Crohns disease (CD) and ulcerative colitis (UC) belong to chronic inflammatory 
bowel diseases, which are induced by autoimmune processes. While CD is 
characterized by over-activity of Th1, ILC1, and MAIT cells, UC is mediated by 
exaggerated activities of Th2 and ILC2 cells and cytokines they produce. 
Knowledge of the pathogenesis enabled a rational therapy based mostly on 
biologics and small molecules. TNF is the principal proinflammatory cytokine in 
both diseases. Anti-TNF monoclonal antibodies, mostly infliximab or adalimumab 
were therefore introduced to their treatment. Approximately 50-70 % of CD and 
more than 33 % of UC patients respond to primary treatment only, which resulted 
in the development of other biologics and small molecules. Out of them, 
monoclonal antibodies targeting adhesive molecules (vedolizumab, etrolizumab) 
and p40 chains shared by IL12 and IL23 (ustekinumab) have been already in 
clinical practice. There are also other small molecules in clinical trials: 
mongersen, tafacitinib, and ozanimod. Mongersen supports immunosuppressive 
activity of TGFβ; it has been tried for the treatment of CD. Tofacitinib 
inhibits activity of JAK kinases; it was shown to be effective in UC management. 
Ozanimod interferes with migrations of activated T cells to the site of 
inflammation and is a promising drug for the UC treatment.Key words: Crohns 
disease - mongersen - monoclonal antibodies - ozanimod - tofacitinib - 
ulcerative colitis.