Fig. 4 Administration of BMS-986165 to mice inhibits autoimmune-relevant pharmacodynamic endpoints driven by IL-12 and IFNα. Administration of BMS-986165.

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Fig. 4 Administration of BMS-986165 to mice inhibits autoimmune-relevant pharmacodynamic endpoints driven by IL-12 and IFNα. Administration of BMS-986165 to mice inhibits autoimmune-relevant pharmacodynamic endpoints driven by IL-12 and IFNα. (A) Effect of administration of BMS-986165 by oral gavage on IFNγ in the serum of mice challenged with a combination of IL-12 and IL-18. BMS-986165 was administered by oral gavage 1 hour before intraperitoneal administration of IL-12 and a subsequent challenge with IL-18 1 hour later, with serum drawn 3 hours after the IL-18 challenge. A blocking anti-p40 antibody (10 mg/kg, sc) was included as a comparator. The data represent means ± SEM of n = 7 per group. mpk, mg/kg. (B) Effect on elevated expression of IFIT3 in blood and kidney from NZB/W mice after 2 days of treatment with BMS-986165 (PO BID) or a blocking anti-IFNAR antibody (0.5 mg per mouse, SC), with drug PK measurements (C) being obtained in separate littermate-control mice. The gene expression represents mean ± SEM of n = 5 per group and P values from one-way ANOVA with Dunnett’s posttest. (D) Impact on IFNγ-producing splenic T cells after 2 weeks of treatment with BMS-986165 (PO QD) of NZB/W lupus-prone mice, with a representative dot plot of IFNγ and IL-17 intracellular staining of live cells from a vehicle control mouse, and the results showing the dose-responsive effect of BMS-986165 on the number of IFNγ-positive cells. The results represent means ± SEM of n = 6 to 7 per group. James R. Burke et al., Sci Transl Med 2019;11:eaaw1736 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works