Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Determination of the binding affinity of BMS-986165 to recombinant human TYK2 pseudokinase domain.
  • Fig. S2. Relationship between potency of JAK1 pseudokinase domain biochemical binding versus a JAK1-dependent IL-2–induced reporter assay in kit225 T cells.
  • Fig. S3. Erythropoietin-induced STAT5 phosphorylation in TF-1 cells is not inhibited by BMS-986165.
  • Fig. S4. Selectivity of BMS-986165 versus JAK inhibitors in functional cellular assays.
  • Fig. S5. IFNα-induced differentiation of monocytes to antigen-presenting cells is blocked by BMS-986165.
  • Fig. S6. BMS-986165 inhibits IL-10–induced phosphorylation of STAT3 in human peripheral blood T cells and monocytes.
  • Fig. S7. BMS-986165 inhibits IFNα-induced phosphorylation of STAT1 in mouse whole blood.
  • Fig. S8. Inhibition of type I IFN–dependent gene transcription in blood and kidneys and ex vivo IFNα-induced STAT1 phosphorylation from NZB/W mice dosed with BMS-986165 by oral gavage.
  • Fig. S9. Kinetics of the inhibition of ex vivo IFNα-induced STAT1 phosphorylation from NZB/W mice dosed with BMS-986165 (30 mg/kg) by oral gavage.
  • Fig. S10. BMS-986165 (PO QD) provides protection from nephritis in NZB/W lupus-prone mice, suppresses splenic TH1 cells, and reduces kidney infiltration of B and T lymphocytes.
  • Fig. S11. PK analysis on the last day of the study in NZB/W lupus-prone mice.
  • Fig. S12. Hemoglobin, hematocrit, platelets, neutrophils, and lymphocytes were not affected by treatment with BMS-986165 in the multiple ascending dose cohorts of the phase 1 study in normal healthy volunteers.
  • Table S1. Potency of BMS-986165 and JAK inhibitors against signaling and transcriptional responses in human cellular assays.
  • Reference (50)

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