| Drug Name: | Fentanyl (437-38-7) |
|---|---|
| PubChem ID: | 3345 |
| SMILES: | CCC(=O)N(C1CCN(CC1)CCC2=CC=CC=C2)C3=CC=CC=C3 |
| InchiKey: | PJMPHNIQZUBGLI-UHFFFAOYSA-N |
| Therapeutic Category: |
| Molecular Weight (dalton) | : | 336.479 |
| LogP | : | 4.1367 |
| Ring Count | : | 2 |
| Hydrogen Bond Acceptor Count | : | 2 |
| Hydrogen Bond Donor Count | : | 0 |
| Total Polar Surface Area | : | 23.55 |
This panel provides information on interacting drugs and their ADRs along with references
| Interacting drug | Toxicity | Interaction Type | Mechanism | Reference |
|---|---|---|---|---|
| Amiodarone (1951-25-3) | Bradycardia | Antagonistic | Fentanyl is a substrate for the cytochrome P450 isoenzyme CYP3A4, and that amiodarone might inhibit CYP3A4, thereby increasing the toxicity of fentanyl | Amiodarone-induced complications during coronary artery surgery |
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Development Of Tolerance | Adenylate cyclase (Q08828) | Three-hour pretreatment of mu receptors with fentanyl and its analogs desensitized the mu receptor by uncoupling it from adenylyl cyclase@indicating that desensitization of the mu receptor may be a molecular basis for the development of tolerance to fentanyl and its analogs [ ADR Type 1 ] | Fentanyl and its analogs desensitize the cloned mu opioid receptor |
| Development Of Tolerance | Mu-Type opioid receptor (P35372) | Fentanyl and its analogs desensitize the cloned mu opioid receptor@indicate that desensitization of the mu receptor may be a molecular basis for the development of tolerance to fentanyl and its analogs. [ ADR Type 1 ] | Fentanyl and its analogs desensitize the cloned mu opioid receptor |
| Pain | Abscisic acid-inducible protein kinase (Q02066) | PKCgamma as a key element that links opioid receptor activation with the recruitment of opposite systems to opioid analgesia involved in a physiological compensatory pain enhancement [ ADR Type 2 ] | Prevention of fentanyl-induced delayed pronociceptive effects in mice lacking the protein kinase Cgamma gene |
| Pain Enhancement | Opioid growth factor receptor (Q9NZT2) | PKCgamma as a key element that links opioid receptor activation with the recruitment of opposite systems to opioid analgesia involved in a physiological compensatory pain enhancement [ ADR Type 2 ] | Prevention of fentanyl-induced delayed pronociceptive effects in mice lacking the protein kinase Cgamma gene |
This panel provides drug-food interactions and their ADRs along with references
| Food | Toxicity | Reference |
|---|---|---|
| Grapefruit Juice | Respiratory Depression | Grapefruit-medication interactions: forbidden fruit or avoidable consequences? |
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