| Drug Name: | Acetylsalicylic acid (50-78-2) |
|---|---|
| PubChem ID: | 2244 |
| SMILES: | CC(=O)OC1=CC=CC=C1C(=O)O |
| InchiKey: | BSYNRYMUTXBXSQ-UHFFFAOYSA-N |
| Therapeutic Category: | Analgesics, Anti-Inflammatory Agents, Antipyretics, Antirheumatic Agents, Cardiovascular Agents, Cyclooxygenase Inhibitors, Enzyme Inhibitors, Fibrin Modulating Agents, Fibrinolytic Agents, Hematologic Agents, Peripheral Nervous System Agents, Platelet Aggregation Inhibitors, Sensory System Agents |
| Molecular Weight (dalton) | : | 180.159 |
| LogP | : | 1.3101 |
| Ring Count | : | 1 |
| Hydrogen Bond Acceptor Count | : | 3 |
| Hydrogen Bond Donor Count | : | 1 |
| Total Polar Surface Area | : | 63.6 |
This panel provides information on interacting drugs and their ADRs along with references
| Interacting drug | Toxicity | Interaction Type | Mechanism | Reference |
|---|---|---|---|---|
| Streptokinase ((9002-01-1)) | Cerebral Haemorrhage | Additive | Additive effects of both drugs | Negative Interaction of Aspirin and Streptokinase in Acute Ischemic Stroke: Further Analysis of the Multicenter Acute Stroke Trial-Italy |
| Clopidogrel (113665-84-2) | Bleeding | Additive | increase in life-threatening bleeding due to additive effect of both drugs | Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial |
| Acetazolamide (59-66-5) | Toxic Reaction | Antagonistic | Carbonic anhydrase inhibitors affect the plasma pH, so that more of the salicylate exists in the un-ionised form, which can enter the CNS and other tissues more easily, leading to salicylate toxicity | Toxicity of combined therapy with carbonic anhydrase inhibitors and aspirin |
| Auranofin (34031-32-8) | Liver Damage | Antagonistic | Not Established | Fenoprofen, aspirin, and gold induction in rheumatoid arthritis |
| Corticotropin (12427-33-7) | Ulceration Of Intestine | Antagonistic | Corticosteroid increases the glomerular filtration rate, which increases salicylate clearance | Patterns of plasma concentrations and urinary excretion of salicylate in rheumatoid arthritis |
| Diclofenac (15307-86-5) | Disorder Gastrointestinal | Additive | Mechanisms behind the pharmacokinetic changes is the rates of absorption and renal clearance and competition for plasma protein binding | Upper gastrointestinal bleeding among users of NSAIDs: a population-based cohort study in Denmark |
| Fluoxetine (54910-89-3) | Gastrointestinal Bleeding | Additive | Fluoxetine being an SSRIs can block this reuptake of serotonin by platelets leading to serotonin depletion, impairment of haemostatic function and so increase the risk of bleeding | Inhibition of serotonin reuptake by antidepressants and upper gastrointestinal bleeding in elderly patients: retrospective cohort study |
| Ibuprofen (15687-27-1) | Gastrointestinal Hemorrhage | Antagonistic | Aspirin irreversibly blocks the production of thromboxane A2 by binding to COX-1 in platelets, and so inhibits platelet aggregation. Ibuprofen also have this effect, but it is more short-lived since they bind reversibly. Therefore competitively inhibit the binding of aspirin to platelets. When Ibuprofen is present in sufficient quantit and a daily low-dose of aspirin is given, then reduce its antiplatelet effect | Effect of ibuprofen on cardioprotective effect of aspirin |
| Misoprostol (59122-46-2) | Abdominal Pain | Antagonistic | Not Established | Effect of nonsteroidal anti-inflammatory drugs on the action of misoprostol in a regimen for early abortion |
| Pentazocine (359-83-1) | Renal Papillary Necrosis | Antagonistic | Pentazocine-induced reduction in blood flow through the kidney potentiated the adverse effects of chronic aspirin use | Renal papillary necrosis caused by long-term ingestion of pentazocine and aspirin |
| Phenylbutazone (50-33-9) | Disorder Gastrointestinal | Antagonistic | Not understood | Suppression of salicylate-induced uricosuria by phenylbutazone |
| Quinidine (56-54-2) | Gastrointestinal Bleeding | Additive | The underlying mechanism is not totally understood both of which can reduce platelet aggregation, although with quinidine this antiplatelet effect usually only occurs as the result of a hypersensitivity reaction. | Cumulative effects of quinidine and aspirin on bleeding time and platelet alpha 2-adrenoceptors: potential mechanism of bleeding diathesis in patients receiving this combination |
| Methotrexate (59-05-2) | Pancytopenia | Synergistic | salicylates competitively inhibit the tubular secretion of methotrexate, which would further reduce its clearance | The effect of organic acids on renal clearance of methotrexate in man |
| Captopril (62571-86-2) | Reduced Hypertensive Efficacy Of Captopril | Antagonistic | Prostaglandins are involved in the hypotensive action of ACE inhibitors and hence, aspirin inhibits prostaglandin synthesis to antagonize effect of captopril | Effect of low-dose aspirin on thromboxane production and the antihypertensive effect of captopril |
| Valproic Acid (99-66-1) | Ataxia | Synergistic | Aspirin displaces valproate from its protein binding sites and also alters its metabolism by the liver so that the levels of free (and pharmacologically active) valproate rise | Interaction between valproic acid and aspirin in epileptic children: serum protein binding and metabolic effects |
| Valproic Acid (99-66-1) | Drowsiness | Synergistic | Aspirin displaces valproate from its protein binding sites and also alters its metabolism by the liver so that the levels of free (and pharmacologically active) valproate rise | Interaction between valproic acid and aspirin in epileptic children: serum protein binding and metabolic effects |
| Valproic Acid (99-66-1) | Nystagmus | Synergistic | Aspirin displaces valproate from its protein binding sites and also alters its metabolism by the liver so that the levels of free (and pharmacologically active) valproate rise | Interaction between valproic acid and aspirin in epileptic children: serum protein binding and metabolic effects |
| Valproic Acid (99-66-1) | Tremor | Synergistic | Aspirin displaces valproate from its protein binding sites and also alters its metabolism by the liver so that the levels of free (and pharmacologically active) valproate rise | Interaction between valproic acid and aspirin in epileptic children: serum protein binding and metabolic effects |
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Antiplatelet Effect | Integrin Alpha-IIb precursor (P08514) | Antiplatelet effect [ ADR Type 1 ] | Increased platelet aggregability associated with platelet GPIIIa PlA2 polymorphism: the Framingham Offspring Study. |
| Antiplatelet Effect | Integrin beta-3 precursor (P05106) | Antiplatelet effect [ ADR Type 1 ] | Increased platelet aggregability associated with platelet GPIIIa PlA2 polymorphism: the Framingham Offspring Study. |
| Apoptosis | Nuclear factor NF-kappa-B (P19838) | Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells [ ADR Type 1 ] | Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells |
| Apoptosis In Human Colon Cancer Cells | wild-type p53 (P00062) | Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells [ ADR Type 1 ] | Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells |
| Gastric Mucosal Microvessels Injury | Vimentin (P08670) | Vimentin fluorescence was reduced three-fold@suggesting gastric mucosal microvessels are the major target for aspirin-induced injury and arachidonic acid protection [ ADR Type 1 ] | Gastric microvascular endothelium: a major target for aspirin-induced injury and arachidonic acid protection An ultrastructural analysis in the rat |
| Haemorrhagic Erosions | Myeloperoxidase precursor (P05164) | Aspirin caused more extensive haemorrhagic erosions (33 1 (12 3) mm2) associated with greater Myeloperoxidase (MPO)activity (1887 7 (598 5) microU/mg protein) and TBARS (0 33 (0 14) nmol/mg protein) and KC/GRO concentrations (28 3 (9 5) pg/mg protein) in infected than in uninfected gerbils (13 7 (2 3); 204 0 (68 9); 0 12 (0 06); 3 1 (0 8)@ respectively) [ ADR Type 2 ] | Aspirin injury and H pylori |
| Hepatotoxicity | Esterase (P00015) | Associated with idiosyncratic hepatotoxicity. [ ADR Type 2 ] | Clinical pharmacokinetics of salicylates: a re-assessment |
| Increases Anticoagulant Effects | Cytochrome P450 1A2 (P05177) | Methyl salicylate is systemically absorbed through the skin in measurable amounts@ and may increase warfarin action by affecting vitamin K metabolism or by displacing warfarin from protein-binding sites@ which increases anticoagulant effects [ ADR Type 4 ] | Potentiation of warfarin anticoagulation associated with topical methyl salicylate |
| Inflammation | Prostaglandin E2 receptor (Q9BGL8) | Inhibition of the vasodilator prostaglandins@ prostaglandin E2 and prostacyclin@ as well as the leukotrienes@ may reduce their inflammatory effects in several disease states. [ ADR Type 1 ] | Prostaglandins and the mechanism of action of anti-inflammatory drugs |
| Inflammation | vasodilator prostaglandins (P00059) | Inhibition of the vasodilator prostaglandins, prostaglandin E2 and prostacyclin, as well as the leukotrienes, may reduce their inflammatory effects in several disease states [ ADR Type 1 ] | Prostaglandins and the mechanism of action of anti-inflammatory drugs |
| Necrosis Of Endothelial Cells | Angiopoietin-related protein (Q9BY76) | Aspirin produced significant damage to both superficial and deeper microvessels consisting of: rupture of capillary walls@ necrosis of endothelial cells@ damage to endothelial organelles@ deposition of fibrin and adherence of platelets to damaged endothelium [ ADR Type 2 ] | Gastric microvascular endothelium: a major target for aspirin-induced injury and arachidonic acid protection An ultrastructural analysis in the rat |
| Thrombotic Complications | Thromboxane A2 receptor (P21731) | Aspirin completely abolished thromboxane A2 generation by both control and uraemic platelets@exposing patients to the thrombotic complications of arteriovenous shunts [ ADR Type 2 ] | Moderate doses of aspirin and risk of bleeding in renal failure |
This panel provides drug-food interactions and their ADRs along with references
This panel provides information on metabolites and their ADRs along with references
| Metabolite | Toxicity | Place of Metabolism | Mechanism | Reference |
|---|
This panel provides information on drug category