Great resource for drug information, reviews and discussions
Nemasol Sodium ICN (Aminosalicylate Sodium)
How do you rate this drug's effectiveness?
Pharmacology
Aminosalicylic acid is bacteriostatic in action. The mechanism of action of the drug is similar to that of sulfonamides. Aminosalicylic acid suppresses growth and reproduction of M.tuberculosis by competitively inhibiting the synthesis of folic acid. The activity of aminosalicylic acid may be partially inhibited by aminobenzoic acid.
Aminosalicylic acid and its salt are a highly specific agent and is active only against M.tuberculosis . In vitro, the minimum inhibitory concentration of aminosalicylic acid for most susceptible M.tuberculosis is 0.5to 2.0µg/mL.
Natural and acquired resistance to aminosalicylic acid have been demonstrated in vitro and in vivo. Resistant strains of initially susceptible organisms develop rapidly if aminosalicylic acid or its salt is used alone in the treatment of clinical tuberculosis. When aminosalicylic acid is combined with other antituberculosis agents in the treatment of the disease, emergence of resistant strains may be delayed or prevented. There is no evidence of cross-resistance between aminosalicylic acid and other antituberculosis agents currently available.
Pharmacokinetics: Absorption: Aminosalicylate sodium is rapidly and well absorbed from the gastrointestinal tract.
Distribution: Aminosalicylate sodium diffuses readily into various tissues and fluids including peritoneal fluid, pleural fluid, and synovial fluid in concentrations approximately equal to plasma concentrations of the drug. The drug does not cross the blood-brain barrier in patients with uninflamed meninges; however, CSF concentrations of aminosalicylic sodium are reported to be 10to 50% of concurrent plasma concentrations of the drug in patients with inflamed meninges. It is not known if aminosalicylic sodium crosses the placenta. Small amounts of the drug are also distributed into milk and bile. It diffuses readily into kidneys, lungs and liver, and achieves high concentrations in caseous tissue.
Aminosalicylic sodium is 50to 73% bound to plasma proteins.
Elimination: The plasma half-life of aminosalicylic acid is approximately 1hour. Plasma concentrations of the drug are not substantially affected by renal or hepatic insufficiency; however, the half-lives of the inactive metabolites may be prolonged in patients with impaired renal function (up to 23hours).
Aminosalicylic acid is inactivated in the intestinal mucosa and liver primarily by acetylation. The major metabolites are N-acetyl-p-aminosalicylic acid and p-aminosalicyluric acid. The degree of metabolism is concentration-dependent and capacity-limited; the larger the dose absorbed, the lower the percentage of drug metabolised.
Aminosalicylic sodium and its metabolites are excreted in urine by glomerular filtration and tubular secretion. Following a single 4g dose of aminosalicylic acid in adults with normal renal function, approximately 77% of the dose is excreted in urine within 24hours; 56% is excreted as the acetylated metabolite. Following a single 4g dose of the sodium salt in adults with normal renal function, 93to 99% of the dose is excreted in urine within 24hours; 52to 57% is excreted as the acetylated metabolite. It is not known if the drug is removed by hemodialysis or peritoneal dialysis.
Aminosalicylic acid is bacteriostatic in action. The mechanism of action of the drug is similar to that of sulfonamides. Aminosalicylic acid suppresses growth and reproduction of M.tuberculosis by competitively inhibiting the synthesis of folic acid. The activity of aminosalicylic acid may be partially inhibited by aminobenzoic acid.
Aminosalicylic acid and its salt are a highly specific agent and is active only against M.tuberculosis . In vitro, the minimum inhibitory concentration of aminosalicylic acid for most susceptible M.tuberculosis is 0.5to 2.0µg/mL.
Natural and acquired resistance to aminosalicylic acid have been demonstrated in vitro and in vivo. Resistant strains of initially susceptible organisms develop rapidly if aminosalicylic acid or its salt is used alone in the treatment of clinical tuberculosis. When aminosalicylic acid is combined with other antituberculosis agents in the treatment of the disease, emergence of resistant strains may be delayed or prevented. There is no evidence of cross-resistance between aminosalicylic acid and other antituberculosis agents currently available.
Pharmacokinetics: Absorption: Aminosalicylate sodium is rapidly and well absorbed from the gastrointestinal tract.
Distribution: Aminosalicylate sodium diffuses readily into various tissues and fluids including peritoneal fluid, pleural fluid, and synovial fluid in concentrations approximately equal to plasma concentrations of the drug. The drug does not cross the blood-brain barrier in patients with uninflamed meninges; however, CSF concentrations of aminosalicylic sodium are reported to be 10to 50% of concurrent plasma concentrations of the drug in patients with inflamed meninges. It is not known if aminosalicylic sodium crosses the placenta. Small amounts of the drug are also distributed into milk and bile. It diffuses readily into kidneys, lungs and liver, and achieves high concentrations in caseous tissue.
Aminosalicylic sodium is 50to 73% bound to plasma proteins.
Elimination: The plasma half-life of aminosalicylic acid is approximately 1hour. Plasma concentrations of the drug are not substantially affected by renal or hepatic insufficiency; however, the half-lives of the inactive metabolites may be prolonged in patients with impaired renal function (up to 23hours).
Aminosalicylic acid is inactivated in the intestinal mucosa and liver primarily by acetylation. The major metabolites are N-acetyl-p-aminosalicylic acid and p-aminosalicyluric acid. The degree of metabolism is concentration-dependent and capacity-limited; the larger the dose absorbed, the lower the percentage of drug metabolised.
Aminosalicylic sodium and its metabolites are excreted in urine by glomerular filtration and tubular secretion. Following a single 4g dose of aminosalicylic acid in adults with normal renal function, approximately 77% of the dose is excreted in urine within 24hours; 56% is excreted as the acetylated metabolite. Following a single 4g dose of the sodium salt in adults with normal renal function, 93to 99% of the dose is excreted in urine within 24hours; 52to 57% is excreted as the acetylated metabolite. It is not known if the drug is removed by hemodialysis or peritoneal dialysis.
Indications
Aminosalicylic Acid Is Bacteriostatic In Action. The Mechanism Of Action Of The Drug Is Similar To That Of Sulfonamides. Aminosalicylic Acid Suppresses Growth And Reproduction Of M.tuberculosis By Competitively Inhibiting The Synthesis Of Folic Acid. The Activity Of Aminosalicylic Acid May Be Partially Inhibited By Aminobenzoic Acid.
Aminosalicylic Acid And Its Salt Are A Highly Specific Agent And Is Active Only Against M.tuberculosis . In Vitro, The Minimum Inhibitory Concentration Of Aminosalicylic Acid For Most Susceptible M.tuberculosis Is 0.5to 2.0µg/mL.
Natural And Acquired Resistance To Aminosalicylic Acid Have Been Demonstrated In Vitro And In Vivo. Resistant Strains Of Initially Susceptible Organisms Develop Rapidly If Aminosalicylic Acid Or Its Salt Is Used Alone In The Treatment Of Clinical Tuberculosis. When Aminosalicylic Acid Is Combined With Other Antituberculosis Agents In The Treatment Of The Disease, Emergence Of Resistant Strains May Be Delayed Or Prevented. There Is No Evidence Of Cross-resistance Between Aminosalicylic Acid And Other Antituberculosis Agents Currently Available.
Pharmacokinetics: Absorption: Aminosalicylate Sodium Is Rapidly And Well Absorbed From The Gastrointestinal Tract.
Distribution: Aminosalicylate Sodium Diffuses Readily Into Various Tissues And Fluids Including Peritoneal Fluid, Pleural Fluid, And Synovial Fluid In Concentrations Approximately Equal To Plasma Concentrations Of The Drug. The Drug Does Not Cross The Blood-brain Barrier In Patients With Uninflamed Meninges; However, CSF Concentrations Of Aminosalicylic Sodium Are Reported To Be 10to 50% Of Concurrent Plasma Concentrations Of The Drug In Patients With Inflamed Meninges. It Is Not Known If Aminosalicylic Sodium Crosses The Placenta. Small Amounts Of The Drug Are Also Distributed Into Milk And Bile. It Diffuses Readily Into Kidneys, Lungs And Liver, And Achieves High Concentrations In Caseous Tissue.
Aminosalicylic Sodium Is 50to 73% Bound To Plasma Proteins.
Elimination: The Plasma Half-life Of Aminosalicylic Acid Is Approximately 1hour. Plasma Concentrations Of The Drug Are Not Substantially Affected By Renal Or Hepatic Insufficiency; However, The Half-lives Of The Inactive Metabolites May Be Prolonged In Patients With Impaired Renal Function (up To 23hours).
Aminosalicylic Acid Is Inactivated In The Intestinal Mucosa And Liver Primarily By Acetylation. The Major Metabolites Are N-acetyl-p-aminosalicylic Acid And P-aminosalicyluric Acid. The Degree Of Metabolism Is Concentration-dependent And Capacity-limited; The Larger The Dose Absorbed, The Lower The Percentage Of Drug Metabolised.
Aminosalicylic Sodium And Its Metabolites Are Excreted In Urine By Glomerular Filtration And Tubular Secretion. Following A Single 4g Dose Of Aminosalicylic Acid In Adults With Normal Renal Function, Approximately 77% Of The Dose Is Excreted In Urine Within 24hours; 56% Is Excreted As The Acetylated Metabolite. Following A Single 4g Dose Of The Sodium Salt In Adults With Normal Renal Function, 93to 99% Of The Dose Is Excreted In Urine Within 24hours; 52to 57% Is Excreted As The Acetylated Metabolite. It Is Not Known If The Drug Is Removed By Hemodialysis Or Peritoneal Dialysis.
Aminosalicylic Acid Is Bacteriostatic In Action. The Mechanism Of Action Of The Drug Is Similar To That Of Sulfonamides. Aminosalicylic Acid Suppresses Growth And Reproduction Of M.tuberculosis By Competitively Inhibiting The Synthesis Of Folic Acid. The Activity Of Aminosalicylic Acid May Be Partially Inhibited By Aminobenzoic Acid.
Aminosalicylic Acid And Its Salt Are A Highly Specific Agent And Is Active Only Against M.tuberculosis . In Vitro, The Minimum Inhibitory Concentration Of Aminosalicylic Acid For Most Susceptible M.tuberculosis Is 0.5to 2.0µg/mL.
Natural And Acquired Resistance To Aminosalicylic Acid Have Been Demonstrated In Vitro And In Vivo. Resistant Strains Of Initially Susceptible Organisms Develop Rapidly If Aminosalicylic Acid Or Its Salt Is Used Alone In The Treatment Of Clinical Tuberculosis. When Aminosalicylic Acid Is Combined With Other Antituberculosis Agents In The Treatment Of The Disease, Emergence Of Resistant Strains May Be Delayed Or Prevented. There Is No Evidence Of Cross-resistance Between Aminosalicylic Acid And Other Antituberculosis Agents Currently Available.
Pharmacokinetics: Absorption: Aminosalicylate Sodium Is Rapidly And Well Absorbed From The Gastrointestinal Tract.
Distribution: Aminosalicylate Sodium Diffuses Readily Into Various Tissues And Fluids Including Peritoneal Fluid, Pleural Fluid, And Synovial Fluid In Concentrations Approximately Equal To Plasma Concentrations Of The Drug. The Drug Does Not Cross The Blood-brain Barrier In Patients With Uninflamed Meninges; However, CSF Concentrations Of Aminosalicylic Sodium Are Reported To Be 10to 50% Of Concurrent Plasma Concentrations Of The Drug In Patients With Inflamed Meninges. It Is Not Known If Aminosalicylic Sodium Crosses The Placenta. Small Amounts Of The Drug Are Also Distributed Into Milk And Bile. It Diffuses Readily Into Kidneys, Lungs And Liver, And Achieves High Concentrations In Caseous Tissue.
Aminosalicylic Sodium Is 50to 73% Bound To Plasma Proteins.
Elimination: The Plasma Half-life Of Aminosalicylic Acid Is Approximately 1hour. Plasma Concentrations Of The Drug Are Not Substantially Affected By Renal Or Hepatic Insufficiency; However, The Half-lives Of The Inactive Metabolites May Be Prolonged In Patients With Impaired Renal Function (up To 23hours).
Aminosalicylic Acid Is Inactivated In The Intestinal Mucosa And Liver Primarily By Acetylation. The Major Metabolites Are N-acetyl-p-aminosalicylic Acid And P-aminosalicyluric Acid. The Degree Of Metabolism Is Concentration-dependent And Capacity-limited; The Larger The Dose Absorbed, The Lower The Percentage Of Drug Metabolised.
Aminosalicylic Sodium And Its Metabolites Are Excreted In Urine By Glomerular Filtration And Tubular Secretion. Following A Single 4g Dose Of Aminosalicylic Acid In Adults With Normal Renal Function, Approximately 77% Of The Dose Is Excreted In Urine Within 24hours; 56% Is Excreted As The Acetylated Metabolite. Following A Single 4g Dose Of The Sodium Salt In Adults With Normal Renal Function, 93to 99% Of The Dose Is Excreted In Urine Within 24hours; 52to 57% Is Excreted As The Acetylated Metabolite. It Is Not Known If The Drug Is Removed By Hemodialysis Or Peritoneal Dialysis.
Safety Information / Warning
Hypersensitivity reactions including fever, skin eruptions of various types, pruritus, vasculitis, joint pain, eosinophilia, leukopenia, agranulocytosis, thrombocytopenia, hepatitis, and jaundice have been reported in patients receiving aminosalicylic acid or its salts. Rarely, Löffler's syndrome, an infectious mononucleosis-like syndrome, encephalopathy, and psychotic reactions have also been reported. If symptoms of hypersensitivity occur, all drugs should be discontinued. When the symptoms have abated, the drugs may be reinstituted one at a time in small and gradually increasing doses to determine which drug was responsible for the reaction.
Aminosalicylic acid or its salt may cause hemolytic anemia and hematuria in patients with G-6-PD deficiency. Hypokalemia, acidosis, albuminuria, and crystalluria have occurred occasionally in patients receiving aminosalicylic acid. Crystalluria may be prevented by administering the sodium salt of the drug or by maintaining the urine at a neutral or alkaline pH.
Goiter, with and without myxedema, has occurred in patients receiving prolonged high-dose aminosalicylic acid therapy. This effect is rare in patients receiving usual dosages of the drug.
Aminosalicylic acid or its salt should be used with caution in patients with impaired renal or hepatic function and in patients with gastric ulcer. Aminosalicylate sodium should be used with caution in patients with known or impending congestive heart failure and in other patients in whom excess sodium is potentially harmful.
Pregnancy: Safe use of aminosalicylic acid or its salt during pregnancy has not been established.
Hypersensitivity reactions including fever, skin eruptions of various types, pruritus, vasculitis, joint pain, eosinophilia, leukopenia, agranulocytosis, thrombocytopenia, hepatitis, and jaundice have been reported in patients receiving aminosalicylic acid or its salts. Rarely, Löffler's syndrome, an infectious mononucleosis-like syndrome, encephalopathy, and psychotic reactions have also been reported. If symptoms of hypersensitivity occur, all drugs should be discontinued. When the symptoms have abated, the drugs may be reinstituted one at a time in small and gradually increasing doses to determine which drug was responsible for the reaction.
Aminosalicylic acid or its salt may cause hemolytic anemia and hematuria in patients with G-6-PD deficiency. Hypokalemia, acidosis, albuminuria, and crystalluria have occurred occasionally in patients receiving aminosalicylic acid. Crystalluria may be prevented by administering the sodium salt of the drug or by maintaining the urine at a neutral or alkaline pH.
Goiter, with and without myxedema, has occurred in patients receiving prolonged high-dose aminosalicylic acid therapy. This effect is rare in patients receiving usual dosages of the drug.
Aminosalicylic acid or its salt should be used with caution in patients with impaired renal or hepatic function and in patients with gastric ulcer. Aminosalicylate sodium should be used with caution in patients with known or impending congestive heart failure and in other patients in whom excess sodium is potentially harmful.
Pregnancy: Safe use of aminosalicylic acid or its salt during pregnancy has not been established.
Precautions
Hypersensitivity reactions including fever, skin eruptions of various types, pruritus, vasculitis, joint pain, eosinophilia, leukopenia, agranulocytosis, thrombocytopenia, hepatitis, and jaundice have been reported in patients receiving aminosalicylic acid or its salts. Rarely, Löffler's syndrome, an infectious mononucleosis-like syndrome, encephalopathy, and psychotic reactions have also been reported. If symptoms of hypersensitivity occur, all drugs should be discontinued. When the symptoms have abated, the drugs may be reinstituted one at a time in small and gradually increasing doses to determine which drug was responsible for the reaction.
Aminosalicylic acid or its salt may cause hemolytic anemia and hematuria in patients with G-6-PD deficiency. Hypokalemia, acidosis, albuminuria, and crystalluria have occurred occasionally in patients receiving aminosalicylic acid. Crystalluria may be prevented by administering the sodium salt of the drug or by maintaining the urine at a neutral or alkaline pH.
Goiter, with and without myxedema, has occurred in patients receiving prolonged high-dose aminosalicylic acid therapy. This effect is rare in patients receiving usual dosages of the drug.
Aminosalicylic acid or its salt should be used with caution in patients with impaired renal or hepatic function and in patients with gastric ulcer. Aminosalicylate sodium should be used with caution in patients with known or impending congestive heart failure and in other patients in whom excess sodium is potentially harmful.
Pregnancy: Safe use of aminosalicylic acid or its salt during pregnancy has not been established.
Hypersensitivity reactions including fever, skin eruptions of various types, pruritus, vasculitis, joint pain, eosinophilia, leukopenia, agranulocytosis, thrombocytopenia, hepatitis, and jaundice have been reported in patients receiving aminosalicylic acid or its salts. Rarely, Löffler's syndrome, an infectious mononucleosis-like syndrome, encephalopathy, and psychotic reactions have also been reported. If symptoms of hypersensitivity occur, all drugs should be discontinued. When the symptoms have abated, the drugs may be reinstituted one at a time in small and gradually increasing doses to determine which drug was responsible for the reaction.
Aminosalicylic acid or its salt may cause hemolytic anemia and hematuria in patients with G-6-PD deficiency. Hypokalemia, acidosis, albuminuria, and crystalluria have occurred occasionally in patients receiving aminosalicylic acid. Crystalluria may be prevented by administering the sodium salt of the drug or by maintaining the urine at a neutral or alkaline pH.
Goiter, with and without myxedema, has occurred in patients receiving prolonged high-dose aminosalicylic acid therapy. This effect is rare in patients receiving usual dosages of the drug.
Aminosalicylic acid or its salt should be used with caution in patients with impaired renal or hepatic function and in patients with gastric ulcer. Aminosalicylate sodium should be used with caution in patients with known or impending congestive heart failure and in other patients in whom excess sodium is potentially harmful.
Pregnancy: Safe use of aminosalicylic acid or its salt during pregnancy has not been established.
Side Effects / Adverse Effects
The most frequent adverse effects of aminosalicylic acid or its salt are gastrointestinal disturbances, including nausea, vomiting, abdominal pain, diarrhea, and anorexia. Rarely, aminosalicylic acid has caused peptic ulcer and gastric hemorrhage. Adverse gastrointestinal effects may be minimised in some patients by administering the drug with meals or by the concomitant administration of aluminium hydroxide gel. However, symptoms may be severe enough to require discontinuation of the drugs. Malabsorption of vitamin B 12, folic acid, iron, and lipids has also occurred occasionally in patients receiving aminosalicylic acid or its salt, possibly as the result of increased peristalsis.
The most frequent adverse effects of aminosalicylic acid or its salt are gastrointestinal disturbances, including nausea, vomiting, abdominal pain, diarrhea, and anorexia. Rarely, aminosalicylic acid has caused peptic ulcer and gastric hemorrhage. Adverse gastrointestinal effects may be minimised in some patients by administering the drug with meals or by the concomitant administration of aluminium hydroxide gel. However, symptoms may be severe enough to require discontinuation of the drugs. Malabsorption of vitamin B 12, folic acid, iron, and lipids has also occurred occasionally in patients receiving aminosalicylic acid or its salt, possibly as the result of increased peristalsis.
Overdose
Information not available
Information not available
Recommended Dosage
Aminosalicylic sodium may be taken with or after meals or with an antacid if gastric irritation occurs. If gastric irritation persists, a temporary reduction in dose or a brief rest period of up to 2weeks may be helpful. Aminosalicylate sodium may then be restarted in small daily doses and gradually increased to full therapeutic doses. If tolerated, the total daily dose may be given as a single dose.
Therapy may have to be continued for 1to 2years, and may even be required for up to several years or indefinitely, although in some patients shorter treatment regimens may also be effective.
Patient compliance may be poor because of gastric irritation or hypersensitivity reactions. Children may tolerate aminosalicylate sodium better than do adults.
Usual Adult and Adolescent Dose: in combination with other antimycobacterials: oral, 3.3 to 4g every 8hours; or 5to 6g every 12hours.
Usual Adult Prescribing Limits: up to 20g daily.
Usual Pediatric Dose: in combination with other antimycobacterials: oral, 50to 75mg/kg of body weight every 6hours; or 66.7to 100mg/kg of body weight every 8hours. The maximum daily dose in children should not exceed 12g.
Stability and Storage Recommendations: Aminosalicylate sodium deteriorates rapidly if exposed to moisture, heat, or light. If deterioration occurs, as indicated by a brownish or purplish discoloration of the tablets, the drug should be discarded.
Aminosalicylic sodium may be taken with or after meals or with an antacid if gastric irritation occurs. If gastric irritation persists, a temporary reduction in dose or a brief rest period of up to 2weeks may be helpful. Aminosalicylate sodium may then be restarted in small daily doses and gradually increased to full therapeutic doses. If tolerated, the total daily dose may be given as a single dose.
Therapy may have to be continued for 1to 2years, and may even be required for up to several years or indefinitely, although in some patients shorter treatment regimens may also be effective.
Patient compliance may be poor because of gastric irritation or hypersensitivity reactions. Children may tolerate aminosalicylate sodium better than do adults.
Usual Adult and Adolescent Dose: in combination with other antimycobacterials: oral, 3.3 to 4g every 8hours; or 5to 6g every 12hours.
Usual Adult Prescribing Limits: up to 20g daily.
Usual Pediatric Dose: in combination with other antimycobacterials: oral, 50to 75mg/kg of body weight every 6hours; or 66.7to 100mg/kg of body weight every 8hours. The maximum daily dose in children should not exceed 12g.
Stability and Storage Recommendations: Aminosalicylate sodium deteriorates rapidly if exposed to moisture, heat, or light. If deterioration occurs, as indicated by a brownish or purplish discoloration of the tablets, the drug should be discarded.
Supplied / Packaging
Each white, compressed tablet, imprinted ICN N11, contains: aminosalicylate sodium, USP 500mg. Nonmedicinal ingredients: microcrystalline cellulose, povidone, starch and stearic acid. Bottles of 500 and 1000. Store in well-closed, light-resistant container at controlled room temperature (15to 30°C).
Each white, compressed tablet, imprinted ICN N11, contains: aminosalicylate sodium, USP 500mg. Nonmedicinal ingredients: microcrystalline cellulose, povidone, starch and stearic acid. Bottles of 500 and 1000. Store in well-closed, light-resistant container at controlled room temperature (15to 30°C).
Search for a drug
Brand Name
Nemasol Sodium ICN
Nemasol Sodium ICN
Generic Name
Aminosalicylate Sodium
Aminosalicylate Sodium
General Indications
Antibacterial Antimycobacterial
Antibacterial Antimycobacterial
