| Drug Name: | Cyclophosphamide (50-18-0) |
|---|---|
| PubChem ID: | 2907 |
| SMILES: | C1CNP(=O)(OC1)N(CCCl)CCCl |
| InchiKey: | CMSMOCZEIVJLDB-UHFFFAOYSA-N |
| Therapeutic Category: | Alkylating Agents, Antineoplastic Agents, Antirheumatic Agents, Immunologic Factors, Immunosuppressive Agents, Mutagens, Myeloablative Agonists, Noxae |
| Molecular Weight (dalton) | : | 261.089 |
| LogP | : | 1.884 |
| Ring Count | : | 0 |
| Hydrogen Bond Acceptor Count | : | 2 |
| Hydrogen Bond Donor Count | : | 1 |
| Total Polar Surface Area | : | 41.57 |
This panel provides information on interacting drugs and their ADRs along with references
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Bladder Inflammation | Intravesical NO donors (P00026) | The effect of NO donors is due to an inhibitory effect on bladder afferent pathways that was manifested by an increase in intercontraction interval without changes in contraction amplitude,which may be considered as a possible treatment of CYP-induced and other types of bladder inflammation [ ADR Type 5 ] | Effect of intravesical nitric oxide therapy on cyclophosphamide-induced cystitis |
| Cardiotoxicity | Troponin I (P48788) | Troponins@in particular troponin I (cTnI)@ have been found to represent a uniquely sensitive and specific marker of myocyte membrane integrity and therefore to increase in response to minimal myocardial cell damage in different settings@ including doxorubicin-induced cardiotoxicity. [ ADR Type 1 ] | Serum cardiac troponin I levels and ECG/Echo monitoring in breast cancer patients undergoing high-dose (7 g/m(2)) cyclophosphamide Bone Marrow |
| Dark Urine | Uroporphyrinogen decarboxylase (P06132) | Hepatic uroporphyrinogen decarboxylase activity is markedly reduced in patients with the disorder of porphyria cutanea tarda@ a metabolic disorder of heme biosynthesis@characterized by dark urine. [ ADR Type 1 ] | Development of porphyria cutanea tarda after treatment with cyclophosphamide |
| Effects On The Gut Immune System | IgG (P00024) | Mitogen induced secretion of IgA and IgG by Peyer#s patch cells was markedly decreased 24 hrs after drug administration,which demonstrates that a single dose cyclophosphamide can have profound effects on the gut immune system [ ADR Type 5 ] | Effect of oral vs parenteral cyclophosphamide on in vitro IgA and IgG production by murine Peyer's patches and cultured jejunal fragments |
| Excess Porphyrin | Uroporphyrinogen decarboxylase (P06132) | Hepatic uroporphyrinogen decarboxylase activity is markedly reduced in patients with the disorder of porphyria cutanea tarda@ a metabolic disorder of heme biosynthesis@characterized by distinctive pattern of excess porphyrin production. [ ADR Type 1 ] | Development of porphyria cutanea tarda after treatment with cyclophosphamide |
| Facial Hypertrichosis | Uroporphyrinogen decarboxylase (P06132) | Hepatic uroporphyrinogen decarboxylase activity is markedly reduced in patients with the disorder of porphyria cutanea tarda@ a metabolic disorder of heme biosynthesis@ characterized by facial hypertrichosis. [ ADR Type 1 ] | Development of porphyria cutanea tarda after treatment with cyclophosphamide |
| Hemolytic Anemia | Glucose-6-phosphate 1-dehydrogenase (P11413) | Contraindicated in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency because this can precipitate hemolytic anemia [ ADR Type 3 ] | Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung |
| Hyperpigmentation | Uroporphyrinogen decarboxylase (P06132) | Hepatic uroporphyrinogen decarboxylase activity is markedly reduced in patients with the disorder of porphyria cutanea tarda@ a metabolic disorder of heme biosynthesis@characterized by cutaneous hyperpigmentation [ ADR Type 1 ] | Development of porphyria cutanea tarda after treatment with cyclophosphamide |
| Lung Toxicity | Glucose-6-phosphate 1-dehydrogenase (P11413) | Significant reductions (P less than 0.005) in G6PD@ GSH-R@ and GSH-P activities occurred on days 1-5@indicating that Cyclophosphamide causes lung toxicity. [ ADR Type 2 ] | Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung |
| Lung Toxicity | Glutathione peroxidase 1 (P07203) | Significant reductions (P less than 0 005) in G6PD@ GSH-R@ and GSH-P activities occurred on days 1-5@indicating that Cyclophosphamide causes lung toxicity [ ADR Type 2 ] | Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung |
| Lung Toxicity | Glutathione reductase (P00390) | Significant reductions (P less than 0 005) in G6PD, GSH-R, and GSH-P activities occurred on days 1-5,indicating that Cyclophosphamide causes lung toxicity [ ADR Type 2 ] | Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung |
| Lung Toxicity | Superoxide dismutase (P00441) | Significant reductions (P less than 0 005) in G6PD, GSH-R, and GSH-P activities occurred on days 1-5,indicating that Cyclophosphamide causes lung toxicity [ ADR Type 2 ] | Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung |
| Profound Effects On The Gut Immune System | IgA (P00025) | Mitogen induced secretion of IgA and IgG by Peyer#s patch cells was markedly decreased 24 hrs after drug administration,which demonstrates that a single dose cyclophosphamide can have profound effects on the gut immune system. [ ADR Type 5 ] | Effect of oral vs parenteral cyclophosphamide on in vitro IgA and IgG production by murine Peyer's patches and cultured jejunal fragments |
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