ArticleBritish journal of clinical pharmacology2026
Modelling immune gene expression profiles as pharmacodynamic endpoints of antileishmanial treatment.
Article in British journal of clinical pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCutaneous leishmaniasis (CL), a neglected infectious disease caused by the intracellular protozoan parasite Leishmania, affects over one million people annually. The type and magnitude of the inflammatory response elicited during infection lead to skin-specific immunopathology, resulting in the clinical manifestations of CL. Systemic antileishmanial drugs are the main control measure; however, these are highly toxic, of long duration, and difficult to access for affected populations. New drugs and optimized regimens are urgently needed. Despite the known participation of immune responses in the pathology of CL, preclinical drug evaluations target parasite elimination as the efficacy measure. This overlooks the potential of host immune responses to influence therapeutic success.
methodsIn this study, we evaluated the performance of non-linear pharmacokinetic/pharmacodynamic (PK/PD) models in recreating the exposure-response relationships between plasma antimony (Sb) concentrations in CL patients treated with Glucantime (Sb
resultsA one-compartment PK model, coupled to an indirect PD model with endogenous regulators, fitted the data well, explaining 80%-90% of the variance. Our results suggest a mechanism of drug-dependent immune gene regulation involving modulation of cell signalling and RNA stability in CL patients who have been cured after treatment.
conclusionsThe model presented herein can be used for evaluating immune gene expression, alongside parasite kill, as PD endpoints of antileishmanials, both for new drug developments and in optimization of available drug regimens.
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