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Salofalk (5-Aminosalicylic Acid)
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Pharmacology
5-Aminosalicylic Acid (5-ASA) is the active metabolite of the prodrug sulfasalazine (SAS), a drug which acts to suppress inflammatory bowel disease. Sulfasalazine is also an effective agent to both treat active disease and maintain remission in ulcerative colitis, however its use in Crohn's disease is minimal. Furthermore its use is limited by numerous adverse reactions. Over the past decade, human trials have shown that 5-ASA is the active principle of sulfasalazine and that it is effective in treating acute episodes of ulcerative colitis as well as maintaining remission.
When sulfasalazine is given orally, the majority of the dose migrates intact to the large bowel where bacterial enzymatic action cleaves the azo bond releasing sulfapyridine and 5-ASA. Sulfapyridine serves as a carrier for the active 5-ASA and has been cited by investigators as being responsible for the majority of adverse reactions and sensitivities of sulfasalazine.
The mode of action of 5-ASA is still under investigation with several biochemical mechanisms being proposed. At present, the action of5-ASA in treating inflammatory bowel disease appears to be associated with the metabolism of arachidonic acid. Studies suggest that interference of5-ASA with either leukotriene or prostaglandin metabolism may play a major role in suppressing the inflammatory response mechanism.
Regardless of the mode of action, 5-ASA appears to be active only topically. Rectal administration, therefore, allows for direct targeting of free 5-ASA to the sites of inflammation along the mucosal lumen of the rectum, sigmoid and distal large bowel. Systemic absorption of rectally administered 5-ASA is low as shown by urinary recoveries which range from 5to 35% of the amount given. Rectally administered 5-ASA thus acts locally on the recto-sigmoidal colon. In contrast, oral administration of free 5-ASA leads to high systemic absorption with little chance of topical effectiveness in the distal bowel. Salofalk tablets are therefore enteric-coated to allow passage through the stomach intact, despite an average gastric dwell time of close to 3 hours in nonfasting patients and delivery, at pH of 6.0, to sites of topical action in the lower gastrointestinal tract. Disintegration of Saloflak enteric-coated tablets usually occurs in the terminal ileum and proximal colon, allowing patients with ileal involvement to benefit from the drug. At the same time, most side effects attributed to the sulfapyridine moiety of SAS are avoided.
The only major metabolite of5-ASA identified in man is N-acetyl-5-aminosalicylic acid. Following rectal administration, both free and acetylated forms can be found in plasma within 1to2hours post administration. Usually plasma concentrations are low and do not exceed a maximum of about 10µg/mL at rectal daily doses of up to 4g. Urinary clearance of absorbed drug occurs rapidly, mainly as the acetylated metabolite. Plasma levels are therefore negligible approximately 24hours after dosing. Unabsorbed drug is excreted as both the free and acetylated forms via feces.
5-ASA and its major metabolite N-acetyl-5-aminosalicylic acid are short lived in serum being excreted rapidly with a half-life reported to range from 5to10hours and up to 24hours. In patients with active ulcerative colitis or Crohn's disease receiving 500mg of5-ASA t.i.d. orally, mean steady-state plasma levels of5-ASA and N-acetyl-5-ASA averaged 0.7and 1.2µg/mL respectively and were reached within 4to 6hours after administration. Treatment with a smaller dose (250mg t.i.d.) achieved levels of 0.4and 1µg/mL respectively. The elimination half-life thus appears to be dose dependent (1.4±0.6hours at 500mg t.i.d. vs 0.6±0.2hours at 250mg t.i.d.).
5-Aminosalicylic Acid (5-ASA) is the active metabolite of the prodrug sulfasalazine (SAS), a drug which acts to suppress inflammatory bowel disease. Sulfasalazine is also an effective agent to both treat active disease and maintain remission in ulcerative colitis, however its use in Crohn's disease is minimal. Furthermore its use is limited by numerous adverse reactions. Over the past decade, human trials have shown that 5-ASA is the active principle of sulfasalazine and that it is effective in treating acute episodes of ulcerative colitis as well as maintaining remission.
When sulfasalazine is given orally, the majority of the dose migrates intact to the large bowel where bacterial enzymatic action cleaves the azo bond releasing sulfapyridine and 5-ASA. Sulfapyridine serves as a carrier for the active 5-ASA and has been cited by investigators as being responsible for the majority of adverse reactions and sensitivities of sulfasalazine.
The mode of action of 5-ASA is still under investigation with several biochemical mechanisms being proposed. At present, the action of5-ASA in treating inflammatory bowel disease appears to be associated with the metabolism of arachidonic acid. Studies suggest that interference of5-ASA with either leukotriene or prostaglandin metabolism may play a major role in suppressing the inflammatory response mechanism.
Regardless of the mode of action, 5-ASA appears to be active only topically. Rectal administration, therefore, allows for direct targeting of free 5-ASA to the sites of inflammation along the mucosal lumen of the rectum, sigmoid and distal large bowel. Systemic absorption of rectally administered 5-ASA is low as shown by urinary recoveries which range from 5to 35% of the amount given. Rectally administered 5-ASA thus acts locally on the recto-sigmoidal colon. In contrast, oral administration of free 5-ASA leads to high systemic absorption with little chance of topical effectiveness in the distal bowel. Salofalk tablets are therefore enteric-coated to allow passage through the stomach intact, despite an average gastric dwell time of close to 3 hours in nonfasting patients and delivery, at pH of 6.0, to sites of topical action in the lower gastrointestinal tract. Disintegration of Saloflak enteric-coated tablets usually occurs in the terminal ileum and proximal colon, allowing patients with ileal involvement to benefit from the drug. At the same time, most side effects attributed to the sulfapyridine moiety of SAS are avoided.
The only major metabolite of5-ASA identified in man is N-acetyl-5-aminosalicylic acid. Following rectal administration, both free and acetylated forms can be found in plasma within 1to2hours post administration. Usually plasma concentrations are low and do not exceed a maximum of about 10µg/mL at rectal daily doses of up to 4g. Urinary clearance of absorbed drug occurs rapidly, mainly as the acetylated metabolite. Plasma levels are therefore negligible approximately 24hours after dosing. Unabsorbed drug is excreted as both the free and acetylated forms via feces.
5-ASA and its major metabolite N-acetyl-5-aminosalicylic acid are short lived in serum being excreted rapidly with a half-life reported to range from 5to10hours and up to 24hours. In patients with active ulcerative colitis or Crohn's disease receiving 500mg of5-ASA t.i.d. orally, mean steady-state plasma levels of5-ASA and N-acetyl-5-ASA averaged 0.7and 1.2µg/mL respectively and were reached within 4to 6hours after administration. Treatment with a smaller dose (250mg t.i.d.) achieved levels of 0.4and 1µg/mL respectively. The elimination half-life thus appears to be dose dependent (1.4±0.6hours at 500mg t.i.d. vs 0.6±0.2hours at 250mg t.i.d.).
Indications
5-Aminosalicylic Acid (5-ASA) Is The Active Metabolite Of The Prodrug Sulfasalazine (SAS), A Drug Which Acts To Suppress Inflammatory Bowel Disease. Sulfasalazine Is Also An Effective Agent To Both Treat Active Disease And Maintain Remission In Ulcerative Colitis, However Its Use In Crohn's Disease Is Minimal. Furthermore Its Use Is Limited By Numerous Adverse Reactions. Over The Past Decade, Human Trials Have Shown That 5-ASA Is The Active Principle Of Sulfasalazine And That It Is Effective In Treating Acute Episodes Of Ulcerative Colitis As Well As Maintaining Remission.
When Sulfasalazine Is Given Orally, The Majority Of The Dose Migrates Intact To The Large Bowel Where Bacterial Enzymatic Action Cleaves The Azo Bond Releasing Sulfapyridine And 5-ASA. Sulfapyridine Serves As A Carrier For The Active 5-ASA And Has Been Cited By Investigators As Being Responsible For The Majority Of Adverse Reactions And Sensitivities Of Sulfasalazine.
The Mode Of Action Of 5-ASA Is Still Under Investigation With Several Biochemical Mechanisms Being Proposed. At Present, The Action Of5-ASA In Treating Inflammatory Bowel Disease Appears To Be Associated With The Metabolism Of Arachidonic Acid. Studies Suggest That Interference Of5-ASA With Either Leukotriene Or Prostaglandin Metabolism May Play A Major Role In Suppressing The Inflammatory Response Mechanism.
Regardless Of The Mode Of Action, 5-ASA Appears To Be Active Only Topically. Rectal Administration, Therefore, Allows For Direct Targeting Of Free 5-ASA To The Sites Of Inflammation Along The Mucosal Lumen Of The Rectum, Sigmoid And Distal Large Bowel. Systemic Absorption Of Rectally Administered 5-ASA Is Low As Shown By Urinary Recoveries Which Range From 5to 35% Of The Amount Given. Rectally Administered 5-ASA Thus Acts Locally On The Recto-sigmoidal Colon. In Contrast, Oral Administration Of Free 5-ASA Leads To High Systemic Absorption With Little Chance Of Topical Effectiveness In The Distal Bowel. Salofalk Tablets Are Therefore Enteric-coated To Allow Passage Through The Stomach Intact, Despite An Average Gastric Dwell Time Of Close To 3 Hours In Nonfasting Patients And Delivery, At PH Of 6.0, To Sites Of Topical Action In The Lower Gastrointestinal Tract. Disintegration Of Saloflak Enteric-coated Tablets Usually Occurs In The Terminal Ileum And Proximal Colon, Allowing Patients With Ileal Involvement To Benefit From The Drug. At The Same Time, Most Side Effects Attributed To The Sulfapyridine Moiety Of SAS Are Avoided.
The Only Major Metabolite Of5-ASA Identified In Man Is N-acetyl-5-aminosalicylic Acid. Following Rectal Administration, Both Free And Acetylated Forms Can Be Found In Plasma Within 1to2hours Post Administration. Usually Plasma Concentrations Are Low And Do Not Exceed A Maximum Of About 10µg/mL At Rectal Daily Doses Of Up To 4g. Urinary Clearance Of Absorbed Drug Occurs Rapidly, Mainly As The Acetylated Metabolite. Plasma Levels Are Therefore Negligible Approximately 24hours After Dosing. Unabsorbed Drug Is Excreted As Both The Free And Acetylated Forms Via Feces.
5-ASA And Its Major Metabolite N-acetyl-5-aminosalicylic Acid Are Short Lived In Serum Being Excreted Rapidly With A Half-life Reported To Range From 5to10hours And Up To 24hours. In Patients With Active Ulcerative Colitis Or Crohn's Disease Receiving 500mg Of5-ASA T.i.d. Orally, Mean Steady-state Plasma Levels Of5-ASA And N-acetyl-5-ASA Averaged 0.7and 1.2µg/mL Respectively And Were Reached Within 4to 6hours After Administration. Treatment With A Smaller Dose (250mg T.i.d.) Achieved Levels Of 0.4and 1µg/mL Respectively. The Elimination Half-life Thus Appears To Be Dose Dependent (1.4±0.6hours At 500mg T.i.d. Vs 0.6±0.2hours At 250mg T.i.d.).
5-Aminosalicylic Acid (5-ASA) Is The Active Metabolite Of The Prodrug Sulfasalazine (SAS), A Drug Which Acts To Suppress Inflammatory Bowel Disease. Sulfasalazine Is Also An Effective Agent To Both Treat Active Disease And Maintain Remission In Ulcerative Colitis, However Its Use In Crohn's Disease Is Minimal. Furthermore Its Use Is Limited By Numerous Adverse Reactions. Over The Past Decade, Human Trials Have Shown That 5-ASA Is The Active Principle Of Sulfasalazine And That It Is Effective In Treating Acute Episodes Of Ulcerative Colitis As Well As Maintaining Remission.
When Sulfasalazine Is Given Orally, The Majority Of The Dose Migrates Intact To The Large Bowel Where Bacterial Enzymatic Action Cleaves The Azo Bond Releasing Sulfapyridine And 5-ASA. Sulfapyridine Serves As A Carrier For The Active 5-ASA And Has Been Cited By Investigators As Being Responsible For The Majority Of Adverse Reactions And Sensitivities Of Sulfasalazine.
The Mode Of Action Of 5-ASA Is Still Under Investigation With Several Biochemical Mechanisms Being Proposed. At Present, The Action Of5-ASA In Treating Inflammatory Bowel Disease Appears To Be Associated With The Metabolism Of Arachidonic Acid. Studies Suggest That Interference Of5-ASA With Either Leukotriene Or Prostaglandin Metabolism May Play A Major Role In Suppressing The Inflammatory Response Mechanism.
Regardless Of The Mode Of Action, 5-ASA Appears To Be Active Only Topically. Rectal Administration, Therefore, Allows For Direct Targeting Of Free 5-ASA To The Sites Of Inflammation Along The Mucosal Lumen Of The Rectum, Sigmoid And Distal Large Bowel. Systemic Absorption Of Rectally Administered 5-ASA Is Low As Shown By Urinary Recoveries Which Range From 5to 35% Of The Amount Given. Rectally Administered 5-ASA Thus Acts Locally On The Recto-sigmoidal Colon. In Contrast, Oral Administration Of Free 5-ASA Leads To High Systemic Absorption With Little Chance Of Topical Effectiveness In The Distal Bowel. Salofalk Tablets Are Therefore Enteric-coated To Allow Passage Through The Stomach Intact, Despite An Average Gastric Dwell Time Of Close To 3 Hours In Nonfasting Patients And Delivery, At PH Of 6.0, To Sites Of Topical Action In The Lower Gastrointestinal Tract. Disintegration Of Saloflak Enteric-coated Tablets Usually Occurs In The Terminal Ileum And Proximal Colon, Allowing Patients With Ileal Involvement To Benefit From The Drug. At The Same Time, Most Side Effects Attributed To The Sulfapyridine Moiety Of SAS Are Avoided.
The Only Major Metabolite Of5-ASA Identified In Man Is N-acetyl-5-aminosalicylic Acid. Following Rectal Administration, Both Free And Acetylated Forms Can Be Found In Plasma Within 1to2hours Post Administration. Usually Plasma Concentrations Are Low And Do Not Exceed A Maximum Of About 10µg/mL At Rectal Daily Doses Of Up To 4g. Urinary Clearance Of Absorbed Drug Occurs Rapidly, Mainly As The Acetylated Metabolite. Plasma Levels Are Therefore Negligible Approximately 24hours After Dosing. Unabsorbed Drug Is Excreted As Both The Free And Acetylated Forms Via Feces.
5-ASA And Its Major Metabolite N-acetyl-5-aminosalicylic Acid Are Short Lived In Serum Being Excreted Rapidly With A Half-life Reported To Range From 5to10hours And Up To 24hours. In Patients With Active Ulcerative Colitis Or Crohn's Disease Receiving 500mg Of5-ASA T.i.d. Orally, Mean Steady-state Plasma Levels Of5-ASA And N-acetyl-5-ASA Averaged 0.7and 1.2µg/mL Respectively And Were Reached Within 4to 6hours After Administration. Treatment With A Smaller Dose (250mg T.i.d.) Achieved Levels Of 0.4and 1µg/mL Respectively. The Elimination Half-life Thus Appears To Be Dose Dependent (1.4±0.6hours At 500mg T.i.d. Vs 0.6±0.2hours At 250mg T.i.d.).
Contraindications
Existing gastric or duodenal ulcer. Hypersensitivity to salicylates. Infants under 2years of age. Urinary tract obstructions.
Existing gastric or duodenal ulcer. Hypersensitivity to salicylates. Infants under 2years of age. Urinary tract obstructions.
Safety Information / Warning
5-ASA should be used only after critical appraisal of the risk to benefit ratio in the following situations: liver and kidney disease; bleeding or clotting disorders; pregnancy and lactation. Caution should be exercised in patients with elevated BUN.
Patients with pyloric stenosis may have prolonged retention of Salofalk enteric-coated tablets.
5-ASA should be used only after critical appraisal of the risk to benefit ratio in the following situations: liver and kidney disease; bleeding or clotting disorders; pregnancy and lactation. Caution should be exercised in patients with elevated BUN.
Patients with pyloric stenosis may have prolonged retention of Salofalk enteric-coated tablets.
Precautions
Periodic urinalysis to assess kidney function is recommended since prolonged therapy may damage the kidneys. Caution should be exercised when 5-ASA is first used in patients known to be allergic to sulfasalazine. These patients should be instructed to discontinue therapy at first sign of rash or fever.
Epigastric pain, also commonly associated with inflammatory bowel disease and prednisone or sulfasalazine therapy should be investigated in order to exclude pericarditis, pancreatitis or hepatitis either as adverse drug reactions to 5-ASA or secondary manifestations of inflammatory bowel disease.
Drug Interactions : No known drug interactions exist. The hypoglycemic effect of sulfonylureas may be enhanced. Interactions with coumarins, methotrexate, probenecid, sulfinpyrazone, spironolactone, furosemide and rifampin cannot be excluded. Potentiation of undesirable glucocorticoid effects on the stomach is possible.
Children: In children between the ages of 2 and 12, information on the safety and efficacy of 5-ASA is limited. Use of the drug should be limited to situations where a clear benefit is expected.
Periodic urinalysis to assess kidney function is recommended since prolonged therapy may damage the kidneys. Caution should be exercised when 5-ASA is first used in patients known to be allergic to sulfasalazine. These patients should be instructed to discontinue therapy at first sign of rash or fever.
Epigastric pain, also commonly associated with inflammatory bowel disease and prednisone or sulfasalazine therapy should be investigated in order to exclude pericarditis, pancreatitis or hepatitis either as adverse drug reactions to 5-ASA or secondary manifestations of inflammatory bowel disease.
Drug Interactions : No known drug interactions exist. The hypoglycemic effect of sulfonylureas may be enhanced. Interactions with coumarins, methotrexate, probenecid, sulfinpyrazone, spironolactone, furosemide and rifampin cannot be excluded. Potentiation of undesirable glucocorticoid effects on the stomach is possible.
Children: In children between the ages of 2 and 12, information on the safety and efficacy of 5-ASA is limited. Use of the drug should be limited to situations where a clear benefit is expected.
Side Effects / Adverse Effects
Adverse reactions linked to the sulfapyridine moiety of sulfasalazine are avoided with Salofalk. Hypersensitivity reactions have been reported in a sub-group of patients known to be allergic to sulfasalazine including rash, fever, and dizziness. The apparent frequency is estimated at 3to 4%, with reactions occurring at the onset of therapy and resolving promptly following discontinuance.
In rare cases, following 5-ASA administration, exacerbation of ulcerative colitis characterized by cramping, acute abdominal pain and diarrhea has been reported. Acute pancreatitis, hepatitis and pleural effusion have also been reported in association both with 5-ASA and SAS, as have rare instances of pericarditis. Both pancreatitis and pericarditis have also been reported as manifestations of inflammatory bowel disease. Finally, acute or chronic interstitial nephritis has been reported in association with orally-administered 5-ASA.
Other reported side effects include headache, flatulence, nausea, and alopecia, but do not appear to be common. During controlled clinical trials involving the administration of rectal 5-ASA or placebo, the following adverse reactions were reported in more than 0.1%
Adverse reactions linked to the sulfapyridine moiety of sulfasalazine are avoided with Salofalk. Hypersensitivity reactions have been reported in a sub-group of patients known to be allergic to sulfasalazine including rash, fever, and dizziness. The apparent frequency is estimated at 3to 4%, with reactions occurring at the onset of therapy and resolving promptly following discontinuance.
In rare cases, following 5-ASA administration, exacerbation of ulcerative colitis characterized by cramping, acute abdominal pain and diarrhea has been reported. Acute pancreatitis, hepatitis and pleural effusion have also been reported in association both with 5-ASA and SAS, as have rare instances of pericarditis. Both pancreatitis and pericarditis have also been reported as manifestations of inflammatory bowel disease. Finally, acute or chronic interstitial nephritis has been reported in association with orally-administered 5-ASA.
Other reported side effects include headache, flatulence, nausea, and alopecia, but do not appear to be common. During controlled clinical trials involving the administration of rectal 5-ASA or placebo, the following adverse reactions were reported in more than 0.1%
Overdose
Information not available
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Recommended Dosage
Rectal Suspension: Acute Episodes: Adults: The rectal suspension is self-administered on a daily basis during acute episodes of disease. Usually 1 unit-dose (4g/60g 5-ASA) is taken upon retiring and retained during the entire rest period. Best results are expected with prolonged retention.
The usual course of therapy is 1 unit of 4g/60g daily at bedtime. Response to treatment and adjustment in dosing frequency should be determined by periodic examinations including endoscopy and the assessment of symptomatology including rectal bleeding, stool frequency, and general well-being.
Daily dosing is continued until a significant response is achieved or the patient achieves remission.
Prevention of Relapse: Rectal suspension 2 g/60g is self-administered in the same manner on a daily basis. If alternatively the 4g/60g preparation is used, the dose can usually be reduced to alternate days or every third day, depending upon disease activity. Abrupt discontinuance of5-ASA is not recommended. Dose tapering is recommended and each patient should be titrated to meet individual needs. Maintenance therapy is recommended to assure continued remission. If symptoms, diarrhea and rectal bleeding recur, dosage should be increased to the previous effective level.
Suppositories: Two 250mg or one 500mg suppository are self-administered on a daily t.i.d. or b.i.d. basis. One 1000mg suppository is self-administered on a once daily basis. The usual adult dose is 1to 1.5g/day, and dosing is continued until a significant response is achieved or until the patient achieves remission. Dose tapering is recommended. Abrupt discontinuance is not recommended. Best results are expected with prolonged retention.
Tablets: In the acute ulcerative colitis inflammatory stage, and in the prevention of recurrence of Crohn's disease, 5-ASA enteric coated tablets must be taken reliably and consistently by the patient in order to ensure therapeutic success. Tablets should be swallowed whole before meals with plenty of fluid. For the treatment of acute ulcerative colitis, two 500mg tablets, 3or 4times/day (total adult dose: 3g/day to 4g/day). Abrupt discontinuance is not recommended. Prolonged treatment may be required.
For the prevention of recurrence of Crohn's disease in patients following bowel resection, the total adult dose is 3g/day in divided doses. Prolonged treatment is required.
Information for the Patient: See Blue Section--Information for the Patient “Salofalk”.
Rectal Suspension: Acute Episodes: Adults: The rectal suspension is self-administered on a daily basis during acute episodes of disease. Usually 1 unit-dose (4g/60g 5-ASA) is taken upon retiring and retained during the entire rest period. Best results are expected with prolonged retention.
The usual course of therapy is 1 unit of 4g/60g daily at bedtime. Response to treatment and adjustment in dosing frequency should be determined by periodic examinations including endoscopy and the assessment of symptomatology including rectal bleeding, stool frequency, and general well-being.
Daily dosing is continued until a significant response is achieved or the patient achieves remission.
Prevention of Relapse: Rectal suspension 2 g/60g is self-administered in the same manner on a daily basis. If alternatively the 4g/60g preparation is used, the dose can usually be reduced to alternate days or every third day, depending upon disease activity. Abrupt discontinuance of5-ASA is not recommended. Dose tapering is recommended and each patient should be titrated to meet individual needs. Maintenance therapy is recommended to assure continued remission. If symptoms, diarrhea and rectal bleeding recur, dosage should be increased to the previous effective level.
Suppositories: Two 250mg or one 500mg suppository are self-administered on a daily t.i.d. or b.i.d. basis. One 1000mg suppository is self-administered on a once daily basis. The usual adult dose is 1to 1.5g/day, and dosing is continued until a significant response is achieved or until the patient achieves remission. Dose tapering is recommended. Abrupt discontinuance is not recommended. Best results are expected with prolonged retention.
Tablets: In the acute ulcerative colitis inflammatory stage, and in the prevention of recurrence of Crohn's disease, 5-ASA enteric coated tablets must be taken reliably and consistently by the patient in order to ensure therapeutic success. Tablets should be swallowed whole before meals with plenty of fluid. For the treatment of acute ulcerative colitis, two 500mg tablets, 3or 4times/day (total adult dose: 3g/day to 4g/day). Abrupt discontinuance is not recommended. Prolonged treatment may be required.
For the prevention of recurrence of Crohn's disease in patients following bowel resection, the total adult dose is 3g/day in divided doses. Prolonged treatment is required.
Information for the Patient: See Blue Section--Information for the Patient “Salofalk”.
Supplied / Packaging
Rectal Suspension: 2g/60g: Each unit of use rectal retention enema contains: 5-ASA 2g/60g (58.25mL). Also contains sodium benzoate and potassium metabisulfite. Boxes of7. Store in a cool place, below 25°C.
4g/60g: Each unit of use rectal retention enema contains: 5-ASA 4g/60g. Store in a cool place, below 25°C.
Suppositories: 250mg: Each suppository contains: 5-ASA 250mg. Strips of 5 suppositories, boxes of 30. Store in a cool place, preferably between 20 and 25°C.
500mg: Each suppository contains: 5-ASA 500mg. Strips of 5suppositories, boxes of 30. Store in a cool place, preferably between 20 and 25°C.
1000mg: Each suppository contains: 5-ASA 1000mg. Strips of 5 suppositories, boxes of 30. Store in a cool place, preferably between 20 and 25°C.
Tablets: Each ochre, oblong, enteric-coated tablet contains: 5-ASA 500mg. Bottles of 150 and 500. Store at controlled room temperature (15to30°C).
Rectal Suspension: 2g/60g: Each unit of use rectal retention enema contains: 5-ASA 2g/60g (58.25mL). Also contains sodium benzoate and potassium metabisulfite. Boxes of7. Store in a cool place, below 25°C.
4g/60g: Each unit of use rectal retention enema contains: 5-ASA 4g/60g. Store in a cool place, below 25°C.
Suppositories: 250mg: Each suppository contains: 5-ASA 250mg. Strips of 5 suppositories, boxes of 30. Store in a cool place, preferably between 20 and 25°C.
500mg: Each suppository contains: 5-ASA 500mg. Strips of 5suppositories, boxes of 30. Store in a cool place, preferably between 20 and 25°C.
1000mg: Each suppository contains: 5-ASA 1000mg. Strips of 5 suppositories, boxes of 30. Store in a cool place, preferably between 20 and 25°C.
Tablets: Each ochre, oblong, enteric-coated tablet contains: 5-ASA 500mg. Bottles of 150 and 500. Store at controlled room temperature (15to30°C).
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Brand Name
Salofalk
Salofalk
Generic Name
5-Aminosalicylic Acid
5-Aminosalicylic Acid
General Indications
Lower Gastrointestinal Anti-inflammatory
Lower Gastrointestinal Anti-inflammatory
