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. 2020 Jan 2;37(2):19. doi: 10.1007/s11095-019-2727-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Schematic representation of the proposed PK/PD model to describe changes in TNF-α plasma levels in male Wistar rats with LPS-induced endotoxemia a and PK/PD/DIS model of arthritis progression in female Lewis rats b treated with the studied compounds; Prec are the hypothetical precursors of TNF-α production a or relative paw edema b in the precursor compartments, I_max is the maximal inhibitory effect of each compound, C_p is a plasma concentration of the test compound (GRMS-55, (±)-LSF, rolipram, and additionally PTX in the case of endotoxemic rats), IC₅₀ is the concentration of each compound that produce 50% of I_max, Paw is a relative paw swelling, τ is the mean transit time, k_in is the zero-order rate constant of production of Prec, while k_in(t) is the zero-order production component of Prec, k_deg is the first-order rate constant of k_in(t) reduction, T₁-T₄ are precursors of TNF-α production a or relative paw edema b in subsequent transit compartments, k_out is the first-order rate constant of Prec degradation, and k_grow is the zero-order rate constant accounting for natural paw growth.