measure the test solution and control solution, inject them into a liquid chromatograph, and record the chromatogram until the retention time of the main component peak is 3 times.

Limit: If there are impurity peaks in the chromatogram of the test solution, the area of a single impurity peak shall not be greater than 0.2 times (0.2%) of the main peak area of the reference solution, and the sum of the impurity peak areas shall not be greater than the main peak area of the reference solution (1.0%).

Loss on drying

Take this product and dry it to constant weight at 105 ℃. The weight loss should not exceed 0.5% (general rule 0831).

Scorching residue

Shall not exceed 0.1% (General Rule 0841).

heavy metal

Take 0.50g of this product and inspect it according to the law (General Rule 0821, Third Method). The content of heavy metals should not exceed 20 parts per million.

Arsenic salt

Take 1.0g of this product, add 1g of Calcium hydroxide, mix it, add a small amount of water, stir it evenly, heat it with a small fire, burn it until it is completely ashed, cool it, add 5mL of hydrochloric acid and 23mL of water, and check according to the law (General Rule 0822, the first method), which should meet the requirements (0.0002%).

Content determination

Take about 0.5g of this product, weigh it accurately, add 30mL of ethanol, dissolve it at a slight temperature, cool it, add 4 drops of Cresol Red indicator solution and 1 drop of thymol blue indicator solution, titrate with sodium hydroxide titrant (0.1mol/L) until the solution turns purple red, and correct the titration result with blank test. Every 1mL of sodium hydroxide titrant (0.1mol/L) is equivalent to 33.07mg of C12H11ClN2O5S. [3]

Drug Description Broadcast


Circulating system drugs>antihypertensive drugs>diuretic and antihypertensive drugs


1. Effect on water and electrolyte excretion: It can increase the excretion of water, sodium, chlorine, potassium, calcium, magnesium, phosphorus, etc. Different from thiazide diuretics, loop diuretics such as Furosemide have obvious dose-response relationship. As the dosage increases, the diuretic effect is significantly enhanced, and the drug dosage range is large. This kind of drugs mainly inhibits the active reabsorption of NaCl in the thick wall segment of the medullary loop of the renal tubule. As a result, the concentration of Na+and Cl – in the lumen fluid increases, while the concentration of Na+and Cl – in the medullary interstitial fluid decreases, reducing the gradient difference of Osmotic pressure and the concentration function of the renal tubule, leading to increased excretion of water, Na+and Cl -. Due to a decrease in Na+reabsorption, the concentration of Na+in the distal tubules increases. As for the mechanism of Furosemide inhibiting the reabsorption of Cl – in the thick wall segment of the ascending branch of the medullary loop of the renal tubule, it is believed that there is a chlorine pump in this area. Research shows that there is a Na+, Cl – paired transport system related to Na+- K+ATPase outside the Basement membrane in this area. Furosemide reduces the reabsorption of Na+, Cl – by inhibiting the function of this system. In addition, Furosemide may also inhibit the reabsorption of Na+and Cl – by proximal and distal tubules, and promote the secretion of K+by distal tubules. Furosemide increases the excretion of Ca2+and Mg2+by inhibiting the reabsorption of Ca2+and Mg2+by Heinz loop. Short term medication can increase uric acid excretion, while long-term medication can cause Hyperuricemia.

2. Effect on hemodynamics: Furosemide can inhibit the activity of Prostaglandin decomposing enzyme, increase the content of Prostaglandin E2, and thus has the effect of vasodilation. The expansion of renal vessels, the reduction of renal vascular resistance, and the increase of Renal blood flow, especially in the deep Renal cortex, are of great significance in the diuretic effect of Furosemide, and are also the theoretical basis for its use in the prevention of acute renal failure. In addition, unlike other diuretics, loop diuretics do not decrease the glomerular filtration rate when the flow of Tubular fluid increases, which may be related to the decrease of chlorine flowing through Macula densa, thus weakening or blocking the bulb tube balance. Furosemide can expand the pulmonary volumetric vein, reduce the permeability of pulmonary capillaries, and its diuretic effect can reduce the amount of blood returning to the heart and the end diastolic pressure of the Right ventricle, which is helpful to the treatment of acute right heart failure. Because Furosemide can reduce the permeability of pulmonary capillaries, it provides a theoretical basis for its treatment of adult respiratory distress syndrome.


The oral absorption rate is 60-70%. Eating can slow down absorption, but it does not affect the absorption rate and its therapeutic effect. The oral absorption rate of end-stage kidney disease patients decreased to 43-46%. In edematous diseases such as congestive heart failure and nephrotic syndrome, due to intestinal wall edema, the oral absorption rate also decreases. Therefore, parenteral medication should be used in these situations. It is mainly distributed in Extracellular fluid, with an average distribution volume of 11.4% of body weight. The Plasma protein binding rate is 91~97%, almost all of which are bound with albumin. This drug can pass through the placental barrier and secrete into milk. The onset time of action after oral and intravenous administration is 30-60 minutes and 5 minutes, respectively, and the peak time is 1-2 hours and 0.33-1 hours. The duration of action is 6-8 hours and 2 hours, respectively. half life β There are significant individual differences, ranging from 30 to 60 minutes for normal individuals, 75 to 155 minutes for patients with anuria, and 11 to 20 hours for those with severe damage to liver and kidney function. Newborns have a half-life due to poor liver and kidney clearance ability β Extend to 4-8 hours. 88% of this drug is excreted through the kidneys in its original form, 12% is metabolized by the liver and excreted by bile. Patients with impaired renal function experience increased liver metabolism. This drug is not cleared by dialysis.


1. Edematous diseases include congestive heart failure, liver cirrhosis, kidney diseases (nephritis, kidney disease, and acute and chronic renal failure caused by various reasons), especially when other diuretics are not effective, the use of these drugs may still be effective. Combined with other drugs to treat acute Pulmonary edema and acute brain edema.

2. Hypertension is not the first choice drug for the treatment of primary hypertension in the stepwise therapy of hypertension. However, when thiazide drugs have poor efficacy, especially when accompanied by renal dysfunction or hypertension crisis, this type of drug is particularly suitable.

3. The prevention of acute renal failure is used to prevent renal blood perfusion insufficiency caused by various reasons, such as dehydration, shock, poisoning, anesthesia accident and circulatory insufficiency. Timely application can reduce the chance of Acute tubular necrosis.

4. Hyperkalemia and hypercalcemia.

5. Dilutive hyponatremia, especially when the blood sodium concentration is below 120mmol/L.

6. Hypersecretion of Vasopressin (SIADH).

7. Acute drug poisoning, such as Barbiturate poisoning.

Usage and dosage

Oral administration

Adult usage:

① Edematous disease: The initial dose is 20-40mg once a day, and if necessary, 20-40mg is added after 6-8 hours until satisfactory diuretic effect is achieved. The maximum daily dose can reach 600mg, but it should generally be controlled within 100mg and taken 2-3 times. Some patients can reduce the dosage to 20-40mg once a day, once every other day (or 20-40mg daily, continuously taking medication for 2-4 days per week).

② Hypertension: The initial dose is 40-80mg per day, taken in two doses, and the dosage may be adjusted accordingly.

③ Hypercalcemia: Take 80-120mg daily, 1-3 times a day.

Children’s commonly used amount

The initial dose for edematous diseases is 2mg/kg based on body weight, with an additional 1-2mg/kg added every 4-6 hours if necessary. Newborns should extend the medication interval.

intravenous injection

Adult usage:

① Edematous diseases:

a. General dose: The initial dose is 20-40mg, and if necessary, an additional dose is added every 2 hours until satisfactory therapeutic effect is achieved. The maintenance medication phase can be administered in stages.

b. Acute left heart failure: The initial dose is 40mg, and if necessary, an additional 80mg per hour is added until satisfactory therapeutic effect is achieved.

c. Chronic renal insufficiency: The daily dose is generally 40-120mg.

② Hypertension crisis: The initial dose is 40-80mg, and when accompanied by acute left heart failure or acute renal failure, the dosage can be increased as appropriate.

③ Hypercalcemia: 20-80mg at a time.

Children’s commonly used dosage:

Edematous disease: The initial dose is 1mg/kg, and if necessary, 1mg/kg is added every 2 hours. The maximum daily dose can reach 6mg/kg.

Prohibit and use with caution

1. Cross allergy. Individuals who are allergic to sulfonamide drugs and thiazide diuretics may also be allergic to this drug.

2. This drug can pass through the placental barrier, and pregnant women, especially in the first three months of pregnancy, should avoid using it as much as possible. It has no preventive effect on pregnancy induced hypertension syndrome. Animal experiments have shown that this product can cause placental hydronephrosis, miscarriage, and increased fetal mortality.

3. This medicine can be secreted through milk, and lactating women should use it with caution.

4. The half-life of this drug is significantly prolonged in newborns, so the interval between newborns should be extended.

5. The elderly have an increased chance of Hypotension, electrolyte disorder, thrombosis and renal function damage when using this drug.

6. Use with caution in the following situations:

① For those with no urine or severe renal function damage, the interval between medication should be extended to avoid side effects such as ototoxicity due to the need to increase the dosage;

② Diabetes;

③ Hyperuricemia or gout history;

④ In patients with severe liver function damage, liver coma may be induced due to water electrolyte disorder;

⑤ Acute myocardial infarction, excessive diuresis can promote shock;

⑥ Pancreatitis or a history of this disease;

⑦ Those who have a tendency to Hypokalemia, especially those who use digitalis or have ventricular arrhythmia;

⑧ Lupus erythematosus, this medication can worsen the condition or induce activity;

⑨ Prostate hypertrophy. Hypokalemia, excessive use of digitalis, contraindicated for liver coma patients, and cautious use for advanced liver cirrhosis. High doses have great eye toxicity to individuals with high blood uric acid levels.

This product can penetrate the placenta, increase the formation of fetal urine, and increase the acid concentration in maternal, fetal serum, and amniotic fluid. Therefore, for pregnant women, it is only necessary to take this product in the event of heart failure.

Adverse reactions

The common ones are related to water and electrolyte disorders, especially in large doses or long-term use, such as postural Hypotension, shock, Hypokalemia, hypochloremia, hypochloremic alkalosis, hyponatremia, Hypocalcemia, and thirst, fatigue, muscle soreness, arrhythmia, etc.

The rare patients have allergic reactions (including rashes, Interstitial nephritis, and even cardiac arrest), blurred vision, yellow vision, photosensitivity, dizziness, headache, anorexia, nausea, vomiting, abdominal pain, diarrhea, pancreatitis, muscle rigidity, etc., Bone marrow suppression leads to granulocytopenia, Thrombocytopenic purpura and aplastic anemia, liver function damage, abnormal sensation of fingers and toes, hyperglycemia, positive urine sugar, and aggravation of original diabetes, Hyperuricemia. Tinnitus and hearing impairment are mostly seen in rapid intravenous injection of large doses (more than 4-5mg per minute), most of which are temporary, and a few are Irreversible process, especially when used together with other ototoxic drugs. In hypercalcemia, it can cause Kidney stone disease. There are still reports that this drug can exacerbate idiopathic edema. It can cause hypokalemia, hypochloremia, decreased blood magnesium, nausea, vomiting, diarrhea, rash, itching, muscle spasms, dizziness, fatigue, drowsiness, and dry mouth. Injecting too quickly can cause temporary deafness. Individual cases of leukopenia, thrombocytopenia, erythema multiforme, postural Hypotension. Long term use can lead to Peptic ulcer disease, hyperacidemia, gastrointestinal irritation or discomfort, acute pancreatitis, jaundice, and hallucination in individual cases. Intravenous injection can cause cardiac arrest or even death. Cardiovascular system: In addition to diuretic effect, Furosemide also has a short-term but definite vasodilation effect. This product can change the venous blood volume and peripheral vascular resistance of patients with kidney damage, resulting in postural Hypotension and syncope. When used in combination with other antihypertensive drugs, the symptoms are more serious.

Endocrine and metabolic: The effect of this product on lipid metabolism is similar to that of thiazide drugs. Furosemide can cause Vasopressin imbalance syndrome (IADHS). The concentration of Vasopressin (ADH) in patients’ plasma increases, the total sodium content of the body is normal, and the total potassium content decreases significantly. If the product is used quickly, it will cause a sharp increase in the secretion of high blood proteasome and Aldosterone. Animal experiments have shown that long-term use of this product can lead to thiamine deficiency and damage heart function. Therefore, for patients who have been using this product for a long time, attention should be paid to the concentration of thiamine in the blood. Similar to thiazide drugs, this product can also cause high blood uric acid and promote gout, with a higher frequency and severity. Elderly patients may develop gout after taking it for 3 months.

Electrolyte and body fluid balance: Similar to thiazide drugs, loop diuretics also cause changes in electrolyte balance,

The characteristics and degree of action vary. The incidence rate is approximately 23%.

1. Calcium metabolism is different from thiazides. Furosemide does not promote calcium reabsorption in distal renal tubules, but can cause transient Hypercalcaemia. This product can cause secondary Parathyroid gland in newborns, resulting in bone calcium loss. The excretion rate of calcium is 10~20 times larger than that of normal children, and there is a risk of Kidney stone disease formation. There is also a possibility of secondary sepsis.

2. Low blood magnesium, although this product can cause kidney damage caused by magnesium

Post time: Jul-13-2023