III-53 Divakar Budda

Prediction of CNS Target Engagement of Pain reliving Drugs in Health and Chronic Pain conditions

Divakar Budda (1), J. G. Coen van Hasselt (1), Elizabeth C.M. de Lange (1)

(1) Division of Systems Biomedicine and Pharmacology, LACDR, Leiden University, The Netherlands

Introduction: Chronic pain is a prevalent medical problem affecting 20% of Europeans [1] with an annual economic burden of approx. €300 billion [2]. Current analgesics and their combinations have shown inadequate response in ~60% of the patients in terms of efficacy or safety [1,3] The European consortium QSPainRelief (www.qspainrelief.eu) focuses on identifying new combinations of CNS active drugs [4], by the development of an in-silico QSPainRelief model platform to improve chronic pain relief and reduce side-effects.

The drug-target binding kinetics (BK) is important as it governs the magnitude, duration of effects, and side effects [5]. In the case of chronic pain, multiple studies have reported the changes in receptor availability, occupancy, and pain relief owing to their gender, age, physiological conditions, and dependent variables [6,7]. A good correlation between mu-opioid receptor agonists occupancy and analgesia has also been reported recently [8]. We intend to develop a BK model that takes into account these multiple factors and predicts target occupancy, which can be used to inform the selection of optimal dose depending on the patient-specific, disease-specific characters to achieve desired analgesia (individualized therapy).

Objectives:  We aim to develop a mathematical BK model for CNS active drugs & their combinations to predict target occupancy (engagement) in chronic pain patients with different characteristics. Here we present the initial simulation results of BK model development.

Methods: A differential equation-based BK model using drug-specific CNS target site pharmacokinetic profiles [6,7], BK parameters association rate constant (Kon), and dissociation rate constant (Koff) was developed using R package RxODE [9]. The simulations were performed under the following assumptions: constant receptor expression (1 mole; arbitrary value for simulations), in healthy conditions, and no role of endogenous ligands, non-specific binding, patient, disease-specific variables. Receptor expression differences between different brain regions were also not implemented in this model yet, assuming homogenous expression for these simulations.

Results: The BK model simulations with Kon (1.78 x 107 M-1min-1(SEM ± 0.08)), Koff (1.39 min-1(SEM ± 0.1)) [10] for morphine revealed that Kon is the major determinant of target occupancy at mu-opioid receptors (1 mole). Upon sensitivity analysis with Koff = Kon/2, target-site concentration was shown to be the determinant for target occupancy.

Conclusion: For morphine at the mu-opioid receptor, the Kon appears to be the major determining factor for mu-opioid receptor occupancy. Data about the disease- and patient-specific variables- including target expression, endogenous ligands, non-specific binding, and target turnover [11-15] is being collected, further simulation results will be presented. Future objectives are to (i) Link the predictions to drug effects via a neural circuit model, and (ii) Validate BK predictions with real-world patient treatment responses.

Funding: This project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No 848068 (https://QSPainRelief.eu/).

References:
[1] Van Hecke et al. Br J Anaesth 2013;111(1):13-18
[2] Pain Proposal: A European Consensus report 2016. Accessible at: [3] https://europeanpainfederation.eu/wp-content/uploads/2016/06/pain_proposal.pdf
[3] Elliott et al. Pain 2002;99(1-2): 299-307
[4] Gilron et al. Lancet Neurol 2013;12(11): 1084-95
[5] Yin et al. Mol Biosyst 2013;9(6):1381-89
[6] Yamamoto et al. Eur J Pharm Sci 2018;112:168-179
[7] Saleh, de Lange M, Pharmaceutics 2021;13(1), 95
[8] Takai N et al. Brain Res. 2018; 1680:105-109
[9] Wang W. CPT Pharmacometrics Syst Pharmacol. 2016
[10] Pederson MF et al. Neuropharmacology 2020;166:107718
[11] De Witte et al. Trends Pharmacol Sci 2016;37(10): 831-42
[12] De Witte et al. Eur J Pharm Sci 2017;109S: S83-89
[13] De Witte et al. Br J Pharmacol 2018;175(21): 4121-36
[14] De Witte et al. Nat Rev Drug Discov 2018;18(1): 82-84
[15] Jones et al. Eur J Pain 2004;8(5): 479-85

Reference: PAGE 29 (2021) Abstr 9622 [www.page-meeting.org/?abstract=9622]

Poster: Drug/Disease Modelling - Other Topics