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It seems that bica actually crosses the blood-brain barrier. Following quote is from Cockshott 2004, Bicalutamide: Clinical Pharmacology and Metabolism:

Bicalutamide is a competitive and pure androgen receptor antagonist in vitro and a potent anti- androgen in vivo.[2] In laboratory animals, bicalu- tamide is a peripherally selective antiandrogen, but in man, elevations of LH, testosterone, oestradiol and, to a lesser degree, follicle-stimulating hormone have been observed.[4,7,15,92-96] From an efficacy per- spective, increases in androgens are of particular importance as the human androgen receptor binding affinity of 5α-dihydrotestosterone is approximately 100-fold higher than that of bicalutamide.[97] During daily administration of bicalutamide 10–200mg to prostate cancer patients, serum testosterone concen- trations increased to reach a plateau at between 4 and 12 weeks. However, the magnitude of the in- crease was relatively small (up to about 80%) and was independent of dose (figure 9), and mean testos- terone concentrations remained within the normal range at all dosage levels.[7] These data indicate that, in man, bicalutamide does not display the peripheral selectivity observed in rats. The observed selectivity in rats may be a consequence of its poor penetration across the blood-brain barrier,[2] as indicated by tissue distribution data,[98] whereas the lack of peripheral selectivity in man suggests that bicalutamide may be blocking androgen receptors within the hypothalamic pituitary axis.