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Risankizumab also known as BI-655066 is a humanized monoclonal antibody targeting interleukin 23A (IL-23A). Risankizumab is part of a collaboration between Boehringer Ingelheim and AbbVie. The therapeutic potential of risankizumab is being evaluated in immunological disorders, including Crohn's disease, psoriasis, psoriatic arthritis, and asthma.
In phase II clinical drug trials, thirty-nine patients received single-dose Risankizumab, 18 of which received the drug intravenously, 13 subcutaneously, and 8 received the placebo drug. There were several instances that adverse effects occurred but in the same frequency for the placebo and the experimental groups. Four considerably serious adverse events occurred, but it was determined that they were not treatment related, in the Risankizumab treated patients. Risankizumab was associated with clinical improvement in individuals treated with the drug, from week 2 and maintained for up to 66 weeks after treatment. At week 12 of treatment, 75%, 90%, and 100% decreases in the psoriasis area and Severity Index were achieved by 87%, 58%, and 16% of Risankizumab treated patients, regardless of dose, respectively, versus individuals receiving placebo. Significant correlation between treatment-associated molecular changes and psoriasis area and severity index improvement was observed (r = 0.73, P = 2 × 10(-6)). The conclusion of this clinical drug trial was that Risankizumab was very well tolerated and associated with quick, significant, and long-lasting clinical improvement in patients with moderate-to-severe psoriasis, supporting a central role for IL-23 in psoriasis pathogenesis.
The IL23/IL17 axis plays an important role in the development of chronic inflammation, with potential genetic links between the IL23 receptor (IL23R) or its ligand identified in inflammatory diseases such as psoriasis, inflammatory bowel disease, and graft-versus-host disease. Signaling through the IL23R induces Janus kinase 2 (JAK2) and tyrosine kinase 2 (tyk2) phosphorylation and leads to increased levels of the inflammatory cytokines IL17 and IL22. Risankizumab binds to the p19 sub-unit of IL23, IL23A, preventing receptor activation and thereby disrupting the IL23/IL17 axis.
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