| Drug Name: | Chloramphenicol (56-75-7) |
|---|---|
| PubChem ID: | 5959 |
| SMILES: | C1=CC(=CC=C1[C@H]([C@@H](CO)NC(=O)C(Cl)Cl)O)[N+](=O)[O-] |
| InchiKey: | WIIZWVCIJKGZOK-RKDXNWHRSA-N |
| Therapeutic Category: | Anti-Bacterial Agents, Anti-Infective Agents, Enzyme Inhibitors, Protein Synthesis Inhibitors |
| Molecular Weight (dalton) | : | 323.132 |
| LogP | : | 0.909 |
| Ring Count | : | 1 |
| Hydrogen Bond Acceptor Count | : | 5 |
| Hydrogen Bond Donor Count | : | 3 |
| Total Polar Surface Area | : | 112.7 |
This panel provides information on interacting drugs and their ADRs along with references
| Interacting drug | Toxicity | Interaction Type | Mechanism | Reference |
|---|---|---|---|---|
| Cyclophosphamide (50-18-0) | Reduce The Production Of The Active Metabolites Of Cyclophosphamide | Antagonistic | Chloramphenicol is an inhibitor of the cytochrome P450 isoenzyme subfamily CYP2B, which is partially responsible for the activation of cyclophosphamide | The effect of chloramphenicol and sulphaphenazole on the biotransformation of cyclophosphamide in man |
| Ampicillin (69-53-4) | Bacterial Meningitis | Antagonistic | By no means fully understood | Antibiotic antagonism in bacterial meningitis |
| Cimetidine (51481-61-9) | Aplastic Anaemia | Additive | Not known | Rapid development of aplastic anemia after intravenous chloramphenicol and cimetidine therapy |
| Cimetidine (51481-61-9) | Pancytopenia | Additive | Not known | Rapid development of aplastic anemia after intravenous chloramphenicol and cimetidine therapy |
| Phenytoin (57-41-0) | Phenytoin Toxicity | Synergistic | Chloramphenicol is a enzyme inducer affects the liver enzymes (possibly cytochrome P450 isoenzyme CYP2C1915) concerned with the metabolism of phenytoin thereby reducing its rate of clearance from the body | Chloramphenicol is a potent inhibitor of cytochrome P450 isoforms CYP2C19 and CYP3A4 in human liver microsomes |
| Warfarin (81-81-2) | International Normalized Ratio Increased | Antagonistic | chloramphenicol inhibits the liver enzymes concerned with the metabolism of the anticoagulants so that their effects are prolonged and increased In vitro work with human liver microsomes showed that chloramphenicol did not inhibit the hydroxylation of S-warfarin, but it did inhibit R-warfarin metabolism, probably via CYP3A4. antibacterial diminishes the gut bacteria thereby decreasing a source of vitamin K, but it is doubtful if these bacteria are normally an important source of the vitamin except in exceptional cases where dietary levels are very inadequate. chloramphenicol blocks production of prothrombin by the liver | Potential interaction between warfarin and ocular chloramphenicol |
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|
This panel provides drug-food interactions and their ADRs along with references
| Food | Toxicity | Reference |
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This panel provides information on metabolites and their ADRs along with references
| Metabolite | Toxicity | Place of Metabolism | Mechanism | Reference |
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This panel provides information on drug category