| Drug Name: | Allopurinol (315-30-0) |
|---|---|
| PubChem ID: | 2094 |
| SMILES: | C1=C2C(=NC=NC2=O)NN1 |
| InchiKey: | OFCNXPDARWKPPY-UHFFFAOYSA-N |
| Therapeutic Category: | Antimetabolites, Antioxidants, Antirheumatic Agents, Enzyme Inhibitors, Free Radical Scavengers, Gout Suppressants, Noxae |
| Molecular Weight (dalton) | : | 136.114 |
| LogP | : | -0.4022 |
| Ring Count | : | 0 |
| Hydrogen Bond Acceptor Count | : | 3 |
| Hydrogen Bond Donor Count | : | 2 |
| Total Polar Surface Area | : | 74.43 |
This panel provides information on interacting drugs and their ADRs along with references
| Interacting drug | Toxicity | Interaction Type | Mechanism | Reference |
|---|---|---|---|---|
| Amoxicillin (26787-78-0) | Skin rash | Additive | Not understood. One suggestion is that the hyperuricaemia was responsible. Another is that hyperuricaemic individuals may possibly have an altered immunological reactivity | Erythema-multiforme-like eruption from amoxycillin and allopurinol |
| Carbamazepine (298-46-4) | Raise Serum Carbamazepine Levels | Synergistic | allopurinol can act as a liver enzyme inhibitor, which reduces the metabolism and clearance of carbamazepin | The effect of atovaquone on etoposide pharmacokinetics in children with acute lymphoblastic leukemia |
| Azathioprine (446-86-6) | Anaemia | Synergistic | Azathioprine is firstly metabolised in the liver to mercaptopurine and then enzymatically oxidised in the liver and intestinal wall by xanthine oxidase to an inactive compound (6-thiouric acid), which is excreted. Allopurinol inhibits first-pass metabolism by xanthine oxidase | Allopurinol-azathioprine interaction |
| Azathioprine (446-86-6) | Leucocytopenia | Synergistic | Azathioprine is firstly metabolised in the liver to mercaptopurine and then enzymatically oxidised in the liver and intestinal wall by xanthine oxidase to an inactive compound (6-thiouric acid), which is excreted. Allopurinol inhibits first-pass metabolism by xanthine oxidase | Allopurinol-azathioprine interaction |
| Azathioprine (446-86-6) | Pancytopenia | Synergistic | Azathioprine is firstly metabolised in the liver to mercaptopurine and then enzymatically oxidised in the liver and intestinal wall by xanthine oxidase to an inactive compound (6-thiouric acid), which is excreted. Allopurinol inhibits first-pass metabolism by xanthine oxidase | Allopurinol-azathioprine interaction |
| Azathioprine (446-86-6) | Thrombocytopenia | Synergistic | Azathioprine is firstly metabolised in the liver to mercaptopurine and then enzymatically oxidised in the liver and intestinal wall by xanthine oxidase to an inactive compound (6-thiouric acid), which is excreted. Allopurinol inhibits first-pass metabolism by xanthine oxidase | Allopurinol-azathioprine interaction |
| Cyclophosphamide (50-18-0) | Concentration Of The Cytotoxic Metabolites Of Cyclophosphamide Increased | Synergistic | Not understood | The pharmacokinetics of cyclophosphamide in man after treatment with allopurinol |
| Mercaptopurine (50-44-2) | Leucopenia | Antagonistic | Not clear | Hazard of combining allopurinol and thiopurine |
| Mercaptopurine (50-44-2) | Thrombocytopenia | Antagonistic | Not clear | Hazard of combining allopurinol and thiopurine |
| Phenytoin (57-41-0) | Nystagmus | Synergistic | not known | Drug interaction between phenytoin and allopurinol |
| Captopril (62571-86-2) | Hypersensitivity | Antagonistic | Not Understood | Fatal Stevens-Johnson syndrome in a patient on captopril and allopurinol |
| Captopril (62571-86-2) | Steven Johnsons Syndrome | Antagonistic | Not Understood | Fatal Stevens-Johnson syndrome in a patient on captopril and allopurinol |
| Ampicillin (69-53-4) | Skin rash | Additive | Not understood. One suggestion is that the hyperuricaemia was responsible. Another is that hyperuricaemic individuals may possibly have an altered immunological reactivity | Excess of ampicillin rashes associated with allopurinol or hyperuricemia A report from the Boston Collaborative Drug Surveillance Program, Boston University Medical Center |
| Enalapril (75847-73-3) | Myocardial Infarction | Antagonistic | Not Understood | Allopurinol and enalapril Drug induced anaphylactic coronary spasm and acute myocardial infarction |
| Pyrazinamide (98-96-4) | Hyperuricaemia | Antagonistic | pyrazinamide is hydrolysed in the body to pyrazinoic acid, which appears to be responsible for the hyperuricaemic effect of pyrazinamide. Pyrazinoic acid is oxidised by the enzyme xanthine oxidase to 5-hydroxypyrazoic acid. Since allopurinol is an inhibitor of xanthine oxidase, its presence increases pyrazinoic acid concentrations | Pharmacology of pyrazinamide: metabolic and renal function studies related to the mechanism of drug-induced urate retention |
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Acute Pure Red Cell Aplasia | Glycophorin A (P02724) | Acute pure red cell aplasia associated with allopurinol therapy.Bone marrow showed severe erythroid hypoplasia with a myeloid/erythroid ratio of 18.6 and low expression of Glycophorin A detected on cell-surface antigen analysis. [ ADR Type 2 ] | Acute pure red cell aplasia associated with allopurinol therapy |
| Intestinal Ischemia | Intercellular adhesion molecule 1 precursor (P05362) | Prereperfusion application of allopurinol and monoclonal antibody to the adhesion molecule ICAM-1 may attenuate the damage caused by intestinal ischemia and reperfusion [ ADR Type 5 ] | Effects of the anti-ICAM-1 monoclonal antibody, allopurinol, and methylene blue on intestinal reperfusion injury |
| Ischemia | Myeloperoxidase precursor (P05164) | The MPO activity was the lowest in ICAMG@ and uric acid level was significantly decreased in ALLOG compared with the other groups Methylene blue decreased TNF-alpha response to reperfusion injury but significantly increased the grade of the mucosal damage and the MPO activity [ ADR Type 5 ] | Effects of the anti-ICAM-1 monoclonal antibody, allopurinol, and methylene blue on intestinal reperfusion injury |
| Reperfusion Injury | Myeloperoxidase precursor (P05164) | The MPO activity was the lowest in ICAMG@ and uric acid level was significantly decreased in ALLOG compared with the other groups Methylene blue decreased TNF-alpha response to reperfusion injury but significantly increased the grade of the mucosal damage and the MPO activity [ ADR Type 5 ] | Effects of the anti-ICAM-1 monoclonal antibody, allopurinol, and methylene blue on intestinal reperfusion injury |
This panel provides drug-food interactions and their ADRs along with references
| Food | Toxicity | Reference |
|---|
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