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Current treatment strategies are not specific to PV pathophysiology and although life\u2010saving, harbour considerable side effects. We aimed to systematically assess the molecules amenable to targeted treatments that follow Ab binding and are associated with PV acantholysis. The resulting scoping review was conducted under PRISMA\u2010ScR guidelines with clear inclusion and exclusion criteria and focused specifically on kinases, caspases, proteases, hydrolytic enzymes and other molecules of interest postulated to take part in the pathophysiology of PV. The review process resulted in the identification of 882 articles, of which 56 were eligible for qualitative synthesis. From the included articles, the majority (<jats:italic>n<\/jats:italic>\u00a0=\u00a042) used PV\u2010IgG as the pathogenic agent, mainly via in vitro (<jats:italic>n<\/jats:italic>\u00a0=\u00a016) and in vivo (<jats:italic>n<\/jats:italic>\u00a0=\u00a010) models. Twenty\u2010five molecules were found to play a pathogenic role in PV, including uPA, ADAM10, EGFR, Src, PKC, cdk2, ERK, PLC, calmodulin, NOS, p38MAPK and caspase\u20103. Selective inhibition of these molecules resulted in varying degrees of reduction in acantholysis and blistering. 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