General
Preferred name
Acetylsalicylic acid
Synonyms
ASPIRIN ()
Apernyl ()
ASA ()
Acetylsalicylate ()
DIHYDROXYALUMINUM ASPIRIN ()
Aloxiprin ()
Carbasalate Calcium ()
ASPIRIN DL-LYSINE ()
Aspirin (NSC 27223) ()
Acetylsalicylic acid, ASA ()
Postmi 300 ()
Disprin Cv ()
Gencardia ()
Acetylsalicylic Acid ()
Postmi 75 ()
Acetylsalicylicum acidum ()
NSC-406186 ()
Acetosalic Acid ()
Levius ()
Ecotrin ()
Nu-Seals 75 ()
Nu-Seals 300 ()
Paynocil ()
Equi-Prin ()
8-Hour Bayer ()
Platet ()
Angettes 75 ()
Measurin ()
Alka Rapid ()
Acetylsalicylic acid (who-ip) ()
NSC-27223 ()
Vazalore ()
BAY1019036 ()
Acetylsalic Acid ()
Durlaza ()
Enprin ()
Acidum acetylsalicylicum (who-ip) ()
Benzoic acid, 2-(acetyloxy)- ()
Anadin All Night ()
Disprin Direct ()
Bayer extra strength aspirin for migraine pain ()
Micropirin EC ()
Acetyl salicylate ()
Nu-Seals Cardio 75 ()
Max Strgh Aspro Clr ()
Platet 300 ()
Danamep ()
Salicylic Acid Acetate ()
Nu-Seals 600 ()
Aspro Clr ()
Acidum acetylsalicylicum ()
Acetylsalicylate lysine ()
Dl-lysine-acetylsalicylate ()
Aspirin lysine ()
Dl-lysine acetylsalicylate ()
Flectadol ()
Aspirisine ()
Venopirin ()
Lysine acetylsalicylate ()
Solpirin ()
Egicalm ()
Laspal ()
L-lysine acetylsalicylate ()
Vetalgine ()
Aspidol ()
Aspegic ()
Acetylsalicylic acid lysinate ()
Aspirin-d4 ()
P&D ID
PD002467
CAS
50-78-2
11126-35-5
107032-89-3
62952-06-1
97781-16-3
Tags
covalent binder
drug candidate
natural product
drug
available
Approved by
FDA
First approval
1950
1898
Drug Status
withdrawn
approved
vet_approved
experimental
investigational
Drug indication
Antipyretic
Myocardial infarction
Pain
Analgesic
Cardiovascular disease
Antirheumatic
Max Phase
Phase 4
Phase 3
Probe control
Probe control not defined
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
HALF-LIFE
The half-life of ASA in the circulation ranges from 13 - 19 minutes. Blood concentrations drop rapidly after complete absorption. The half-life of the salicylate ranges between 3.5 and 4.5 hours [FDA label].
METABOLISM
Acetylsalicylic acid is hydrolyzed in the plasma to salicylic acid. Plasma concentrations of aspirin following after administration of the extended-release form are mostly undetectable 4-8 hours after ingestion of a single dose. Salicylic acid was measured at 24 hours following a single dose of extended-release acetylsalicylic acid [F4405].; ; 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].; ;
ABSORPTION
Absorption is generally rapid and complete following oral administration but absorption may be variable depending on the route, dosage form, and other factors including but not limited to the rate of tablet dissolution, gastric contents, gastric emptying time, and gastric pH [FDA label].; ; **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].
DESCRIPTION
Aspirin is the prototypical cyclooxygenase inhibitor and inhibits the biosynthesis of prostaglandins. Aspirin acid also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis.
(GtoPdb)
PHARMACODYNAMICS
**Effects on pain and fever**; ; 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.
ROE
Excretion of salicylates occurs mainly through the kidney, by the processes of glomerular filtration and tubular excretion, in the form of free salicylic acid, salicyluric acid, and, additionally, phenolic and acyl glucuronides [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].
MOA
Acetylsalicylic acid (ASA) blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes [A177241, A10989, A32682]. Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan). The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins. This process also stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation [FDA label]. Platelet aggregation can result in clots and harmful venous and arterial thromboembolism, leading to conditions such as pulmonary embolism and stroke. ; ; 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].
INDICATION
**Pain, fever, and inflammation**; ; 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].; ; ;
DESCRIPTION
Cytochrome P450 inhibitor; antifungal
(Tocris Bioactive Compound Library)
DESCRIPTION
Cyclooxygenase inhibitor; NSAID
(Tocriscreen Plus)
DESCRIPTION
COX inhibitor; antithrombotic
(LOPAC library)
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Cell lines
5
Organisms
3
Compound Sets
33
ChEMBL Approved Drugs
ChEMBL Drugs
Concise Guide to Pharmacology 2017/18
Concise Guide to Pharmacology 2019/20
Concise Guide to Pharmacology 2021/22
Concise Guide to Pharmacology 2023/24
CovalentInDB
CovBinderInPDB
Drug Repurposing Hub
DrugBank Approved Drugs
DrugCentral
DrugCentral Approved Drugs
DrugMAP
DrugMAP Approved Drugs
Enamine BioReference Compounds
Guide to Pharmacology
Ki Database
LOPAC library
MedChem Express Bioactive Compound Library
NCATS Inxight Approved Drugs
Novartis Chemogenetic Library (NIBR MoA Box)
NPC Screening Collection
Prestwick Chemical Library
ReFrame library
Selleckchem Bioactive Compound Library
TargetMol Bioactive Compound Library
The Spectrum Collection
Tocris Bioactive Compound Library
Tocriscreen Plus
Withdrawn 2.0
ZINC Tool Compounds
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
84
Molecular Weight
180.04
Hydrogen Bond Acceptors
3
Hydrogen Bond Donors
1
Rotatable Bonds
2
Ring Count
1
Aromatic Ring Count
1
cLogP
1.31
TPSA
63.6
Fraction CSP3
0.11
Chiral centers
0.0
Largest ring
6.0
QED
0.55
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Target Type
Enzymes
Selectivity
COX-3 > COX-1 > COX-2
Pathway
Immunology/Inflammation
Neuroscience
Anti-infection
Apoptosis
Autophagy
MAPK/ERK Pathway
NF-κB
Target
COX-1
COX-2
AKR1C1, ASIC3, EDNRA, HSPA5, IKBKB, NFKB1, NFKB2, NFKBIA, PRKAA1, PRKAA2, PRKAB1, PRKAB2, PRKAG1, PRKAG2, PRKAG3, PTGS1, PTGS2, RPS6KA3, TP53
Caspase
COX
Mitophagy
p38 MAPK
Virus Protease
Autophagy,COX,Mitophagy
Primary Target
Cyclooxygenases
MOA
Inhibitor
Cyclooxygenase-2 Inhibitors
TP53 Expression Enhancers
Cyclooxygenase-1 Inhibitors
Nitric Oxide Donors
Non-Steroidal Antiinflammatory Drugs
cyclooxygenase inhibitor
Member status
member
Indication
headache, fever, toothache, muscle pain
Disease Area
neurology/psychiatry, endocrinology, dental
ATC
N02BA51
N02BA71
B01AC06
A01AD05
N02BA01
Toxicity type
hepatic, neurological
Therapeutic Class
Analgesics
Source data
