Psoriasis is a chronic immune-mediated inflammatory skin disease with a multifactorial aetiology and a strong genetic predisposition. In the last two decades, a better understanding of psoriasis pathophysiology allowed the development of targeted therapies, including biologics and small molecules. As to biologics, different classes are now available including tumour necrosis factor (TNF)-α interleukin (IL)-12/23, IL-17 and IL-23 inhibitors. TNF-α inhibitors were the first biologics introduced for psoriasis treatment and include etanercept, infliximab, adalimumab and certolizumab. The class of IL-17 inhibitors encompasses secukinumab, ixekizumab, brodalumab, bimekizumab, netakimab and M1095. The novel class of IL-23 inhibitors, including guselkumab, risankizumab and tildrakizumab, bind the p19 subunit of IL-23 in order to prevent the activation of IL-23 receptor. They differ from ustekinumab as the latter antibody inhibits the p40 subunit shared by both IL-23 and IL-12. The availability of biosimilars at much lower cost compared to originators is dramatically changing the access of patients to these treatments. In the coming years, studies will progress to identify subgroups of patients based on biomarkers for a more personalized treatment approach.