A drug for the treatment of rheumatoid arthritis (RA), psoriasis, inflammatory bowel disease, and other immunological diseases, as well as for the prevention of organ transplant rejection.

Trade name Xeljanz.

Oral agent with half-life 2-5 hours

Dose 5-10 mg twice daily.

An inhibitor of the enzyme Janus kinase 3 (JAK3), interfering with the JAK-STAT signaling pathway, which transmits extracellular information into the cell nucleus, influencing DNA transcription.


An orally administered selective inhibitor of Janus kinase (JAK)1  and JAK3, with functional selectivity for JAK2, that blocks intracellular transduction patheays after a Cytokine is bound to its receptor.
As a consequence, no cellular response is triggered, and cytokine production is indirectly suppressed.
Itbalso modulatesvthe action of interferons and Interleukin6, decreasing the release of cytokines by type 1 and type 17 helper T cells, implicated in the pathogenesis of acute respiratory distress syndrome.
Its action on multiple critical pathways of the inflammatory cascade may ameliorate progressive, inflammatory driven lung injury of acovid-19.

Tofacitinib is a specific inhibitor of JAK3, which blocks the activity of IL-2, IL-4, IL-15 and IL-21.

With Tofacitinib Th2 cell differentiation is blocked and therefore it is effective in treating allergic diseases.

Inhibits the production of inflammatory mediators and suppressing STAT1-dependent genes in joint tissue.

It can repair permeability defects in the gut’s epithelium in ulcerative colitis.


It has a direct effect on cells lining the gut by correcting defects that occur in inflammation. 


Increased intestinal permeability, or leakiness, is a feature of UC and promotes inflammation. 


The epithelium that lines the alimentary canal is comprised of cells that have gaps between them, making them selectively permeable and providing a barrier that keeps out pathogens: in 

UC, this epithelial permeability becomes leaky, allowing bacterial products to cross into the gut and nutrients and water to leak out.

This drug inhibits a pathway that is activated by inflammation.

UC is a chronic inflammatory bowel disease of the large intestine in which the lining of the colon becomes inflamed and leaky. 



Tofacitinib repairs inflammation-induced permeability defects.


RA is an autoimmune disease in which the body’s immune system attacks the joints.



The PTPN2, a protein-coding gene associated with autoimmune diseases such as Crohn disease, UC, and RA. 



Tofacitinib corrects the defects that occur from the loss-of-function mutations of PTPN2 without having to introduce new genes into a cell or patient.

In a monotherapy study of RA patients that did not respond to DMARD therapy the ACR score improved by at least 20% (ACR-20) in 67% of patients versus 25% who received placebo; and a study that combined the drug with methotrexate achieved ACR-20 in 59% of patients versus 35% who received methotrexate alone.

High, medium, and low doses of tofacitinib are all effective for RA patients who have an inadequate response, or intolerance, to MTX.

In naive treated RA patients tofacitinib is superior to methotrexate in reducing signs and symptoms of RA and inhibiting the progression of structural joint damage (ORAL Start Investigators).

In a psoriasis study, the PASI score improved by at at least 75% in between 25 and 67% of patients, depending on the dose, versus 2% in the placebo group.

Side effects include:increased blood cholesterol levels, neutropenia, lymphopenia, and increased creatinine.

Patients are at higher risk of opportunistic infections, tuberculosis, cancers and lymphoma.

Among patients hospitalized with Covid-19 pneumonia tofacitinib led to the fewer deaths a lower risk of respiratory failure through the 28th and placebo.
In a trial comparing combined tofacitinib with TNF inhibitor in a cardiovascular risk enriched population, the risks of major cardiovascular events and cancers was higher with tofacitinib.
Dosage 5 mg twice daily or 11 mg one daily extended release formulation.

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