IndraLab

Statements


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"In addition, tofacitinib suppressed M1 macrophage polarization via STAT1 activation after IFN-γ and lipopolysaccharide stimulation in vitro."

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"Through its ability to inhibit JAK1 activity, tofacitinib is able to block the activation of STAT3 and STAT1 downstream of IL-6 and STAT1 but not STAT4 activation downstream of IL-12 even at a high concentration of the inhibitor (500nM in vitro) [XREF_BIBR] In summary these changes are associated with a reduction in mouse Th1 and Th2 polarization and a reduction in the expression of inflammatory cytokines from both T cells and cells of the innate immune system [XREF_BIBR]."

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"Inhibition of pSTAT1 by tofacitinib accounts for the early improvement of experimental chronic synovitis."

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"Tofacitinib downregulated both p-STAT1 and p-STAT3 to control levels."

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"1muM of Ruxolitinib (JAK1/2 inhibitor) and 5muM of Tofacitinib (JAK1/3 inhibitor) suppressed the IL-27-mediated STAT-1, -3 and -5 activation (XREF_SUPPLEMENTARY) without any significant change in cell viability (data not shown)."

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"Tofacitinib was also shown to inhibit STAT1, STAT3, STAT4, STAT5 and STAT6 activation in cultured anti-CD3-stimulated T cells, which suggests that targeting the cytokine signalling pathway with TKIs may be a consideration for immunosuppression 183."

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"They demonstrated that tofacitinib significantly decreased Signal Transducer and Activator of Transcription (STAT) 3, pSTAT1, Nuclear Factor (NF) kappaBp65 and induced Suppressor of Cytokine Signaling (SOCS) 53 and Protein Inhibitor Of Activated STAT (PIAS) 3 expression in the cells and explant cultures."

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"Tofacitinib is new agent, a selective inhibitor of Janus kinase (JAK) signaling pathways mediated by JAK1 and JAK3 and inhibits the key transcription factors STAT1 and STAT3."

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"Tofacitinib could suppress M1 macrophage polarization and subsequently delay CGR by inhibiting STAT1 activation."

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"XREF_BIBR In this study, tofacitinib inhibited pSTAT1, pSTAT3 and NFkappaBp65 in PsAFLS and PsA explants, an effect that was paralleled by induction of both SOCS3 and PIAS3."

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"At the maximum oral dose tested (i.e., 60mg/kg), tofacitinib inhibited pSTAT1 elevation by 74 +/-12% (mean +/-SEM)."

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"Tofacitinib suppresses Spike protein potentiated STAT1 signaling, whereas this function was unchanged by TNFi."

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"Gao et al. [XREF_BIBR] have administered tofacitinib to synovial cells obtained from patients with psoriatic arthritis and found that tofacitinib statistically significant inhibited STAT3 and STAT1, in addition to stimulating suppressor of cytokine signaling 3 (SOCS3) and protein inhibitor of activated STAT3 (PIAS3)."

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"Tofacitinib inhibited pSTAT1 and pSTAT3, with no effect on tSTAT1 or tSTAT3 compared with DMSO control (XREF_FIG B, D), pSTAT2 was undetectable."