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Home / Brands / Starting with V / Viccillin S / Carmustine
 
Carmustine
 

A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed)
BrandsBecenun
Bi CNU
BiCNU
Carmubris
Gliadel
Gliadel Wafer
Nitrumon
CategoriesAntineoplastic Agents
Antineoplastic Agents, Alkylating
ManufacturersEisai inc
Bristol laboratories inc div bristol myers co
PackagersBristol-Myers Squibb Co.
Eisai Inc.
Mead Johnson and Co.
MGI Pharma
SynonymsBCNU
Bischlorethylnitrosourea
Bischlorethylnitrosurea
Carmustin

indication

For the treatment of brain tumors, multiple myeloma, Hodgkin's disease and Non-Hodgkin's lymphomas.

pharmacology

Carmustine is one of the nitrosoureas indicated as palliative therapy as a single agent or in established combination therapy with other approved chemotherapeutic agents in treatment of brain tumors, multiple myeloma, Hodgkin's disease, and non-Hodgkin's lymphomas. Although it is generally agreed that carmustine alkylates DNA and RNA, it is not cross resistant with other alkylators. As with other nitrosoureas, it may also inhibit several key enzymatic processes by carbamoylation of amino acids in proteins.

mechanism of action

Carmustine causes cross-links in DNA and RNA, leading to the inhibition of DNA synthesis, RNA production and RNA translation (protein synthesis). Carmustine also binds to and modifies (carbamoylates) glutathione reductase. This leads to cell death.

toxicity

The oral LD50s in rat and mouse are 20 mg/kg and 45 mg/kg, respectively. Side effects include leukopenia, thrombocytopenia, nausea. Toxic effects include pulmonary fibrosis (20-0%) and bone marrow toxicity.

biotransformation

Hepatic and rapid with active metabolites. Metabolites may persist in the plasma for several days.

absorption

5 to 28% bioavailability

half life

15-30 minutes

route of elimination

Approximately 60% to 70% of a total dose is excreted in the urine in 96 hours and about 10% as respiratory CO2.

drug interactions

Cimetidine: Increases myelosuppression caused by carmustine

Digoxin: The antineoplasic agent decreases the effect of digoxin

Fosphenytoin: The antineoplasic agent decreases the effect of hydantoin

Leflunomide: Immunosuppressants such as carmustine may enhance the adverse/toxic effect of leflunomide. Specifically, the risk for hematologic toxicity such as pancytopenia, agranulocytosis, and/or thrombocytopenia may be increased. Consider eliminating the use of a leflunomide loading dose in patients who are receiving other immunosuppressants in order to reduce the risk for serious adverse events such as hematologic toxicity. Also, patients receiving both leflunomide and another immunosuppressive medication should be monitored for bone marrow suppression at least monthly throughout the duration of concurrent therapy.

Natalizumab: Immunosuppressants such as carmustine may enhance the adverse/toxic effect of natalizumab. Specifically, the risk of concurrent infection may be increased. Patients receiving natalizumab should not use concurrent immunosuppressants.

Phenytoin: The antineoplasic agent decreases the effect of hydantoin

Pimecrolimus: Pimecrolimus may enhance the adverse/toxic effect of immunosuppressants such as carmustine. Avoid use of pimecrolimus cream in patients receiving immunosuppressants.

Tacrolimus: Tacrolimus (Topical) may enhance the adverse/toxic effect of immunosuppressants such as carmustine. Avoid use of tacrolimus ointment in patients receiving immunosuppressants.

Trastuzumab: Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.