| Drug Name: | Gentamicin (1403-66-3) |
|---|---|
| PubChem ID: | 3467 |
| SMILES: | CC(C1CCC(C(O1)OC2C(CC(C(C2O)OC3C(C(C(CO3)(C)O)NC)O)N)N)N)NC |
| InchiKey: | CEAZRRDELHUEMR-UHFFFAOYSA-N |
| Therapeutic Category: | Anti-Bacterial Agents, Anti-Infective Agents, Enzyme Inhibitors, Protein Synthesis Inhibitors |
| Molecular Weight (dalton) | : | 477.603 |
| LogP | : | -3.3275 |
| Ring Count | : | 0 |
| Hydrogen Bond Acceptor Count | : | 12 |
| Hydrogen Bond Donor Count | : | 8 |
| Total Polar Surface Area | : | 199.73 |
This panel provides information on interacting drugs and their ADRs along with references
| Interacting drug | Toxicity | Interaction Type | Mechanism | Reference |
|---|---|---|---|---|
| Amphotericin B (1397-89-3) | Nephrotoxicity | Antagonistic | Not fully understood | Nephrotoxicity associated with combined gentamicin-amphotericin B therapy |
| Cephalothin (153-61-7) | Nephrotoxicity | Additive | Uncertain. The nephrotoxic effects of gentamicin is well documented, and some (mostly older) cephalosporins are known to be nephrotoxic, especially in high dose. However, it appears that doses that are well tolerated separately can be nephrotoxic when given together | Cephalothin plus an aminoglycoside is more nephrotoxic than methicillin plus an aminoglycoside |
| Clindamycin (18323-44-9) | Nephrotoxicity | Additive | Not known | Renal failure following gentamicin in combination with clindamycin |
| Furosemide (54-31-9) | Nephrotoxicity | Additive | Not known | Incidence of and significant risk factors for aminoglycoside-associated nephrotoxicity in patients dosed by using individualized pharmacokinetic monitoring |
| Magnesium Sulfate (7487-88-9) | Respiratory Arrest | Additive | Magnesium ions and the aminoglycosides have neuromuscular blocking activity, which can be additive it seems that it was enough to block the actions of the respiratory muscles. | Potentiation of magnesium sulfate--induced neuromuscular weakness by gentamicin, tobramycin, and amikacin |
| Piperacillin (66258-76-2) | Nephrotoxicity | Antagonistic | The nephrotoxic effects of gentamicin is well documented. The reason why piperacillin increase the risk of nephrotoxicity is not clear. One suggestion is that sodium loading may protect the kidney from tobramycin toxicity and piperacillin has only 40% as much sodium | Gentamicin inactivation by piperacillin or carbenicillin in patients with end-stage renal disease |
| Vancomycin (1404-90-6) | Nephrotoxicity | Additive | Not clear | Incidence of and significant risk factors for aminoglycoside-associated nephrotoxicity in patients dosed by using individualized pharmacokinetic monitoring |
| Cisplatin (15663-27-1) | Ototoxicity | Additives | Cisplatin is nephrotoxic and it would appear that its damaging effects on the kidney are additive with the nephrotoxic effects of the aminoglycoside antibacterials. | Aminoglycoside- and cisplatin-ototoxicity: from basic science to clinics |
| Cisplatin (15663-27-1) | Renal Toxicity | Additives | Cisplatin is nephrotoxic and it would appear that its damaging effects on the kidney are additive with the nephrotoxic effects of the aminoglycoside antibacterials. | Aminoglycoside- and cisplatin-ototoxicity: from basic science to clinics |
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Aminoglycoside Toxicity | Phospholipase A (P04054) | Gentamicin inhibited both phospholipase A and phospholipase C,which is a possible mechanism of aminoglycoside toxicity. [ ADR Type 1 ] | Inhibition of kidney lysosomal phospholipases A and C by aminoglycoside antibiotics: possible mechanism of aminoglycoside toxicity |
| Aminoglycoside Toxicity | phospholipases C (Q9NQ66) | Gentamicin inhibited both phospholipase A and phospholipase C@which is a possible mechanism of aminoglycoside toxicity. [ ADR Type 1 ] | Inhibition of kidney lysosomal phospholipases A and C by aminoglycoside antibiotics: possible mechanism of aminoglycoside toxicity |
| Consequences Upon Renal Function And Metabolism | Angiotensinase A (P42785) | Angiotensinase A significantly decreased after 3 (p [ ADR Type 1 ] | IFN-alpha is a survival factor for human myeloma cells and reduces dexamethasone-induced apoptosis |
| Consequences Upon Renal Function And Metabolism | Dipeptidylpeptidase IV (P42658) | Dipeptidylpeptidase IV activity was significantly decreased only after 6 days of treatment with gentamicin@which suggests that gentamicin-induced decrease in ectopeptidase activities could compromise vasoactive and other biologically active peptides handling@ with important consequences upon renal function and metabolism [ ADR Type 1 ] | IFN-alpha is a survival factor for human myeloma cells and reduces dexamethasone-induced apoptosis |
| Necrosis | Sodium/potassium-transporting ATPase (P05023) | Treatment with Gentamicin will cause a selective inhibition of Na@K(+)-ATPase in the proximal tubule cells@where it will produce necrosis. [ ADR Type 2 ] | Gentamicin inhibition of Na+,K(+)-ATPase in rat kidney cells |
| Nephrotoxicity | phosphatidylinositol-specific phospholipase C (P09194) | Kidney cortex cytosolic PI-PLC activity is also inhibited by gentamicin@suggesting gentamicin-induced modulation of BBM PI-PLC may be an important factor in ensuing nephrotoxicity. [ ADR Type 1 ] | Effects of aminoglycosides on proximal tubule brush border membrane phosphatidylinositol-specific phospholipase |
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