ChemicalBook--->CAS DataBase List--->89-57-6


89-57-6 Structure

89-57-6 Structure

5-Aminosalicylic acid


IFLAB-BB F1918-0003
5-Aminosalicyclic acid

[Molecular Formula]

[MDL Number]

[Molecular Weight]

[MOL File]

Chemical PropertiesBack Directory

Off-White Crystals
[Melting point ]

275-280 °C (dec.) (lit.)
[Boiling point ]

276.03°C (rough estimate)
[density ]

1.3585 (rough estimate)
[vapor pressure ]

0Pa at 25℃
[refractive index ]

1.5500 (estimate)
[Fp ]

[storage temp. ]

[solubility ]

Soluble in dimethyl sulfoxide.
[form ]


2.74, 5.84(at 25℃)
[color ]

off-white to gray

4.0-4.1 (0.8g/l, H2O, 20℃)
[PH Range]

Non-B uorescence (3.1) to light green B uorescence (4.4)

Stable. Incompatible with acids, acid anhydrides, acid chlorides, chloroformates, strong oxidizing agents.
[Water Solubility ]

<0.1 g/100 mL at 21 ºC
[Decomposition ]

279-281 ºC

The active metabolite of Sulfasalazine. Anti-inflammatory (gastrointestinal)
[Detection Methods]

[Merck ]

[BRN ]

[Major Application]

Detergent, hair dyes, prevention of colorectal cancer, treating inflammatory bowel disease, autoimmune disorders, gastrointestinal inflammation, chemokine-mediated diseases, mucosal tissue disorder, sleep disorders, rectoanal tenesmus, ulcerative colitis

[CAS DataBase Reference]

89-57-6(CAS DataBase Reference)
[NIST Chemistry Reference]

[Storage Precautions]

Air sensitive;Store under nitrogen;Light sensitive
[EPA Substance Registry System]

89-57-6(EPA Substance)
Safety DataBack Directory
[Hazard Codes ]

[Risk Statements ]

R36/37/38:Irritating to eyes, respiratory system and skin .
[Safety Statements ]

S26:In case of contact with eyes, rinse immediately with plenty of water and seek medical advice .
S36:Wear suitable protective clothing .
S24/25:Avoid contact with skin and eyes .
[WGK Germany ]


[F ]

[Autoignition Temperature]

280 °C
[Hazard Note ]


[HazardClass ]

[HS Code ]

[Hazardous Substances Data]

89-57-6(Hazardous Substances Data)

LD50 orally in Rabbit: 2800 mg/kg LD50 dermal Rat > 5000 mg/kg
Raw materials And Preparation ProductsBack Directory
[Raw materials]

Sodium carbonate-->ZINC-->Water-->Sodium dithionite-->Methanesulfonyl chloride-->Salicylic acid-->Tyramine-->5-Nitrosalicylic acid-->Hydrogen-->Hydrazine hydrate-->Aluminium-nickel
[Preparation Products]

Benzoic acid, 2-[[1-amino-7-[[4-[[6-amino-5-[(3-carboxy-4-hydroxyphenyl)azo]-1-hydroxy-3-sulfo-2-naphthalenyl]azo]-2-methoxyphenyl]azo]-8-hydroxy-3,6-disulfo-2-naphthalenyl]azo]-5-[[6-amino-5-[(3-carboxy-4-hydroxyphenyl)azo]-1-hydroxy-3-sul-->Sulfasalazine-->METHYL 5-AMINOSALICYLATE-->BOC-3-AMINOBENZOIC ACID-->OLSALAZINE-->Benzoic acid, 2-[[1-amino-7-[[4-[[6-amino-5-[(3-carboxy-4-hydroxyphenyl)azo]-1-hydroxy-3-sulfo-2-naphthalenyl]azo]-2-methoxyphenyl]azo]-8-hydroxy-3,6-disulfo-2-naphthalenyl]azo]-5-[[6-amino-5-[(3-carboxy-4-hydroxyphenyl)azo]-1-hydroxy-3-sul-->tetrasodium 2-[[2-amino-6-[[4-[[4-[(3-carboxylato-4-hydroxyphenyl)azo]-7-sulphonato-1-naphthyl]azo]-2,5-dimethoxyphenyl]azo]-5-hydroxy-7-sulphonato-1-naphthyl]azo]-5-nitrobenzoate
Hazard InformationBack Directory
[General Description]

Odorless white to pinkish crystals or purplish-tan powder. Aqueous solutions acidic (pH approximately 4.1 at 0.8 mg/L water) .
[Reactivity Profile]

5-AMINOSALICYLIC ACID(89-57-6) is incompatible with acids, acid chlorides, acid anhydrides, chloroformates and strong oxidizers.
[Air & Water Reactions]

Sensitive to moisture. Water insoluble.
[Fire Hazard]

Flash point data for this chemical are not available; however, 5-AMINOSALICYLIC ACID is probably combustible.

Fisalamine is an intestinal metabolite of sulfasalazine useful in the treatment of ulcerative colitis and to a lesser degree in the management of Crohn’s disease. Administered as a suppository, it appears to lack the hypersensitivity-type side effects of sulfasalazine.
[Chemical Properties]

Off-White Crystals

Radcliffe Infirmary (United Kingdom)

anesthetic (local)

For the treatment of active ulcerative proctitis.

In manufacture of light-sensitive paper, azo and sulfur dyes.

peroxidase substrate

The active metabolite of Sulfasalazine (S699084). Anti-inflammatory (gastrointestinal).

ChEBI: A monohydroxybenzoic acid that is salicylic acid which is substituted by an amino group at the 5-position.
[Manufacturing Process]

Procedure A: To 5-nitrosalicylic acid potassium salt (55 g, 246 mmol) dissolved in water (200 mL) was added potassium hydroxide pellets to reach pH 11.5. To this solution 2 g of Raney nickel were added. The mixture was heated-up to reflux and hydrazine hydrate (40 mL, 80% in water, 64 mmol) was added dropwise during 3-4 hrs. The reflux was maintened until HPLC showed the disappearance of the starting material and the complete reduction of 5-nitrosalicylic acid (3-4 hrs). The hot mixture was filtered under nitrogen and the solution was collected. The solution was cooled to 40°C and the pH was adjusted to 2.3 by addition of 35% HCl aqueous solution. The precipitation of 5-aminosalicylic acid occurred. The solution was cooled at 0°C, and after standing at this temperature for 2 hr, the precipitate was filtered, washed with water, and dried at 60-70°C. 5-Aminosalicylic acid was obtained in 89% yield.
Procedure B: To 5-nitrosalicylic acid potassium salt (55 g, 246 mmol) dissolved in water (200 mL) was added potassium hydroxide pellets to reach pH 11.5. The solution was charged in a stainless steel autoclave and 2 g of Raney nickel are added. Hydrogen was introduced into the autoclave reaching a pressure of 8 atm. The mixture was heated-up to 100°C. The temperature was maintained until HPLC-test 5-aminosalicylic acid showed the disappearance of the starting material and the complete reduction of 5- aminosalicylic acid (6-8 hrs). Hydrogen was purged and replaced by nitrogen. The hot mixture was filtered under nitrogen, the filtrate was cooled to 40°C, and the pH was adjusted to 2.3 by addition of 35% HCl aqueous solution. The precipitation of the 5-aminosalicylic acid occurred. The solution was cooled at 0°C, and after standing at this temperature for 2 hr, the precipitate was filtered, washed with ion depleted water, and dried at 60-70°C.
[Brand name]

[Therapeutic Function]

[Flammability and Explosibility]

[Biochem/physiol Actions]

5-Aminosalicylic acid (5-ASA) is a first-line medicine, used to treat inflammatory bowel diseases like ulcerative colitis (UC). It has a high-efficiency rate in maintenance and induction of remission. 5-ASA is an active component of sulfasalazine and also consists of the carbohydrate polymer, inulin. It might exhibit anti-oxidant activity to lessen tissue injury. 5-ASA is vital for the prevention of T cell activation and proliferation. It negatively regulates cyclooxygenase and lipoxygenase pathways and lowers the formation of prostaglandins and leukotrienes. 5-ASA stimulates the membranous expression of E-cadherin and boosts intercellular adhesion.
[Clinical Use]

Induction and maintenance of remission in ulcerative colitis
[Safety Profile]

Poison by intraperitoneal route.Moderately toxic by ingestion. Human systemic effects byingestion: hypermotility, diarrhea, dermatitis, increasedbody temperature. When heated to decomposition it emitstoxic fumes of NOx.
[Drug interactions]

Potentially hazardous interactions with other drugs
None known

The absorbed part of mesalazine is almost completely acetylated in the gut wall and in the liver to acetyl-5- aminosalicylic acid. The acetylated metabolite is excreted mainly in urine by tubular secretion, with traces of the parent compound.
[Purification Methods]

It crystallises as needles from H2O containing a little NaHSO3 to avoid aerial oxidation to the quinone-imine. The Me ester gives needles from *C6H6, m 96o, and the hydrazide has m 180-182o (from H2O). [Fallab et al. Helv Chim Acta 34 26 1951, Shavel J Amer Pharm Assoc 42 402 1953, Beilstein 14 IV 2058.]
Material Safety Data Sheet(MSDS)Back Directory
[msds information]

Questions And AnswerBack Directory

Mesalazine is an anti-inflammatory agent, structurally related to the salicylates, which is active in inflammatory bowel disease. It is considered to be the active moiety of sulphasalazine. A study of the therapeutic properties of sulfasalazine and its constituents[mesalazine (5-amino salicylic acid, 5-ASA) and sulfapyridine] indicated that mesalazine is the therapeutically active component, while sulfapyridine acts as an inert carrier molecule to facilitate delivery to the colon.[2] This discovery, coupled with the implication of sulfapyridine in most of the adverse events associated with sulfasalazine treatment,[3] led to the development of Mesalazine as a pure therapeutic entity.
Mesalazine (fig. 1) is believed to exert its effects via topical actions in the gut lumen. However, orally administered unconjugated mesalazine is extensively absorbed from the proximal small bowel,[4] and alternative oral dosage formulations have been
developed to facilitate the delivery of mesalazine to more distal sites of inflammation. These include microgranules of mesalazine coated with a semipermeable ethylcellulose membrane (Pentasa®), mesalazine encased within a pH-dependent acrylic resin (pH-dependent delayed-release preparations: Salofalk®, Claversal®, Mesasal®, Asacol®), or conjugation of mesalazine via an azo bond to an inert carrier (balsalazide) or to another mesalazine molecule (olsalazine). In each case the properties of the delivery system dictate the site of mesalazine release.

Figure 1 the chemical structure of Mesalazine

It is used for the treatment of active ulcerative proctitis.
[Mode of action]

The pathogenesis of IBD and hence the mechanism by which mesalazine exerts its therapeutic effects in this disease remain elusive. However, lipid mediators[leukotrienes (LT), prostaglandins (PG), platelet-activating factor (PAF)], cytokines[including interleukins (IL), interferon-(IFN)γ and tumour necrosis factor-(TNF)α] and reactive oxygen species have been implicated in the nonspecific inflammation and tissue damage characteristic of IBD.[5-7] The modulation of these molecules by mesalazine may underlie the therapeutic effects of the drug.[8-11]
Numerous in vitro studies have investigated the effects of mesalazine on inflammatory processes in colonic epithelial cell lines or biopsy specimens from patients with active ulcerative colitis or with normal colons. Mesalazine also appears to reduce in vitro levels of LTC4, 5-hydroxyeicosatetraenoic acid (HETE), 11-, 12-, 15-HETE, PGD2 and platelet-activating factor. In addition to inhibiting interferon (IFN)-γ binding, mesalazine reduced IFNγ-induced cell permeability and expression of the HLA-DR product of the major histocompatibility complex in colonic epithelial cell lines. Recent evidence suggests that mesalazine reverses the antiproliferative effects of tumour necrosis factor-(TNF)α and inhibits TNFα signalling events in intestinal cells. Mesalazine may also reduce interleukin (IL)-1/1β and IL-2 production.
A variety of data from experimental work, animal studies and preliminary clinical trials strongly suggest that mesalazine may have antineoplastic and potentially prophylactic (chemo-preventive) properties, which are comparable with those found with aspirin and other NSAIDs. Mesalazine shares similar molecular targets, interfering with inflammation, proliferation and ⁄ or apoptosis, as aspirin and other NSAIDs. This can be explained by the close molecular similarity of mesalazine and aspirin, in which the former differs only in structure by the presence of an amino group at position 5 of the benzene ring. Recent experimental and preliminary clinical work has demonstrated that mesalazine may have in vitro and in vivo inhibitory properties comparable to other NSAIDs.[12-14] Reversible inhibition of COX-1 and COX-2, NF-kB activation, MAP kinases and Bcl-2 by mesalazine, was found in experiments using different cell systems including lymphocytes, polymorphonuclear leucocytes (PMNLs) and cultures from normal and neoplastic cell lines of animal and human origin.[15] In contrast to aspirin, which was shown to inhibit COX irreversibly, mesalazine (and other NSAIDs) inhibit COX and other steps (e.g. Bcl-2) reversibly. The molecular details for the majority of these reactions are only partly known, but recent work has shed light on some of these. Thus, inhibition of NF-kB activation is most likely to be mediated by inhibition of IkB degradation, the inhibitory unit of the NF-kB complex. It is worth noting that mesalazine has rather unspecific COX inhibitory properties with no preference for COX-2.

After a single oral dose of prolonged-release mesalazine 250mg to volunteers, the median lag time (tlag) to the first detectable plasma concentration of mesalazine was 45 minutes (range 15 to 150). A maximum plasma concentration (Cmax) of 0.6 μmol/L (range 0.4 to 1.4) was recorded 240 minutes (tmax; 90 to 300) after dose administration. Corresponding values for acetyl mesalazine were: tlag 22 minutes (15 to 45), Cmax 2.9 μmol/L (1.6 to 3.4) and tmax 105 minutes (60 to 300).[16] The plasma concentration-time profile following a single oral dose of prolonged-release mesalazine 1g to healthy volunteers was consistent with a continuous release of drug throughout the gastrointestinal tract. Plasma concentrations peaked at 0.53 mg/L 4 hours after administration, declined rapidly to 0.03 mg/L at 12 hours, then remained fairly constant over the next 24 hours before resuming the final decline, becoming undetectable 60 hours after administration. The area under the plasma concentrationtime curve (AUC) for mesalazine was 4.37-mg/L • h.
Little is known about the distribution of prolonged-release mesalazine. In 9 pregnant women with IBD who were receiving prolonged-release mesalazine 0.5 to 3 g/day, low concentrations (approximate values from graph) of mesalazine and acetylmesalazine were measured in maternal (≤0.5 and ≤7.5 μmol/L) and fetal plasma (≤0.25 and ≤18 μmol/L). In 2 patients, low concentrations of mesalazine were detected in breast milk. Mean acetyl mesalazine concentrations in breast milk were 4.4 to 47.5 μmol/L.[18, 19]
Mesalazine is primarily metabolized by acetylation in the gut wall and the liver, forming the therapeutically inert metabolite acetyl mesalazine. Both the parent compound and the metabolite are excreted in the urine.[20] After a single oral administration of prolonged-release mesalazine 0.25g in 6 volunteers, the apparent mean elimination half-life of acetyl mesalazine was 802 minutes (range 608 to 993). Determination of the terminal half-life of mesalazine was not possible because of low plasma concentrations.[16] After oral administration of prolonged-release mesalazine 1.5 to 4 g/day to volunteers, excretion of unchanged mesalazine accounted for 8 to 12% of the daily dose. Total urinary excretion of mesalazine plus acetyl mesalazine was 29 to 53%.[21,22,23] In volunteers, renal clearance of acetyl mesalazine was 12 L/h (201 ml/min) at steady state.[21] In a 7-day study of 15 patients with ulcerative colitis, daily urinary excretion of mesalazine and acetyl mesalazine was higher with prolonged-release mesalazine (1.5 g/day) and pH-dependent delayed-release mesalazine (Asacol ®, 1.2 g/day) than with olsalazine (1 g/day).[17]
[Adverse reactions and toxicity]

In an 8-week randomized trial of prolonged release mesalazine 1, 2 and 4 g/day or placebo in patients (n = 314) with ulcerative colitis, 16% of patients receiving active drug experienced treatment-related adverse events, compared with 22% of patients in the placebo group. No dose-response relationship was observed. In total, 5%, 9% and 7% of patients in the 1, 2 and 4 g/day dosage groups discontinued therapy because of treatment-related or unrelated events, compared with 12% of placebo treated patients. The most common treatment limiting adverse events were diarrhoea, abdominal pain, fever and melaena.[24] In another 16-week study, the most common adverse events considered to be related to prolonged-release mesalazine treatment were nausea and/or vomiting (7.4 vs 3.7% in the placebo group), headache (5.2 vs 3.7%) and abdominal pain (4.3 vs 5.0%).[26]
In a 12-month study involving 205 patients with ulcerative colitis, adverse events necessitating withdrawal occurred in 14% and 33% (2% and 6% considered to be treatment-related) of patients receiving prolonged-release mesalazine 4 g/day and placebo, respectively. Treatment-related adverse events (most commonly nausea 2.9%, abdominal pain 1.9% and dyspepsia 1.9%) were experienced in 6.8% of patients receiving prolonged-release mesalazine. In contrast, 11.8% of patients in the placebo group experienced adverse events related to therapy.[25] In a non-comparative study in 467 patients with Crohn’s disease who received prolongedrelease mesalazine at dosages up to 4 g/day for a median of 14 months, 12%of patients discontinued because of treatment-related adverse events, of which the most commonly reported were diarrhoea (4.3%), abdominal pain (3.6%) and dyspepsia (3.1%).[27]

  1. Martin F. Oral 5-aminosalicylic acid preparations in treatment of inflammatory bowel disease: an update. Dig Dis Sci 1987; 32 (12 Suppl.): 57S-63S
  2. Azad Khan AK, Piris J, Truelove SC. An experiment ot determine the active therapeutic moiety of sulphasalazine. Lancet 1979; II (8044): 892-5
  3. Schröder H, Price E, Evans DA. Acetylator phenotype and adverse events of sulphasalazine in healthy subjects. Gut 1972; 13 (4): 278-84
  4. Haagen Nielsen O, Bondesen S. Kinetics of 5-aminosalicylic acid after jejunal instillation in man. Br J Clin Pharmacol 1983; 16 (6): 738-40
  5. Ireland A, Jewell DP. Mechanism of action of 5-aminosalicylic acid and its derivatives. Clin Sci 1990; 78: 119-25
  6. Greenfield SM, Punchard NA, Teare JP, et al. Review article: the mode of action of the aminosalicylates in inflammatory bowel disease. Aliment Pharmacol Ther 1993; 7: 369-83
  7. Travis SPL, Jewell DP. Salicylates for ulcerative colitis – their mode of action. Pharmacol Ther 1994; 63: 135-61
  8. Schmidt C, Fels T, Baumeister B, et al. The effect of 5aminosalicylate and para-aminosalicylate on the synthesis of prostaglandin E2 and leukotriene B4 in isolated colonic mucosal cells. Curr Med Res Opin 1996; 13 (7): 417-25
  9. Capasso F, Tavares IA, BennettA. Release of platelet-activating factor (PAF) from human colon mucosa and its inhibition by 5-aminosalicylic acid. Drugs Exp Clin Res 1991; 17: 351-3
  10. Rachmilewitz D, Karmeli F, Schwartz LW, et al. Effect of aminophenols (5-ASA and 4-ASA) on colonic interleukin-1 generation. Gut 1992; 33: 929-32
  11. Di Paolo MC, Merrett MN, Crotty B, et al. 5-Aminosalicylic acid inhibits the impaired epithelial barrier function induced by gamma interferon. Gut 1996; 38: 115-9
  12. Vainio H, Morgan G. Non-steroidal anti-inflammatory drugs and the chemoprevention of gastrointestinal cancers. Scand J Gastroenterol 1998; 33: 785–9.
  13. Bus PJ, Nagtegaal ID, Verspaget HW, et al. Mesalazine-induced apoptosis of colorectal cancer: on the verge of a new chemopreventive era? Aliment Pharmacol Ther 1999; 13: 1397–402.
  14. Reinacher-Schick A, Seidensticker F, Petrasch S, et al. Mesalazine changes apoptosis and proliferation in normal mucosa of patients with sporadic polyps of the large bowel. Endoscopy 2000; 32: 245–54.
  15. Egan LJ, Mays DC, Huntoon MP, et al. Inhibition of interleukin-1-stimulated NF-jB RelA ⁄ p65 phosphorylation by mesalazine is accompanied by decreased transcriptional activity. J Biol Chem 1999; 274: 26448–53.
  16. Bondesen S, Hegnhoj J, Larsen F, et al. Pharmacokinetics of 5-aminosalicylic acid in man following administration of intravenous bolus and Per Os slow-release formulation. Dig Dis Sci 1991; 36: 1735-40
  17. Daneshmend TK, Hendrickse M, Salzmann M, et al. Does systemic absorption of 5-aminosalicylic acid from olsalazine (Dipentum®) and mesalazine (Asacol® and Pentasa®) differ significantly in ulcerative colitis?[abstract]. Gut 1994; 35 Suppl. 4: 233
  18. Staerk-Laursen L, Stokholm M, Bukhave K, et al. Disposition of 5-aminosalicylic acid by olsalazine and three mesalazine preparations in patients with ulcerative colitis: comparison of intraluminal colonic concentrations, serum values, and urinary excretion. Gut 1990; 31: 1271-6
  19. Christensen LA, Rasmussen SN, Hansen SH. Disposition of 5-aminosalicylic acid and N-acetyl-5-aminosalicylic acid in fetal and maternal body fluids during treatment with different 5-aminosalicylic acid preparations. Acta Obstet Gynecol Scand 1994; 74: 399-402
  20. Lauritsen K, Laursen LS, Rask-Madsen J. Clinical pharmacokinetics of drugs used in the treatment of gastrointestinal diseases (Part II). Clin Pharmacokinet 1990; 19: 94-125
  21. Rasmussen SN, Bondesen S, Hvidberg EF, et al. 5-Aminosalicylic acid in a slow-release prepararation: bioavailability, plasma level, and excretion in humans. Gastroenterolo 1982; 83: 1062-70
  22. Christensen LA, Fallingborg J, Abildgaard K, et al. Topical and systemic availability of 5-amino-salicylate: comparisons of three controlled release preparations in man. Aliment Pharmacol Ther 1990; 4: 523-33
  23. Christensen LA, Fallingborg J, Jacobsen BA, et al. Comparative bioavailability of 5-aminosalicylic acid from a controlled release preparation and an azo-bond preparation. Aliment Pharmacol Ther 1994; 8: 289-94
  24. Hanauer S, Schwartz J, RobinsonM, et al.Mesalamine capsules for the treatment of active ulcerative colitis: results of a controlled trial. Am J Gastroenterol 1993; 88: 1188-97
  25. Miner P, Hanauer S, Robinson M, et al. Safety and efficacy of controlled-release mesalamine for maintenance of remission in ulcerative colitis. Dig Dis Sci 1995; 40: 296-304
  26. Singleton JW, Hanauer SB, Gitnick GL, et al. Mesalamine capsules for the treatment of active Crohn’s disease: results of a 16-week trial. Pentasa Crohn’s Disease Study Group[see comments]. Gastroenterology 1993; 104: 1293-301
  27. Hanauer SB, Krawitt EL, Robinson M, et al. Long-term management of Crohn’s disease with mesalamine capsules (Pentasa ®). Am J Gastroenterol 1993; 88: 1343-51
Spectrum DetailBack Directory
[Spectrum Detail]

5-Aminosalicylic acid(89-57-6)MS
5-Aminosalicylic acid(89-57-6)1HNMR
5-Aminosalicylic acid(89-57-6)IR1
5-Aminosalicylic acid(89-57-6)IR2
Well-known Reagent Company Product InformationBack Directory
[Acros Organics]

5-Aminosalicylic acid, purified, 99%(89-57-6)
[Alfa Aesar]

5-Aminosalicylic acid, 95%(89-57-6)
[Sigma Aldrich]


5-Aminosalicylic Acid,>98.0%(T)(89-57-6)
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