The precise mode of cytotoxic action of procarbazine has not been clearly defined. There is evidence that the drug may act by inhibition of protein, RNA and DNA synthesis. The absence of functional t-RNA could cause the cessation of protein synthesis and consequently DNA and RNA synthesis.
Procarbazine is metabolized primarily in the liver and kidneys.
The drug appears to be auto-oxidized to the azo derivative with the release of hydrogen peroxide. The azo derivative isomerizes to the hydrazone, and following hydrolysis splits into a benzylaldehyde derivative and methylhydrazine. The methylhydrazine is further degraded to CO 2 and CH 4 and possibly hydrazine, whereas the aldehyde is oxidized to N-isopropylterephthalamic acid, which is excreted in the urine. Procarbazine is rapidly and completely absorbed. Following oral administration of 30 mg of 14 C-labeled procarbazine, maximum peak plasma radioactive concentrations were reached within 60 minutes.