To date, a strong link has been established between the polymorphism of the interleukin-23 (IL -23) mediator gene and the risk for the development, treatment, and outcome of various autoimmune diseases, but most of the evidence on this topic has been gathered in Crohn’s disease patients.
What is it really about?
Receptors for IL -23 on T lymphocytes bind IL -23 molecules twice as strongly, meaning that a normal concentration of IL -23 in the blood can overactive T lymphocytes, which activate another cascade that causes Crohn’s disease. Blocking this receptor may prevent another cascade that causes Crohn’s disease flare-ups.
There have been three groups of drugs approved for the treatment of Crohn’s disease:
- TNF-α antagonists, which reverse the harmful effects of TNF-α molecules
- integrin inhibitors, which prevent all leukocytes from entering the tissues and thus also “put out the fire”
- IL -antagonists. -12 and IL -23, which alone potentially act at the beginning of this inflammatory cascade.
The realization that the sensitive receptor for IL -23 is indeed the main culprit in Crohn’s disease has also led to the discovery of drugs that specifically block IL -23 receptors.
Indeed, in the early stages of the study, this group of drugs proved to be effective “joint” inhibitors of IL -12 and IL -23 in Crohn’s disease treatment, psoriasis, and psoriatic arthritis.
Now it is time for a great Phase 3 study to compare the efficacy of a selective IL -23 blocker and a dual IL -23 and IL -12 blocker.
We are pleased that Solmed and Dr. Dominik Kralj are involved in this great project.
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