Palmitoylethanolamide (PEA), a fatty acid amide‐signalling molecule has well‐known anti‐inflammatory and neuroprotective effects. Nevertheless, PEA does not possess the ability to prevent free radical formation. Polydatin (PLD), a biological precursor of resveratrol, has antioxidant activity. A combination of PEA and PLD could, conceivably, have beneficial effects on oxidative stress produced by inflammatory processes. In the present study we investigated the effects of a co‐micronized composite containing PEA and PLD (m(PEA/PLD)) in a model of testosterone‐induced benign hyperplasia (BPH).BPH was provoked in rats by daily administration of testosterone propionate (3 mg/kg) for 14 days. This protocol led to alterations in prostate morphology and increased levels of prostaglandin E2 and dihydrotestosterone as well as of 5α‐reductase 1 and 5α‐reductase 2 expression. Moreover, testosterone induced marked inflammation in terms of an increase in nuclear translocation of nuclear factor‐κB p65 and consequently in IκB‐α degradation as well as disregulation of inducible nitric oxide synthase, cyclooxygenase‐2 expression and manganese superoxide dismutase expression and in the apoptosis pathway. Our results show, for the first time, that m(PEA/PLD) is capable of decreasing prostate weight and dihydrotestosterone production in BPH‐induced rats. These effects were most likely correlated to the anti‐inflammatory and apoptotic effects of m(PEA/PLD).Accordingly, these results support the view that m(PEA/PLD) should be further studied as a potent candidate for the management of BPH.