Mesalazine 1.5g gastro-resistant modified-release granules sachets sugar free
Prescription only
Requires a prescription from a doctor or prescriber
An anti-inflammatory agent, structurally related to the salicylates and non-steroidal anti-inflammatory drugs like acetylsalicylic acid, which is active in inflammatory bowel disease [A174022].
Active ingredients:
Mesalazine
Formulation:Does not contain sugar — suitable for diabetic patients
Sugar-free
No active safety alerts
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Mesalazine
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
EMA
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Suspected adverse reactions reported for Mesalazine
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
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Part of the Octasa brand family (generic: Mesalazine)
1 products
MHRA licensed products
View all licensed products for Mesalazine on the MHRA register
Salofalk 1.5g gastro-resistant modified-release granules sachets
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£48.85indicative price
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
1.5 gram
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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Mesalazine 300mg/5ml oral suspension
Oral suspension
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Same therapeutic group
Mesalazine 4g modified-release granules sachets sugar free
Granules
4g
Same therapeutic group
Mesalazine 3g gastro-resistant modified-release granules sachets sugar free
Granules
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Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Mesalazine
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Crohn's disease: management (NG129)
NG129
NICE guideline
Updated May 2019Ulcerative colitis: management (NG130)
NG130
NICE guideline
Updated May 2019Ozanimod for treating moderately to severely active ulcerative colitis (TA828)
TA828
Technology appraisal
Updated Oct 2022Infliximab, adalimumab and golimumab for treating moderately to severely active ulcerative colitis after the failure of conventional therapy (TA329)
TA329
Technology appraisal
Updated Feb 2015Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
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These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
243 found
Half-life
40 minutes
Mechanism
Although the mechanism of action of mesalazine is not fully understood, it is be…
Food interactions
1 warning
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
14 days
Depending on the formulation administered, prescribing information for orally administered delayed-released tablets of 2.4g…
Half-life
40 minutes
For the delayed-release formulation, after intravenous administration, the elimination half-life of mesalamine is reported to be approximately 40 minutes.…
Protein binding
6%
In an in vitro study, at 2.5 mcg/mL, mesalamine and N-Ac-5-ASA are 43±6% and 78±1% bound, respectively, to plasma
proteins.…
proteins.…
Volume of distribution
18 L
For the extended-release formulation, mesalazine has a Vd of 18 L, confirming minimal extravascular penetration of systemically available drug.
[L44201]…
[L44201]…
Metabolism
Mesalazine is metabolized both pre-systemically by the intestinal mucosa and systemically in the liver to N-acetyl-5-aminosalicylic acid (N-Ac-5-ASA) principally by NAT-1.…
Elimination
21%
Elimination of mesalazine is mainly via the renal route following metabolism to N-acetyl-5-aminosalicylic acid (acetylation) .
[L40848]…
[L40848]…
Clearance
18 to 35 years
The mean (SD) renal clearance in L/h for mesalazine following the single dose administration of mesalazine delayed-release tablets 4.8g…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
An anti-inflammatory agent, structurally related to the salicylates and non-steroidal anti-inflammatory drugs like acetylsalicylic acid, which is active in inflammatory bowel disease [A174022]. Although demonstrably effective in treating and maintaining remission for ulcerative colitis, mesalazine has historically faced a number of issues regarding its lack of stability as a pharmaceutical agent [A174019]. Throughout the late seventies and the eighties, important research initiatives developed stable mesalazine formulations like the eudragit-S coating of Asacol brand mesalazine and the Pentasa brand's encapsulation of mesalazine within microgranules [A174019]. In the present day, contemporary research regarding novel methods to stabilize mesalazine continues and interest in the agent's capacity to decrease inflammatory activity and subsequently potentially reduce the risk of colorectal cancer in conditions like ulcerative colitis is maintained.[A174019][A174022]
Properties:
View FDA drug labelsolid
Avg. mass: 153.14 Da
DrugBank indication
Mesalazine is indicated for the treatment of mildly to moderately active ulcerative colitis in adults and patients 5 years or older..
[L36280][L36275]
Mesalazine is also indicated for the maintenance of remission of ulcerative colitis in adults and maintenance of remission of Crohn's ileocolitis.
[L44196][L5101]
[L36280][L36275]
Mesalazine is also indicated for the maintenance of remission of ulcerative colitis in adults and maintenance of remission of Crohn's ileocolitis.
[L44196][L5101]
Also known as(114)
3-carboxy-4-hydroxyaniline
5-aminosalicylic acid
5-ASA
m-Aminosalicylic acid
Mesalamine
Mesalazina
Mésalazine
Mesalazine
Dosage forms(149)
Capsule, extended release (Oral) — 375 mg/1
Capsule, delayed release (Oral) — 400 MG
Granule, for suspension (Rectal) — 2 G
Suppository (Rectal) — 500.000 mg
Suspension (Rectal) — 2 G/50ML
Suspension (Rectal) — 4 G/50ML
Suspension (Rectal) — 4 G/100ML
Tablet (Oral) — 400 mg/1
Molecular properties(19)
Drug interactions(1522)
Known interactions with other medications. Always consult a healthcare professional.
Amlodipine
Moderate
Mesalazine may decrease the antihypertensive activities of Amlodipine.
Phentermine
Unknown severity
The risk or severity of hypertension can be increased when Phentermine is combined with Mesalazine.
The risk or severity of hypertension can be increased when Midodrine is combined with Mesalazine.
Eletriptan
Unknown severity
The risk or severity of hypertension can be increased when Eletriptan is combined with Mesalazine.
Isoetharine
Unknown severity
The risk or severity of hypertension can be increased when Isoetharine is combined with Mesalazine.
Ziprasidone
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Ziprasidone.
Methysergide
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Methysergide.
Cabergoline
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Cabergoline.
Zolmitriptan
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Zolmitriptan.
Dihydroergotamine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Dihydroergotamine.
Methylergometrine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Methylergometrine.
Norepinephrine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Norepinephrine.
Mirtazapine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Mirtazapine.
Phenylephrine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Phenylephrine.
Phenylpropanolamine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Phenylpropanolamine.
The risk or severity of hypertension can be increased when Mesalazine is combined with Promazine.
Droperidol
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Droperidol.
The risk or severity of hypertension can be increased when Mesalazine is combined with Doxapram.
The risk or severity of hypertension can be increased when Mesalazine is combined with Atropine.
The risk or severity of hypertension can be increased when Mesalazine is combined with Lisuride.
The risk or severity of hypertension can be increased when Mesalazine is combined with Linezolid.
Metaraminol
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Metaraminol.
Furazolidone
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Furazolidone.
Epinephrine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Epinephrine.
Thioridazine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Thioridazine.
Ergotamine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Ergotamine.
Nicergoline
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Nicergoline.
Sufentanil
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Sufentanil.
Methoxamine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Methoxamine.
Risperidone
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Risperidone.
Tranylcypromine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Tranylcypromine.
Isoflurane
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Isoflurane.
Propiomazine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Propiomazine.
Alfentanil
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Alfentanil.
The risk or severity of hypertension can be increased when Mesalazine is combined with Minaprine.
Orciprenaline
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Orciprenaline.
The risk or severity of hypertension can be increased when Mesalazine is combined with Propofol.
Phenmetrazine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Phenmetrazine.
Trifluoperazine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Trifluoperazine.
Pseudoephedrine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Pseudoephedrine.
Benzphetamine
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Benzphetamine.
The risk or severity of hypertension can be increased when Mesalazine is combined with Ritodrine.
Flupentixol
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Flupentixol.
Remifentanil
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Remifentanil.
Bitolterol
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Bitolterol.
Oxymetazoline
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Oxymetazoline.
Diethylpropion
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Diethylpropion.
Salmeterol
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Salmeterol.
Naratriptan
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Naratriptan.
Formoterol
Unknown severity
The risk or severity of hypertension can be increased when Mesalazine is combined with Formoterol.
Showing 50 of 1522 interactions
Food & lifestyle interactions
Advice
Take with or without food. The absorption is unaffected by food.
Toxicity & overdose
Mesalazine caused no increase in the incidence of neoplastic lesions over controls in a two-year study of Wistar rats fed up to 320 mg/kg/day of mesalazine admixed with diet (about 1.7 times the recommended human intra-rectal dose of CANASA, based on body
surface area). Mesalazine was not mutagenic in the Ames test, the mouse lymphoma cell (TK+/-) forward mutation test, or the mouse micronucleus test. No effects on fertility or reproductive performance of the male and female rats were observed at oral mesalamine doses up to 320 mg/kg/day (about 1.7 times the recommended human intra-rectal dose of mesalazine, based on body surface area).
[L36280]
Mesalazine is an aminosalicylate, and symptoms of salicylate toxicity include nausea, vomiting and abdominal pain, tachypnea, hyperpnea, tinnitus, and neurologic symptoms (headache, dizziness, confusion, seizures). Severe salicylate intoxication may lead to electrolyte and blood pH imbalance and potentially to other organ involvement (e.g., renal and liver).
There is no specific antidote for mesalamine overdose; however, conventional therapy for salicylate toxicity may be beneficial in the event of acute
overdosage and may include gastrointestinal tract decontamination to prevent further absorption. Correct fluid and electrolyte imbalance by the administration of appropriate intravenous therapy and maintain adequate renal function.
[L36230]
Mesalazine is known to be substantially excreted by the kidney, and the risk of adverse reactions may be greater in patients with impaired renal function. Evaluate renal function in all patients prior to initiation and periodically while on Asacol HD therapy.
Monitor patients with known renal impairment or a history of renal disease or taking nephrotoxic drugs for decreased renal function and mesalamine-related adverse reactions.
[L36230]
surface area). Mesalazine was not mutagenic in the Ames test, the mouse lymphoma cell (TK+/-) forward mutation test, or the mouse micronucleus test. No effects on fertility or reproductive performance of the male and female rats were observed at oral mesalamine doses up to 320 mg/kg/day (about 1.7 times the recommended human intra-rectal dose of mesalazine, based on body surface area).
[L36280]
Mesalazine is an aminosalicylate, and symptoms of salicylate toxicity include nausea, vomiting and abdominal pain, tachypnea, hyperpnea, tinnitus, and neurologic symptoms (headache, dizziness, confusion, seizures). Severe salicylate intoxication may lead to electrolyte and blood pH imbalance and potentially to other organ involvement (e.g., renal and liver).
There is no specific antidote for mesalamine overdose; however, conventional therapy for salicylate toxicity may be beneficial in the event of acute
overdosage and may include gastrointestinal tract decontamination to prevent further absorption. Correct fluid and electrolyte imbalance by the administration of appropriate intravenous therapy and maintain adequate renal function.
[L36230]
Mesalazine is known to be substantially excreted by the kidney, and the risk of adverse reactions may be greater in patients with impaired renal function. Evaluate renal function in all patients prior to initiation and periodically while on Asacol HD therapy.
Monitor patients with known renal impairment or a history of renal disease or taking nephrotoxic drugs for decreased renal function and mesalamine-related adverse reactions.
[L36230]
How it works
Mechanism of action
Although the mechanism of action of mesalazine is not fully understood, it is believed to possess a topical anti-inflammatory effect on colonic epithelial cells.[L36230] Mucosal production of arachidonic acid metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes and hydroxyeicosatetraenoic acids, is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalazine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin production in the colon.[L36230]
Furthermore, mesalazine also has the potential to inhibit the activation of Nuclear Factor kappa B (NFkB) and consequently the production of key pro-inflammatory cytokines.[A16800][A4391][A16799] It has been proposed that reduced expression of PPAR gamma nuclear receptors (gamma form of peroxisome proliferator-activated receptors) may be implicated in ulcerative colitis, and that mesalazine produces pharmacodynamic effects through direct activation of PPAR gamma receptors in the colonic/rectal epithelium.[A16797][A16798][A16516][A16515] Other research also showed the potential involvement of inducible NO synthase (iNOS) and that mesalazine can inhibit this enzyme to amiliorate the enteropathy in inflammatory bowel diseases.[L37023]
Moreover, since increased leukocyte migration, abnormal cytokine production, increased production of arachidonic acid metabolites, particularly leukotriene B4, and increased free radical formation in the inflamed intestinal tissue are all present in patients with inflammatory bowel disease it is also believed that mesalazine has in-vitro and in-vivo pharmacological effects that inhibit leukocyte chemotaxis, decrease cytokine and leukotriene production and scavenge for free radicals.[L5107]
Furthermore, mesalazine also has the potential to inhibit the activation of Nuclear Factor kappa B (NFkB) and consequently the production of key pro-inflammatory cytokines.[A16800][A4391][A16799] It has been proposed that reduced expression of PPAR gamma nuclear receptors (gamma form of peroxisome proliferator-activated receptors) may be implicated in ulcerative colitis, and that mesalazine produces pharmacodynamic effects through direct activation of PPAR gamma receptors in the colonic/rectal epithelium.[A16797][A16798][A16516][A16515] Other research also showed the potential involvement of inducible NO synthase (iNOS) and that mesalazine can inhibit this enzyme to amiliorate the enteropathy in inflammatory bowel diseases.[L37023]
Moreover, since increased leukocyte migration, abnormal cytokine production, increased production of arachidonic acid metabolites, particularly leukotriene B4, and increased free radical formation in the inflamed intestinal tissue are all present in patients with inflammatory bowel disease it is also believed that mesalazine has in-vitro and in-vivo pharmacological effects that inhibit leukocyte chemotaxis, decrease cytokine and leukotriene production and scavenge for free radicals.[L5107]
Pharmacodynamics
Mesalazine is one of the two components of sulphasalazine, the other being sulphapyridine. It is the latter responsible for most of the side effects associated with sulphasalazine therapy, while mesalazine is known to be the active moiety in the treatment of ulcerative colitis [L5101].
Mesalazine is thought to dampen the inflammatory process through its ability to inhibit prostaglandin synthesis, interfere with leukotriene synthesis, and consequent leukocyte migration as well as act as a potent scavenger of free radicals.[L37023] Regardless of the mode of action, mesalazine appears to be active mainly topically rather than systemically.[L37023]
Intraperitoneally administered mesalazine at 30 and 340 mg/kg daily had similar efficacy in attenuating colitis as prednisolone 4 to 550 mg/kg daily given intraperitoneally or sulphasalazine 0.34 to 5 mg/kg given orally in immune complex-induced colitis mice.[A254851] Mesalazine at 5 mmol/L and sulphasalazine 1.5 mmol/L also reversed the increase in water and chloride secretion and decrease the sodium in dinitrochlorbenzene-induced colitis guinea pig.[A254851]
Mesalazine is thought to dampen the inflammatory process through its ability to inhibit prostaglandin synthesis, interfere with leukotriene synthesis, and consequent leukocyte migration as well as act as a potent scavenger of free radicals.[L37023] Regardless of the mode of action, mesalazine appears to be active mainly topically rather than systemically.[L37023]
Intraperitoneally administered mesalazine at 30 and 340 mg/kg daily had similar efficacy in attenuating colitis as prednisolone 4 to 550 mg/kg daily given intraperitoneally or sulphasalazine 0.34 to 5 mg/kg given orally in immune complex-induced colitis mice.[A254851] Mesalazine at 5 mmol/L and sulphasalazine 1.5 mmol/L also reversed the increase in water and chloride secretion and decrease the sodium in dinitrochlorbenzene-induced colitis guinea pig.[A254851]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Depending on the formulation administered, prescribing information for orally administered delayed-released tablets of 2.4g or 4.8g of mesalazine given once daily for 14 days to healthy volunteers was to found to be about 21% to 22% of the administered dose [FDA Label] while prescribing information for an orally administered controlled-release capsule formulation suggests 20% to 30% of the mesalazine in the formulation is absorbed.F3001 In contrast, when mesalamine is administered orally as an unformulated 1-g aqueous suspension, mesalazine is approximately 80% absorbed.F3001
Half-life
For the delayed-release formulation, after intravenous administration, the elimination half-life of mesalamine is reported to be approximately 40 minutes. After oral dosing, the median terminal half life values for mesalamine are usually about 25 hours, but are variable, ranging from 1.5 to 296 hours. There is a large inter-subject and intra-subject variability in the plasma concentrations of mesalamine and N-acetyl-5-aminosalicylic acid and in their terminal half-lives following the administration of mesalazine.
[L36275]
For the extended-release formulation, following single and multiple doses of mesalazine, the mean half-lives were 9 to 10 hours for 5-ASA, and 12 to 14 hours for N-Ac-5-ASA.
[L44196]
The mean elimination half-life was 5 hours (CV=73%) for 5-ASA and 5 hours (CV=63%) for N-acetyl-5-ASA in patients taking 500 mg mesalazine as a rectal suppository every 8 hours for 6 days.
[L36280]
For the rectal enema suspension formulation, the elimination half-life was 0.5 to 1.5 hours for 5-ASA and 5 to 10 hours for N-acetyl-5-ASA.
[L40978]
[L36275]
For the extended-release formulation, following single and multiple doses of mesalazine, the mean half-lives were 9 to 10 hours for 5-ASA, and 12 to 14 hours for N-Ac-5-ASA.
[L44196]
The mean elimination half-life was 5 hours (CV=73%) for 5-ASA and 5 hours (CV=63%) for N-acetyl-5-ASA in patients taking 500 mg mesalazine as a rectal suppository every 8 hours for 6 days.
[L36280]
For the rectal enema suspension formulation, the elimination half-life was 0.5 to 1.5 hours for 5-ASA and 5 to 10 hours for N-acetyl-5-ASA.
[L40978]
Protein binding
In an in vitro study, at 2.5 mcg/mL, mesalamine and N-Ac-5-ASA are 43±6% and 78±1% bound, respectively, to plasma
proteins. Protein binding of N-Ac-5-ASA does not appear to be concentration dependent at concentrations ranging from 1
to 10 mcg/mL.
[L44196]
proteins. Protein binding of N-Ac-5-ASA does not appear to be concentration dependent at concentrations ranging from 1
to 10 mcg/mL.
[L44196]
Volume of distribution
For the extended-release formulation, mesalazine has a Vd of 18 L, confirming minimal extravascular penetration of systemically available drug.
[L44201]
For the delayed-release formulation, the apparent volume of distribution was estimated to be 4.8 L.
[L44206]
[L44201]
For the delayed-release formulation, the apparent volume of distribution was estimated to be 4.8 L.
[L44206]
Metabolism
Mesalazine is metabolized both pre-systemically by the intestinal mucosa and systemically in the liver to N-acetyl-5-aminosalicylic acid (N-Ac-5-ASA) principally by NAT-1. Some acetylation also occurs through the action of colonic bacteria.
[L5107][L44196]
[L5107][L44196]
Route of elimination
Elimination of mesalazine is mainly via the renal route following metabolism to N-acetyl-5-aminosalicylic acid (acetylation) .
[L40848]
However, there is also limited excretion of the parent mesalazine drug in the urine.
[L40848]
After the oral administration of the extended-release formulation of mesalazine, of the approximately 21% to 22% of the drug absorbed, less than 8% of the dose was excreted unchanged in the urine after 24 hours, compared with greater than 13% for N-acetyl-5-aminosalicylic acid.
[L40848]
When given the controlled-release formulation, about 130 mg free mesalazine was recovered in the feces following a single 1-g dose, which was comparable to the 140 mg of mesalazine recovered from the molar equivalent sulfasalazine tablet dose of 2.5 g F3001]. Elimination of free mesalazine and salicylates in feces increased proportionately with the dose given. N-acetylmesalazine was the primary compound excreted in the urine (19% to 30%) following the controlled-release dosing.F3001
In patients with ulcerative proctitis treated with mesalamine 500 mg as a rectal suppository every 8 hours for 6 days, 12% or less of the dose was eliminated in urine as unchanged 5-ASA and 8% to 77% was eliminated as N-acetyl-5-ASA following the initial dose.
At steady state, 11% or less of the dose was eliminated in the urine as unchanged 5-ASA and 3% to 35% was eliminated as N-acetyl-5-ASA.
[L36280]
[L40848]
However, there is also limited excretion of the parent mesalazine drug in the urine.
[L40848]
After the oral administration of the extended-release formulation of mesalazine, of the approximately 21% to 22% of the drug absorbed, less than 8% of the dose was excreted unchanged in the urine after 24 hours, compared with greater than 13% for N-acetyl-5-aminosalicylic acid.
[L40848]
When given the controlled-release formulation, about 130 mg free mesalazine was recovered in the feces following a single 1-g dose, which was comparable to the 140 mg of mesalazine recovered from the molar equivalent sulfasalazine tablet dose of 2.5 g F3001]. Elimination of free mesalazine and salicylates in feces increased proportionately with the dose given. N-acetylmesalazine was the primary compound excreted in the urine (19% to 30%) following the controlled-release dosing.F3001
In patients with ulcerative proctitis treated with mesalamine 500 mg as a rectal suppository every 8 hours for 6 days, 12% or less of the dose was eliminated in urine as unchanged 5-ASA and 8% to 77% was eliminated as N-acetyl-5-ASA following the initial dose.
At steady state, 11% or less of the dose was eliminated in the urine as unchanged 5-ASA and 3% to 35% was eliminated as N-acetyl-5-ASA.
[L36280]
Clearance
The mean (SD) renal clearance in L/h for mesalazine following the single dose administration of mesalazine delayed-release tablets 4.8g under fasting conditions to young and elderly subjects were documented as 2.05 ± 1.33 in young subjects aged 18 to 35 years old, 2.04 ± 1.16 in elderly subjects aged 65 to 75 years old and 2.13 ± 1.20 in elderly subjects older than 75 years.
[L40848]
[L40848]
Drug targets(7)
Proteins and enzymes this drug interacts with in the body
Prostaglandin G/H synthase 2
PTGS2
inhibitor
Specific functionenzyme binding
Cellular location
Microsome membrane
General function & pharmacology
Dual cyclooxygenase and peroxidase in the biosynthesis pathway of prostanoids, a class of C20 oxylipins mainly derived from arachidonate ((5Z,8Z,11Z,14Z)-eicosatetraenoate, AA, C20:4(n-6)), with a particular role in the inflammatory response .
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
Prostaglandin G/H synthase 1
PTGS1
inhibitor
Specific functionheme binding
Cellular location
Microsome membrane
General function & pharmacology
Dual cyclooxygenase and peroxidase that plays an important role in the biosynthesis pathway of prostanoids, a class of C20 oxylipins mainly derived from arachidonate ((5Z,8Z,11Z,14Z)-eicosatetraenoate, AA, C20:4(n-6)), with a particular role in the inflammatory response. The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes. This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins.
The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:7947975
Involved in the constitutive production of prostanoids in particular in the stomach and platelets. In gastric epithelial cells, it is a key step in the generation of prostaglandins, such as prostaglandin E2 (PGE2), which plays an important role in cytoprotection. In platelets, it is involved in the generation of thromboxane A2 (TXA2), which promotes platelet activation and aggregation, vasoconstriction and proliferation of vascular smooth muscle cells (Probable).
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity)
The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:7947975
Involved in the constitutive production of prostanoids in particular in the stomach and platelets. In gastric epithelial cells, it is a key step in the generation of prostaglandins, such as prostaglandin E2 (PGE2), which plays an important role in cytoprotection. In platelets, it is involved in the generation of thromboxane A2 (TXA2), which promotes platelet activation and aggregation, vasoconstriction and proliferation of vascular smooth muscle cells (Probable).
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity)
Polyunsaturated fatty acid 5-lipoxygenase
ALOX5
inhibitor
Specific functionarachidonate 12(S)-lipoxygenase activity
Cellular location
Cytoplasm
General function & pharmacology
Catalyzes the oxygenation of arachidonate ((5Z,8Z,11Z,14Z)-eicosatetraenoate) to 5-hydroperoxyeicosatetraenoate (5-HPETE) followed by the dehydration to 5,6- epoxyeicosatetraenoate (Leukotriene A4/LTA4), the first two steps in the biosynthesis of leukotrienes, which are potent mediators of inflammation .
PMID:19022417 PMID:21233389 PMID:22516296 PMID:23246375 PMID:24282679 PMID:24893149 PMID:31664810 PMID:8615788 PMID:8631361
Also catalyzes the oxygenation of arachidonate into 8-hydroperoxyicosatetraenoate (8-HPETE) and 12-hydroperoxyicosatetraenoate (12-HPETE) .
PMID:23246375
Displays lipoxin synthase activity being able to convert (15S)-HETE into a conjugate tetraene .
PMID:31664810
Although arachidonate is the preferred substrate, this enzyme can also metabolize oxidized fatty acids derived from arachidonate such as (15S)-HETE, eicosapentaenoate (EPA) such as (18R)- and (18S)-HEPE or docosahexaenoate (DHA) which lead to the formation of specialized pro-resolving mediators (SPM) lipoxin and resolvins E and D respectively, therefore it participates in anti-inflammatory responses .
PMID:17114001 PMID:21206090 PMID:31664810 PMID:32404334 PMID:8615788
Oxidation of DHA directly inhibits endothelial cell proliferation and sprouting angiogenesis via peroxisome proliferator-activated receptor gamma (PPARgamma) (By similarity). It does not catalyze the oxygenation of linoleic acid and does not convert (5S)-HETE to lipoxin isomers .
PMID:31664810
In addition to inflammatory processes, it participates in dendritic cell migration, wound healing through an antioxidant mechanism based on heme oxygenase-1 (HO-1) regulation expression, monocyte adhesion to the endothelium via ITGAM expression on monocytes (By similarity). Moreover, it helps establish an adaptive humoral immunity by regulating primary resting B cells and follicular helper T cells and participates in the CD40-induced production of reactive oxygen species (ROS) after CD40 ligation in B cells through interaction with PIK3R1 that bridges ALOX5 with CD40 .
PMID:21200133
May also play a role in glucose homeostasis, regulation of insulin secretion and palmitic acid-induced insulin resistance via AMPK (By similarity).
Can regulate bone mineralization and fat cell differentiation increases in induced pluripotent stem cells (By similarity)
PMID:19022417 PMID:21233389 PMID:22516296 PMID:23246375 PMID:24282679 PMID:24893149 PMID:31664810 PMID:8615788 PMID:8631361
Also catalyzes the oxygenation of arachidonate into 8-hydroperoxyicosatetraenoate (8-HPETE) and 12-hydroperoxyicosatetraenoate (12-HPETE) .
PMID:23246375
Displays lipoxin synthase activity being able to convert (15S)-HETE into a conjugate tetraene .
PMID:31664810
Although arachidonate is the preferred substrate, this enzyme can also metabolize oxidized fatty acids derived from arachidonate such as (15S)-HETE, eicosapentaenoate (EPA) such as (18R)- and (18S)-HEPE or docosahexaenoate (DHA) which lead to the formation of specialized pro-resolving mediators (SPM) lipoxin and resolvins E and D respectively, therefore it participates in anti-inflammatory responses .
PMID:17114001 PMID:21206090 PMID:31664810 PMID:32404334 PMID:8615788
Oxidation of DHA directly inhibits endothelial cell proliferation and sprouting angiogenesis via peroxisome proliferator-activated receptor gamma (PPARgamma) (By similarity). It does not catalyze the oxygenation of linoleic acid and does not convert (5S)-HETE to lipoxin isomers .
PMID:31664810
In addition to inflammatory processes, it participates in dendritic cell migration, wound healing through an antioxidant mechanism based on heme oxygenase-1 (HO-1) regulation expression, monocyte adhesion to the endothelium via ITGAM expression on monocytes (By similarity). Moreover, it helps establish an adaptive humoral immunity by regulating primary resting B cells and follicular helper T cells and participates in the CD40-induced production of reactive oxygen species (ROS) after CD40 ligation in B cells through interaction with PIK3R1 that bridges ALOX5 with CD40 .
PMID:21200133
May also play a role in glucose homeostasis, regulation of insulin secretion and palmitic acid-induced insulin resistance via AMPK (By similarity).
Can regulate bone mineralization and fat cell differentiation increases in induced pluripotent stem cells (By similarity)
Peroxisome proliferator-activated receptor gamma
PPARG
agonist
Specific functionalpha-actinin binding
Cellular location
Nucleus
General function & pharmacology
Nuclear receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the nuclear receptor binds to DNA specific PPAR response elements (PPRE) and modulates the transcription of its target genes, such as acyl-CoA oxidase. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids.
Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated pro-inflammatory responses.
Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of BMAL1 in the blood vessels (By similarity)
Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated pro-inflammatory responses.
Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of BMAL1 in the blood vessels (By similarity)
Inhibitor of nuclear factor kappa-B kinase subunit alpha
CHUK
inhibitor
Specific functionATP binding
Cellular location
Cytoplasm
General function & pharmacology
Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses .
PMID:18626576 PMID:9244310 PMID:9252186 PMID:9346484
Acts as a part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on serine residues .
PMID:18626576 PMID:35952808 PMID:9244310 PMID:9252186 PMID:9346484
These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome .
PMID:18626576 PMID:9244310 PMID:9252186 PMID:9346484
In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis .
PMID:18626576 PMID:9244310 PMID:9252186 PMID:9346484
Negatively regulates the pathway by phosphorylating the scaffold protein TAXBP1 and thus promoting the assembly of the A20/TNFAIP3 ubiquitin-editing complex (composed of A20/TNFAIP3, TAX1BP1, and the E3 ligases ITCH and RNF11) .
PMID:21765415
Therefore, CHUK plays a key role in the negative feedback of NF-kappa-B canonical signaling to limit inflammatory gene activation. As part of the non-canonical pathway of NF-kappa-B activation, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes .
PMID:20501937
In turn, these complexes regulate genes encoding molecules involved in B-cell survival and lymphoid organogenesis. Also participates in the negative feedback of the non-canonical NF-kappa-B signaling pathway by phosphorylating and destabilizing MAP3K14/NIK.
Within the nucleus, phosphorylates CREBBP and consequently increases both its transcriptional and histone acetyltransferase activities .
PMID:17434128
Modulates chromatin accessibility at NF-kappa-B-responsive promoters by phosphorylating histones H3 at 'Ser-10' that are subsequently acetylated at 'Lys-14' by CREBBP .
PMID:12789342
Additionally, phosphorylates the CREBBP-interacting protein NCOA3. Also phosphorylates FOXO3 and may regulate this pro-apoptotic transcription factor .
PMID:15084260
Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity). Phosphorylates AMBRA1 following mitophagy induction, promoting AMBRA1 interaction with ATG8 family proteins and its mitophagic activity PMID:30217973
PMID:18626576 PMID:9244310 PMID:9252186 PMID:9346484
Acts as a part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on serine residues .
PMID:18626576 PMID:35952808 PMID:9244310 PMID:9252186 PMID:9346484
These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome .
PMID:18626576 PMID:9244310 PMID:9252186 PMID:9346484
In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis .
PMID:18626576 PMID:9244310 PMID:9252186 PMID:9346484
Negatively regulates the pathway by phosphorylating the scaffold protein TAXBP1 and thus promoting the assembly of the A20/TNFAIP3 ubiquitin-editing complex (composed of A20/TNFAIP3, TAX1BP1, and the E3 ligases ITCH and RNF11) .
PMID:21765415
Therefore, CHUK plays a key role in the negative feedback of NF-kappa-B canonical signaling to limit inflammatory gene activation. As part of the non-canonical pathway of NF-kappa-B activation, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes .
PMID:20501937
In turn, these complexes regulate genes encoding molecules involved in B-cell survival and lymphoid organogenesis. Also participates in the negative feedback of the non-canonical NF-kappa-B signaling pathway by phosphorylating and destabilizing MAP3K14/NIK.
Within the nucleus, phosphorylates CREBBP and consequently increases both its transcriptional and histone acetyltransferase activities .
PMID:17434128
Modulates chromatin accessibility at NF-kappa-B-responsive promoters by phosphorylating histones H3 at 'Ser-10' that are subsequently acetylated at 'Lys-14' by CREBBP .
PMID:12789342
Additionally, phosphorylates the CREBBP-interacting protein NCOA3. Also phosphorylates FOXO3 and may regulate this pro-apoptotic transcription factor .
PMID:15084260
Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity). Phosphorylates AMBRA1 following mitophagy induction, promoting AMBRA1 interaction with ATG8 family proteins and its mitophagic activity PMID:30217973
Metabolizing enzymes(1)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
NAT1Arylamine N-acetyltransferase 1
substrate
Transporters(3)
Proteins that transport this drug across cell membranes
Solute carrier organic anion transporter family member 1B1
SLCO1B1
substrate
Specific functionbile acid transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Mediates the Na(+)-independent uptake of organic anions .
PMID:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
PMID:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
Solute carrier organic anion transporter family member 1B3
SLCO1B3
substrate
Specific functionbile acid transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Mediates the Na(+)-independent uptake of organic anions .
PMID:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins) such as pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver PMID:16624871 PMID:16627748
PMID:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins) such as pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver PMID:16624871 PMID:16627748
Solute carrier organic anion transporter family member 2B1
SLCO2B1
substrate
Specific functionbile acid transmembrane transporter activity
Cellular location
Cell membrane
General function & pharmacology
Mediates the Na(+)-independent transport of steroid sulfate conjugates and other specific organic anions .
PMID:10873595 PMID:11159893 PMID:11932330 PMID:12724351 PMID:14610227 PMID:16908597 PMID:18501590 PMID:20507927 PMID:22201122 PMID:23531488 PMID:25132355 PMID:26383540 PMID:27576593 PMID:28408210 PMID:29871943 PMID:34628357
Responsible for the transport of estrone 3-sulfate (E1S) through the basal membrane of syncytiotrophoblast, highlighting a potential role in the placental absorption of fetal-derived sulfated steroids including the steroid hormone precursor dehydroepiandrosterone sulfate (DHEA-S) .
PMID:11932330 PMID:12409283
Also facilitates the uptake of sulfated steroids at the basal/sinusoidal membrane of hepatocytes, therefore accounting for the major part of organic anions clearance of liver .
PMID:11159893
Mediates the intestinal uptake of sulfated steroids .
PMID:12724351 PMID:28408210
Mediates the uptake of the neurosteroids DHEA-S and pregnenolone sulfate (PregS) into the endothelial cells of the blood-brain barrier as the first step to enter the brain .
PMID:16908597 PMID:25132355
Also plays a role in the reuptake of neuropeptides such as substance P/TAC1 and vasoactive intestinal peptide/VIP released from retinal neurons .
PMID:25132355
May act as a heme transporter that promotes cellular iron availability via heme oxygenase/HMOX2 and independently of TFRC .
PMID:35714613
Also transports heme by-product coproporphyrin III (CPIII), and may be involved in their hepatic disposition .
PMID:26383540
Mediates the uptake of other substrates such as prostaglandins D2 (PGD2), E1 (PGE1) and E2 (PGE2), taurocholate, L-thyroxine, leukotriene C4 and thromboxane B2 (PubMed:10873595, PubMed:14610227, PubMed:19129463, PubMed:29871943, Ref.25). May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable). Shows a pH-sensitive substrate specificity which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:14610227 PMID:19129463 PMID:22201122
The exact transport mechanism has not been yet deciphered but most likely involves an anion exchange, coupling the cellular uptake of organic substrate with the efflux of an anionic compound .
PMID:19129463 PMID:20507927 PMID:26277985
Hydrogencarbonate/HCO3(-) acts as a probable counteranion that exchanges for organic anions .
PMID:19129463
Cytoplasmic glutamate may also act as counteranion in the placenta .
PMID:26277985
An inwardly directed proton gradient has also been proposed as the driving force of E1S uptake with a (H(+):E1S) stoichiometry of (1:1) PMID:20507927
PMID:10873595 PMID:11159893 PMID:11932330 PMID:12724351 PMID:14610227 PMID:16908597 PMID:18501590 PMID:20507927 PMID:22201122 PMID:23531488 PMID:25132355 PMID:26383540 PMID:27576593 PMID:28408210 PMID:29871943 PMID:34628357
Responsible for the transport of estrone 3-sulfate (E1S) through the basal membrane of syncytiotrophoblast, highlighting a potential role in the placental absorption of fetal-derived sulfated steroids including the steroid hormone precursor dehydroepiandrosterone sulfate (DHEA-S) .
PMID:11932330 PMID:12409283
Also facilitates the uptake of sulfated steroids at the basal/sinusoidal membrane of hepatocytes, therefore accounting for the major part of organic anions clearance of liver .
PMID:11159893
Mediates the intestinal uptake of sulfated steroids .
PMID:12724351 PMID:28408210
Mediates the uptake of the neurosteroids DHEA-S and pregnenolone sulfate (PregS) into the endothelial cells of the blood-brain barrier as the first step to enter the brain .
PMID:16908597 PMID:25132355
Also plays a role in the reuptake of neuropeptides such as substance P/TAC1 and vasoactive intestinal peptide/VIP released from retinal neurons .
PMID:25132355
May act as a heme transporter that promotes cellular iron availability via heme oxygenase/HMOX2 and independently of TFRC .
PMID:35714613
Also transports heme by-product coproporphyrin III (CPIII), and may be involved in their hepatic disposition .
PMID:26383540
Mediates the uptake of other substrates such as prostaglandins D2 (PGD2), E1 (PGE1) and E2 (PGE2), taurocholate, L-thyroxine, leukotriene C4 and thromboxane B2 (PubMed:10873595, PubMed:14610227, PubMed:19129463, PubMed:29871943, Ref.25). May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable). Shows a pH-sensitive substrate specificity which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:14610227 PMID:19129463 PMID:22201122
The exact transport mechanism has not been yet deciphered but most likely involves an anion exchange, coupling the cellular uptake of organic substrate with the efflux of an anionic compound .
PMID:19129463 PMID:20507927 PMID:26277985
Hydrogencarbonate/HCO3(-) acts as a probable counteranion that exchanges for organic anions .
PMID:19129463
Cytoplasmic glutamate may also act as counteranion in the placenta .
PMID:26277985
An inwardly directed proton gradient has also been proposed as the driving force of E1S uptake with a (H(+):E1S) stoichiometry of (1:1) PMID:20507927
Scientific references(11)
Mayberry J.
Ulcerative colitis associated with gastric heterotopia in the rectum: a case report.
Journal of Gastrointestinal and Liver Diseases
201928(1). doi: 10.15403/jgld.2014.1121.281.ulc
Stolfi C., De Simone V., Pallone F., Monteleone G.
Mechanisms of action of non-steroidal anti-inflammatory drugs (NSAIDs) and mesalazine in the chemoprevention of colorectal cancer.
International Journal Molecular Science
2013 Sep 314(9):17972-85. doi: 10.3390/ijms140917972
Bantel H., Berg C., Vieth M., Stolte M., Kruis W., Schulze-Osthoff K.
Mesalazine Inhibits Activation of Transcription Factor Nf-κB in Inflamed Mucosa of Patients With Ulcerative Colitis.
American Journal of Gastroenterology
200095(12):3452-3457. doi: 10.1111/j.1572-0241.2000.03360.x
Allgayer H.
Review article: mechanisms of action of mesalazine in preventing colorectal carcinoma in inflammatory bowel disease.
Alimentary Pharmacology & Therapeutics
200318(s2):10-14. doi: 10.1046/j.1365-2036.18.s2.1.x
Weber C.K., Liptay S., Wirth T., Adler G., Schmid R.M.
Suppression of NF-κB activity by sulfasalazine is mediated by direct inhibition of IκB kinases α and β.
Gastroenterology
2000119(5):1209-1218. doi: 10.1053/gast.2000.19458
Schwab M., Reynders V., Loitsch S., Shastri Y.M., Steinhilber D., Schroder O., Stein J.
PPARgamma is involved in mesalazine-mediated induction of apoptosis and inhibition of cell growth in colon cancer cells.
Carcinogenesis
2008 Jul29(7):1407-14. doi: 10.1093/carcin/bgn118. Epub 2008 Jun 9
Linard C., Gremy O., Benderitter M.
Reduction of Peroxisome Proliferation-Activated Receptor γ Expression by γ-Irradiation as a Mechanism Contributing to Inflammatory Response in Rat Colon: Modulation by the 5-Aminosalicylic Acid Agonist.
The Journal of Pharmacology and Experimental Therapeutics
2008324(3):911-920. doi: 10.1124/jpet.107.129122
Desreumaux P., Ghosh S.
Review article: mode of action and delivery of 5‐aminosalicylic acid – new evidence.
Alimentary Pharmacology & Therapeutics
200624(s1):2-9. doi: 10.1111/j.1365-2036.2006.03069.x
Rousseaux C., Lefebvre B., Dubuquoy L., Lefebvre P., Romano O., Auwerx J., Metzger D., Wahli W., Desvergne B., Naccari G.C., Chavatte P., Farce A., Bulois P., Cortot A., Colombel J.F., Desreumaux P.
Intestinal antiinflammatory effect of 5-aminosalicylic acid is dependent on peroxisome proliferator–activated receptor-γ.
The Journal of Experimental Medicine
2005201(8):1205-1215. doi: 10.1084/jem.20041948
Nandi J., Saud B., Zinkievich J.M., Palma D.T., Levine R.A.
5-Aminosalicylic Acid Improves Indomethacin-Induced Enteropathy by Inhibiting iNOS Transcription in Rats.
Digestive Diseases and Sciences
200853(1):123-132. doi: 10.1007/s10620-007-9832-2
Brogden R.N., Sorkin E.M.
Mesalazine.
A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in chronic inflammatory bowel disease
Drugs. 1989 Oct38(4):500-23. doi: 10.2165/00003495-198938040-00003
ATC classification(1 code)
ATC A07EC02
Affected organisms(1)
Humans and other mammals
International brands(5)
Experimental properties(2)
Commercial products(157)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Mesalazine
Additional database identifiers
Drugs Product Database (DPD)
14088
ChemSpider
3933
BindingDB
60918
Guide to Pharmacology
2700
ZINC
ZINC000000001688
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9604
GenAtlas
PTGS1
GeneCards
PTGS1
GenBank Gene Database
M31822
GenBank Protein Database
387018
Guide to Pharmacology
1375
UniProt Accession
PGH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:435
GenAtlas
ALOX5
GeneCards
ALOX5
GenBank Gene Database
J03600
GenBank Protein Database
187193
Guide to Pharmacology
1385
UniProt Accession
LOX5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9236
GenAtlas
PPARG
GeneCards
PPARG
GenBank Gene Database
U79012
GenBank Protein Database
1711117
Guide to Pharmacology
595
UniProt Accession
PPARG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1974
GeneCards
CHUK
Guide to Pharmacology
1989
UniProt Accession
IKKA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5960
GenAtlas
IKBKB
GeneCards
IKBKB
GenBank Gene Database
AF029684
GenBank Protein Database
2599558
Guide to Pharmacology
2039
UniProt Accession
IKKB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7873
GenAtlas
NOS2A
GeneCards
NOS2
GenBank Gene Database
L09210
GenBank Protein Database
292242
Guide to Pharmacology
1250
UniProt Accession
NOS2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7645
GeneCards
NAT1
GenBank Gene Database
D90041
GenBank Protein Database
219414
UniProt Accession
ARY1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10959
GenAtlas
SLCO1B1
GeneCards
SLCO1B1
GenBank Gene Database
AF060500
GenBank Protein Database
5051630
Guide to Pharmacology
1220
UniProt Accession
SO1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10961
GeneCards
SLCO1B3
GenBank Gene Database
AJ251506
GenBank Protein Database
9187497
Guide to Pharmacology
1221
UniProt Accession
SO1B3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10962
GenAtlas
SLCO2B1
GeneCards
SLCO2B1
GenBank Gene Database
AB026256
GenBank Protein Database
5006263
Guide to Pharmacology
1224
UniProt Accession
SO2B1_HUMAN
International reference pricing
22 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
From $0.41/ml
To $488.32/box
Rowasa 4 gm/60 ml enema
$0.41/ml
Novo-5 Asa 400 mg Enteric-Coated Tablet
$0.42/tablet
Salofalk 500 mg Enteric-Coated Tablet
$0.56/tablet
Asacol 400 mg Enteric-Coated Tablet
$0.59/tablet
Pentasa 500 mg Sustained-Release Tablet
$0.63/tablet
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
4 active patents, 14 expired
8865688
United States
Approved 21 Oct 2014 · Expires 1 May 2030
4 years
8436051
United States
Approved 7 May 2013 · Expires 6 Jun 2028
2y 2m
8217083
United States
Approved 10 Jul 2012 · Expires 6 Jun 2028
2y 2m
7645801
United States
Approved 12 Jan 2010 · Expires 24 Jul 2027
1y 3m
6893662
United States
Approved 17 May 2005 · Expires 15 Nov 2021
Expired
The earliest active patent expires July 2027. Generic versions may become available after this date.
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)