IndraLab
Statements
Baricitinib inhibits JAK1. 122 / 131
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"Early clinical trial results of baricitinib, by itself or in combination with remdesivir, on hospitalized COVID‐19 patients, showed reduced inflammation and favorable clinical outcomes [156, 157], supporting the efficacy of JAK1/JAK2 inhibitors in resolving SARS‐CoV‐2 infection‐induced inflammation."
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"Therefore, it is likely that JAK inhibitors such as tofacitinib (a selective inhibitor of JAK1 and 3) and baricitinib (a selective inhibitor of JAK1 and 2) interupt the intracellular signaling of IL-20R ligands as well as the signaling of other members of the type I/II cytokine family (Table 1) (76)."
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"As for upadacitinib, abrocitinib is a selective oral JAK1 inhibitor recently FDA-approved for patients ≥ 18 years old with moderate-to-severe AD (163), whereas baricitinib, recently approved in Europe and Japan for the treatment of AD in adult patients (164), is an oral inhibitor of JAK1 and JAK2 with modest activity against JAK3 and TYK2."
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"From the studies conducted, various strategies that block ACE2 receptor; TMPRSS2 inhibitors like Camostat mesylate; anti-IFN-gamma drugs like Emapalumab that target STAT1; JAK1 and JAK2 inhibitors like Baricitinib, Ruxolinib that inhibit ACE2 mediated endocytosis; monoclonal antibody targeting S protein; PARPs intervening antiviral ADP ribosylation can aid in the treatment of this disease [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"38 Notably, in spite of the (partially) distinct pharmacodynamic effects of the two compounds (ie, tofacitinib predominantly inhibiting JAK1 and JAK3, baricitinib predominantly inhibiting JAK1 and JAK2), their safety profile is very similar, suggesting that the actual in vivo effects might not be predicted entirely by in vitro " selectivity " assays."
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"The success of such new molecular target drugs may have an influence on the research and development of the subsequent compounds, and further development may provide clues to advance the elucidation of the clinical characteristics of RA and provide benefits to patients as a result.Key issues * Baricitinib selectively inhibits the activation of JAK1 and JAK2."
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"Subsequently, additional JAK inhibitors, including tofacitinib (a pan JAK inhibitor with greater selectivity for JAK1/JAK3), baricitinib (BARI, a JAK1/JAK2), upadacitinib (JAK1), filgotinib (JAK1), pacritinib (JAK2), and abrocitinib (JAK1), have been approved for treating various inflammatory and autoimmune diseases, such as atopic dermatitis, psoriasis, alopecia areata, psoriatic arthritis, juvenile idiopathic arthritis, rheumatoid arthritis, ankylosing spondylitis, ulcerative colitis, and most recently, vitiligo [9,10,11]."
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"Several other agents, including sarilumab (a monoclonal antibody against IL-6Rα), ustekinumab (a monoclonal antibody targeting both IL-12 and IL-23), mavrilimumab (a human monoclonal antibody inhibiting the GM-CSF receptor), and baricitinib (inhibitor of JAK1 and JAK2 enzymes), are currently undergoing clinical investigation [21]."
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"For example, the ACTT-2 trial investigating baricitinib (small-molecule inhibitor of JAK1/JAK2 which arrests downstream immune signalling) in combination with remdesivir described 30% higher odds of improvement in clinical status at day 15 in hospitalised adults with COVID-19 [2]."
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"The use of JAK1 and JAK2 inhibitors such as ruxolitinib and baricitinib for GvHD prophylaxis may limit the need for expensive and labor-intensive ex vivo cellular manipulations 38 and may also reduce the use of broadly immunosuppressive agents that may themselves contribute to disease relapse, morbidity, and mortality after allo-HSCT."
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"As many of these molecules play a central role in the RA network, the use of agents targeting JAK inhibition allows modulation of multiple pathways simultaneously and potentially a broader effect on disease pathogenesis.Tofacitinib, the first JAKi approved (in 2012 by the FDA and in 2017 by the EMA), is a selective inhibitor of JAK1,3 with minor activity against JAK2 and TYK2, whereas baricitinib is a selective inhibitor of JAK1,2 with moderate activity against TYK2 and minimal activity against JAK3."
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"Current Food and Drug Administration (FDA) and European Medical Agency (EMA) licensed JAK inhibitors include two first-generation agents [11]; i) tofacitinib which inhibits JAK3 and JAK1 with some affinity for JAK2 and limited affinity for TYK2 and was licensed in 2012, and ii) baricitinib which inhibits JAK1 and JAK2 (and to a much lesser extent TYK2) and was licensed in 2017."
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"Baricitinib and ruxolitinib are specific inhibitors of JAK1/JAK2, a protein implicated in various cellular signals, including the pro-inflammatory IL-6, that function as immunomodulators by lowering cytotoxic T lymphocytes while increasing regulatory T cells (Modi et al., 2019; Zhang et al., 2020c)."
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"In this regard, in vitro assays using human peripheral blood mononuclear cells showed that baricitinib inhibited the signalling of several JAK1 and JAK2 dependent cytokines, including IL-6 signalling [XREF_BIBR, XREF_BIBR] and also reduced the mean change from baseline of plasma IL-6 in adult patients with active RA [XREF_BIBR]."