The mean oral bioavailability of finasteride is approximately 65%.  Its volume of distribution is 76 L/kg.  The plasma protein binding of finasteride is 90%.  The drug has been found to cross the blood–brain barrier , whereas levels in semen were found to be undetectable.  Finasteride is extensively metabolized in the liver , first by hydroxylation via CYP3A4 and then by aldehyde dehydrogenase .  The metabolites of finasteride have about 20% of its potency in inhibiting 5α-reductase and hence its metabolites are not particularly active.  The drug has a terminal half-life of 5 to 6 hours in adult men (18–60 years of age) and a terminal half-life of 8 hours or more in elderly men (greater than 70 years of age).  It is eliminated as its metabolites 57% in the feces and 40% in the urine . 
In CombAT, after 4 years of treatment, the incidence of the composite term cardiac failure in the combination therapy group (12/1,610; %) was higher than in either monotherapy group: AVODART, 2/1,623 (%) and tamsulosin, 9/1,611 (%). Composite cardiac failure was also examined in a separate 4-year placebo-controlled trial evaluating AVODART in men at risk for development of prostate cancer. The incidence of cardiac failure in subjects taking AVODART was % (26/4,105) compared with % (15/4,126) in subjects on placebo. A majority of subjects with cardiac failure in both trials had comorbidities associated with an increased risk of cardiac failure. Therefore, the clinical significance of the numerical imbalances in cardiac failure is unknown. No causal relationship between AVODART alone or in combination with tamsulosin and cardiac failure has been established. No imbalance was observed in the incidence of overall cardiovascular adverse events in either trial.
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