Aspirin 75mg effervescent tablets
Also known as <em>Aspirin</em>, acetylsalicylic acid (ASA) is a commonly used drug for the treatment of pain and fever due to various causes.
Genetic variations that may affect drug response
2 known genetic variations may influence how your body responds to Aspirin 75mg effervescent tablets.Genes involved: CYP2C9, ITGB3
These are known genetic variations. They don't mean the medicine won't work for you — speak to your doctor or a pharmacogenomics specialist for personalised advice. Source: DrugBank (CC BY-NC 4.0).
Safety information for pregnancy and breastfeeding
Pregnancy
While teratogenic effects were observed in animals nearly lethal doses, no evidence suggests that this drug is teratogenic in humans [FDA label].
Breastfeeding
While teratogenic effects were observed in animals nearly lethal doses, no evidence suggests that this drug is teratogenic in humans [FDA label].
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Safety monitoring data
Yellow Card reports
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.
View Drug Analysis Profile
Suspected adverse reactions reported for Aspirin
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Aspirin
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
2 branded products available
WHO defined daily dose (DDD)
1 tablet
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.
Therapeutically similar medicines
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
Clinical guidelines and formulary information
British National Formulary
Aspirin
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(14)
Stroke and transient ischaemic attack in over 16s: diagnosis and initial management (NG128)
Acute coronary syndromes (NG185)
Acute upper gastrointestinal bleeding in adults (QS38)
Atrial fibrillation (QS93)
Clopidogrel and modified-release dipyridamole for the prevention of occlusive vascular events (TA210)
Rivaroxaban for preventing atherothrombotic events in people with coronary or peripheral artery disease (TA607)
Rivaroxaban for preventing adverse outcomes after acute management of acute coronary syndrome (TA335)
Hypertension in pregnancy (QS35)
Ticagrelor for the treatment of acute coronary syndromes (TA236)
Venous thromboembolism in over 16s: reducing the risk of hospital-acquired deep vein thrombosis or pulmonary embolism (NG89)
Ticagrelor for preventing atherothrombotic events after myocardial infarction (TA420)
Barrett's oesophagus and stage 1 oesophageal adenocarcinoma: monitoring and management (NG231)
Colorectal cancer (NG151)
Headaches in over 12s: diagnosis and management (CG150)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
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
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
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
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
97 found
Half-life
13 - 19 minutes
Mechanism
Acetylsalicylic acid (ASA) blocks prostaglandin synthesis.
Food interactions
4 warnings
Human targets
17 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1-2 hours
Half-life
13 - 19 minutes
Protein binding
50%
Volume of distribution
Metabolism
4-8 hours
Elimination
48 hours
Clearance
10 mL/min
[A177217]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Interestingly, the results of various studies have demonstrated that long-term use of acetylsalicylic acid may decrease the risk of various cancers, including colorectal, esophageal, breast, lung, prostate, liver and skin cancer [A177325]. Aspirin is classified as a non-selective cyclooxygenase (COX) inhibitor [A32682][A177268] and is available in many doses and forms, including chewable tablets, suppositories, extended release formulations, and others [L5968].
Acetylsalicylic acid is a very common cause of accidental poisoning in young children. It should be kept out of reach from young children, toddlers, and infants [FDA label].
Acetylsalicylic acid (ASA), in the regular tablet form (immediate-release), is indicated to relieve pain, fever, and inflammation associated with many conditions, including the flu, the common cold, neck and back pain, dysmenorrhea, headache, tooth pain, sprains, fractures, myositis, neuralgia, synovitis, arthritis, bursitis, burns, and various injuries. It is also used for symptomatic pain relief after surgical and dental procedures [FDA label].
The extra strength formulation of acetylsalicylic acid is also indicated for the management migraine pain with photophobia (sensitivity to light) and phonophobia (sensitivity to sound)[FDA label].
Other indications
ASA is also indicated for various other purposes, due to its ability to inhibit platelet aggregation. These include:
Reducing the risk of cardiovascular death in suspected cases of myocardial infarction (MI) [FDA label].
Reducing the risk of a first non-fatal myocardial infarction in patients, and for reducing the risk of morbidity and mortality in cases of unstable angina and in those who have had a prior myocardial infarction [FDA label].
For reducing the risk of transient ischemic attacks (TIA) and to prevent atherothrombotic cerebral infarction (in conjunction with other treatments) [FDA label].
For the prevention of thromboembolism after hip replacement surgery [FDA label].
For decreasing platelet to platelet adhesion following carotid endarterectomy, aiding in the prevention of transient ischemic attacks (TIA) [FDA label].
Used for patients undergoing hemodialysis with a silicone rubber arteriovenous cannula inserted to prevent thrombosis at the insertion site [FDA Label].
Important note regarding use of the extended-release formulation F4405
In the setting of acute myocardial infarction, or before percutaneous interventions, the extended-release form of acetylsalicylic acid should not be used.
Use immediate-release formulations in scenarios requiring rapid onset of action [Label, F4405]. The extended-release form is taken to decrease the incidence of mortality and myocardial infarction (MI) for individuals diagnosed with chronic coronary artery disease (CAD), including patients with previous myocardial infarction (MI) or unstable angina or with chronic stable angina. Additionally, the extended-release form is used to decrease the risk of death and recurrent episodes of stroke in patients with a history of stroke or TIA F4405.
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1786 interactions
Acute oral LD50 values have been reported as over 1.0 g/kg in humans, cats, and dogs, 0.92 g/kg - 1.48 g/kg in albino rats, 1.19 g/kg in guinea pigs, 1.1 g/kg in mice, and 1.8 g/kg in rabbit models [FDA label].
Acute toxicity
Salicylate toxicity is a problem that may develop with both acute and chronic salicylate exposure .
[A35408]
Multiple organ systems may be affected by salicylate toxicity, including the central nervous system, the pulmonary system, and the gastrointestinal system. Severe bleeding may occur. In the majority of cases, patients suffering from salicylate toxicity are volume-depleted at the time of presentation for medical attention.
Fluid resuscitation should occur immediately and volume status should be monitored closely. Disruptions in acid-base balance are frequent in ASA toxicity .
[A35408]
The acute toxicity of acetylsalicylic in animals has been widely studied. The signs of poisoning in rats from lethal doses are mild to severe gastroenteritis, hepatitis, nephritis, pulmonary edema, encephalopathy, shock and some toxic effects on other organs and tissues. Mortality has been observed following convulsions or cardiovascular shock.
An important differentiating property between various animal species is the ability to vomit toxic doses. Humans, cats and dogs have this ability, but rodents or rabbits do not [FDA label].
Chronic toxicity and carcinogenesis
Chronic ASA toxicity is frequently accompanied by atypical clinical presentations that may be similar to diabetic ketoacidosis, delirium, cerebrovascular accident (CVA), myocardial infarction (MI) or cardiac failure. Plasma salicylate concentrations should be measured if salicylate intoxication is suspected, even if there no documentation available to suggest ASA was ingested.
In older age, nephrotoxicity from salicylates increases, and the risk of upper gastrointestinal hemorrhage is increased, with higher rates of mortality .
[A32954]
It is also important to note that ASA toxicity may occur even with close to normal serum concentrations. Prevention of chronic ASA includes the administration of smallest possible doses, avoidance of concurrent use of salicylate drugs, and therapeutic drug monitoring. Renal function should be regularly monitored and screening for gastrointestinal bleeding should be done at regular intervals .
[A32954]
Chronic toxicity studies were performed in rodents.
ASA was administered at doses measured to be 2 to 20 times the maximum tolerated clinical dose to mice for up to one year. Negative dose-related effects were seen. These include decreased mean survival time, decreased number of births and progeny reaching an appropriate age for weaning.
No evidence of carcinogenesis was found in 1-year studies [FDA label]. At daily doses of 0.24 g/kg/day given for 100 days to albino rats, ASA led to signs to excessive thirst, aciduria, diuresis, drowsiness, hyperreflexia, piloerection, changes in respiration, tachycardia, followed by soft stools, epistaxis, sialorrhea, dacryorrhea and mortality during hypothermic coma in the second study month [FDA label].
Use in pregnancy and lactation
While teratogenic effects were observed in animals nearly lethal doses, no evidence suggests that this drug is teratogenic in humans [FDA label]. It is advisable, however, to avoid ASA use the first and second trimester of pregnancy, unless it is clearly required.
If acetylsalicylic acid containing drugs are ingested by a patient attempting to conceive, or during the first and second trimester of pregnancy, the lowest possible dose at the shortest possible duration should be taken [FDA label]. This drug is contraindicated in the 3rd trimester of pregnancy [FDA label].
It is important to note that there is 60% homology between the protein structures of COX-1 and COX-2. ASA binds to serine 516 residue on the active site of COX-2 in the same fashion as its binding to the serine 530 residue located on the active site of COX-1. The active site of COX-2 is, however, slightly larger than the active site of COX-1, so that arachidonic acid (which later becomes prostaglandins) manages to bypass the aspirin molecule inactivating COX-2 [A32682][A177256]. ASA, therefore, exerts more action on the COX-1 receptor rather than on the COX-2 receptor [A177268]. A higher dose of acetylsalicylic acid is required for COX-2 inhibition [A177325].
Acetylsalicylic acid disrupts the production of prostaglandins throughout the body by targeting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) [A177241][A10989][A32682]. Prostaglandins are potent, irritating substances that have been shown to cause headaches and pain upon injection into humans. Prostaglandins increase the sensitivity of pain receptors and substances such as histamine and bradykinin. Through the disruption of the production and prevention of release of prostaglandins in inflammation, this drug may stop their action at pain receptors, preventing symptoms of pain. Acetylsalicylic acid is considered an antipyretic agent because of its ability to interfere with the production of brain prostaglandin E1. Prostaglandin E1 is known to be an extremely powerful fever-inducing agent [FDA label].
Effects on platelet aggregation
The inhibition of platelet aggregation by ASA occurs because of its interference with thromboxane A2 in platelets, caused by COX-1 inhibition. Thromboxane A2 is an important lipid responsible for platelet aggregation, which can lead to clot formation and future risk of heart attack or stroke [FDA label].
A note on cancer prevention
ASA has been studied in recent years to determine its effect on the prevention of various malignancies [A177325]. In general, acetylsalicylic acid is involved in the interference of various cancer signaling pathways, sometimes inducing or upregulating tumor suppressor genes [A177325][A177403]. Results of various studies suggest that there are beneficial effects of long-term ASA use in the prevention of several types of cancer, including stomach, colorectal, pancreatic, and liver cancers [A177400]. Research is ongoing.
How the body processes this drug — absorption, distribution, metabolism, and elimination
Detailed absorption information
When ingested orally, acetylsalicylic acid is rapidly absorbed in both the stomach and proximal small intestine. The non-ionized acetylsalicylic acid passes through the stomach lining by passive diffusion. Ideal absorption of salicylate in the stomach occurs in the pH range of 2.15 - 4.10.
Intestinal absorption of acetylsalicylic acid occurs at a much faster rate. At least half of the ingested dose is hydrolyzed to salicylic acid in the first-hour post-ingestion by esterases found in the gastrointestinal tract. Peak plasma salicylate concentrations occur between 1-2 hours post-administration [FDA label].
The kidney, liver, heart, and lungs are also found to be rich in salicylate concentration after dosing. Low concentrations of salicylate are usually low, and minimal concentrations are found in feces, bile, and sweat [FDA label].
Salicylate is mainly metabolized in the liver, although other tissues may also be involved in this process [FDA label]. The major metabolites of acetylsalicylic acid are salicylic acid, salicyluric acid, the ether or phenolic glucuronide and the ester or acyl glucuronide.
A small portion is converted to gentisic acid and other hydroxybenzoic acids [FDA label].
Salicylate can be found in the urine soon after administration, however, the entire dose takes about 48 hours to be completely eliminated. The rate of salicylate is often variable, ranging from 10% to 85% in the urine, and heavily depends on urinary pH. Acidic urine generally aids in reabsorption of salicylate by the renal tubules, while alkaline urine increases excretion [FDA label].
After the administration of a typical 325mg dose, the elimination of ASA is found to follow first order kinetics in a linear fashion. At high concentrations, the elimination half-life increases [FDA label].
[A177217]
Dosage adjustments may be required in patients with renal impairment [FDA label]. The extended-release tablet should not be administered to patients with eGFR of less than 10 mL/min F4405.
Proteins and enzymes this drug interacts with in the body
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)
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:21357570 PMID:2991281 PMID:36745799 PMID:6995544
HMGCR is the main target of statins, a class of cholesterol-lowering drugs PMID:11349148 PMID:18540668 PMID:36745799
PMID:19218247
Most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentrations of NADPH .
PMID:14672942
Displays a broad positional specificity acting on positions 3, 17 and 20 of steroids and regulates the metabolism of hormones like estrogens and androgens .
PMID:10998348
May also reduce conjugated steroids such as 5alpha-dihydrotestosterone sulfate .
PMID:19218247
Displays affinity for bile acids PMID:8486699
PMID:14722619 PMID:17878938 PMID:24563466
In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. AMPK also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin.
The AMPK gamma3 subunit is a non-catalytic subunit with a regulatory role in muscle energy metabolism .
PMID:17878938
It mediates binding to AMP, ADP and ATP, leading to AMPK activation or inhibition: AMP-binding results in allosteric activation of alpha catalytic subunit (PRKAA1 or PRKAA2) both by inducing phosphorylation and preventing dephosphorylation of catalytic subunits. ADP also stimulates phosphorylation, without stimulating already phosphorylated catalytic subunit. ATP promotes dephosphorylation of catalytic subunit, rendering the AMPK enzyme inactive
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:11669456 PMID:11907186 PMID:14675047 PMID:22108572 PMID:23832370 PMID:28534121 PMID:9950961
Mediates the uptake of OA across the basolateral side of proximal tubule epithelial cells, thereby contributing to the renal elimination of endogenous OA from the systemic circulation into the urine .
PMID:9887087
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
Transports prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) and may contribute to their renal excretion .
PMID:11907186
Also mediates the uptake of cyclic nucleotides such as cAMP and cGMP .
PMID:26377792
Involved in the transport of neuroactive tryptophan metabolites kynurenate (KYNA) and xanthurenate (XA) and may contribute to their secretion from the brain .
PMID:22108572 PMID:23832370
May transport glutamate .
PMID:26377792
Also involved in the disposition of uremic toxins and potentially toxic xenobiotics by the renal organic anion secretory pathway, helping reduce their undesired toxicological effects on the body .
PMID:11669456 PMID:14675047
Uremic toxins include the indoxyl sulfate (IS), hippurate/N-benzoylglycine (HA), indole acetate (IA), 3-carboxy-4- methyl-5-propyl-2-furanpropionate (CMPF) and urate .
PMID:14675047 PMID:26377792
Xenobiotics include the mycotoxin ochratoxin (OTA) .
PMID:11669456
May also contribute to the transport of organic compounds in testes across the blood-testis-barrier PMID:35307651
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
ATC B01AC06
ATC C07FX04
ATC C10BX04
ATC M01BA03
ATC C10BX02
ATC N02BA71
ATC B01AC56
ATC N02AJ07
ATC N02AJ02
ATC N02BA01
ATC B01AF51
ATC C10BX05
ATC N02BA51
ATC A01AD05
ATC C10BX01
ATC C07FX03
ATC N02AJ18
ATC C10BX12
ATC C10BX08
ATC C10BX06
ATC C07FX02
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)
Acetylsalicylic acid
Matched from: Aspirin
Additional database identifiers
Drugs Product Database (DPD)
150
ChemSpider
2157
BindingDB
22360
PDB
AIN
Guide to Pharmacology
4139
ZINC
ZINC000000000053
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: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:5006
GenAtlas
HMGCR
GeneCards
HMGCR
GenBank Gene Database
M11058
GenBank Protein Database
306865
Guide to Pharmacology
639
UniProt Accession
HMDH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:384
GenAtlas
AKR1C1
GeneCards
AKR1C1
GenBank Gene Database
M86609
GenBank Protein Database
181549
UniProt Accession
AK1C1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9376
GenAtlas
PRKAA1
GeneCards
PRKAA1
GenBank Gene Database
AB022017
GenBank Protein Database
4115829
UniProt Accession
AAPK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9377
GeneCards
PRKAA2
UniProt Accession
AAPK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9378
GenAtlas
PRKAB1
GeneCards
PRKAB1
GenBank Gene Database
AJ224515
GenBank Protein Database
2916800
Guide to Pharmacology
1543
UniProt Accession
AAKB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9379
GenAtlas
PRKAB2
GeneCards
PRKAB2
GenBank Gene Database
AJ224538
GenBank Protein Database
2916802
Guide to Pharmacology
1544
UniProt Accession
AAKB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9385
GeneCards
PRKAG1
UniProt Accession
AAKG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9386
GeneCards
PRKAG2
UniProt Accession
AAKG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9387
GeneCards
PRKAG3
UniProt Accession
AAKG3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3179
GenAtlas
EDNRA
GeneCards
EDNRA
GenBank Gene Database
S63938
GenBank Protein Database
238636
Guide to Pharmacology
219
UniProt Accession
EDNRA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11998
GenAtlas
TP53
GeneCards
TP53
GenBank Gene Database
X02469
UniProt Accession
P53_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5238
GenAtlas
HSPA5
GeneCards
HSPA5
GenBank Gene Database
M19645
GenBank Protein Database
386758
UniProt Accession
BIP_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10432
GeneCards
RPS6KA3
Guide to Pharmacology
1528
UniProt Accession
KS6A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7797
GenAtlas
NFKBIA
GeneCards
NFKBIA
GenBank Gene Database
BC004983
UniProt Accession
IKBA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11898
GeneCards
TNFAIP6
UniProt Accession
TSG6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1499
GenAtlas
CASP1
GeneCards
CASP1
GenBank Gene Database
X65019
GenBank Protein Database
33793
Guide to Pharmacology
1617
UniProt Accession
CASP1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1504
GenAtlas
CASP3
GeneCards
CASP3
GenBank Gene Database
U13737
GenBank Protein Database
561666
Guide to Pharmacology
1619
UniProt Accession
CASP3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1582
GenAtlas
CCND1
GeneCards
CCND1
GenBank Gene Database
X59798
GenBank Protein Database
35632
UniProt Accession
CCND1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7553
GeneCards
MYC
UniProt Accession
MYC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8729
GeneCards
PCNA
UniProt Accession
PCNA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7758
GenAtlas
NEU1
GeneCards
NEU1
GenBank Gene Database
AF040958
GenBank Protein Database
2773339
Guide to Pharmacology
3214
UniProt Accession
NEUR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12538
GeneCards
UGT1A6
UniProt Accession
UD16_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7646
GeneCards
NAT2
GenBank Gene Database
D90040
GenBank Protein Database
219412
UniProt Accession
ARY2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10970
GenAtlas
hROAT1
GeneCards
SLC22A6
GenBank Gene Database
AF057039
GenBank Protein Database
3831566
Guide to Pharmacology
1025
UniProt Accession
S22A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_HUMAN
International reference pricing
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
6 active patents, 8 expired
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: