Yeah, maybe they didn't go up high enough on the anti-IL-20 antibody dose for long enough, and maybe they didn't study enough subjects, but it showed no signs of working, and they dropped its development completely. They also hypothesized that maybe they needed to also block some other cytokines in that family.
This next quote from the paper is a little troubling:
"Although a preclinical study in mice transplanted with human psoriatic plaques or nonlesional psoriatic skin plus activated peripheral blood mononuclear cells showed improvement in the semiquantitative clinical psoriasis scores following treatment with an anti?IL-20 antibody, suggesting that targeting IL-20 may improve PsO symptoms in humans [24], this response is not necessarily predictive of efficacy in humans with PsO because there is no animal model specific to PsO [31]."
In any event, I'm cautiously optimistic about Prurisol results, but it could go either way. I'd feel better about Prurisol if I had some idea of how it's supposed to work. I don't think the IL-20 pathway is necessarily causative for psoriasis, as blocking it didn't show many signs of helping treat psoriasis. Anti-IL-17(A), Anti-IL-22, and Anti-TNFa show more promise.
Here's a very nice recent review article about targeting cytokines for treatment of autoimmune/inflammatory disorders:
Market Data 
Markets 
AI
