Search bioRxiv⌕ Search

bioRxiv · 10.1101/2021.01.21.427533

Predicting transdermal fentanyl delivery using physics-based simulations for tailored therapy

Abstract

Transdermal fentanyl patches are an effective alternative to the sustained-release of oral morphine for chronic pain treatment. Due to the narrow therapeutic range of fentanyl, the fentanyl concentration in the blood needs to be controlled carefully. Only then, effective pain relief can be reached while avoiding adverse effects such as respiratory depression. In this study, a physics-based digital twin of the patient was developed by implementing mechanistic models for transdermal drug uptake and the patients pharmacokinetic and pharmacodynamics response. A digital twin is a virtual representation of the patient and the transdermal drug delivery system, which is linked to the real-world patient by patient feedback, sensor data of specific biomarkers, or customizing the twin to a particular patient characteristic, for example, based on the age. This digital twin can predict the transdermal drug delivery processes in-silico. Our twin is used first to predict conventional therapys effect for using fentanyl patches on a virtual patient at different ages. The results show that by aging, the maximum transdermal fentanyl flux and maximum concentration of fentanyl in the blood decrease by 11.4% and 7.0%, respectively. Nonetheless, by aging, the pain relief increases by 45.2% despite the lower concentration of fentanyl in the blood for older patients. As a next step, the digital twin was used to propose a tailored therapy, based on the patients age, to deliver fentanyl based on the patients needs to alleviate pain. This predesigned therapy consisted of customizing the duration of applying and changing the commercialized fentanyl patches based on the calculated pain intensity. According to this therapy, a patient of 20 years old needs to change the patch 2.1 times more frequently compared to conventional therapy, which led to 30% more pain relief and 315% more time without pain. In addition, the digital twin was updated by the patients pain intensity feedback. Such therapy led to an increase in the patients breathing rate while having effective pain relief, therefore providing a safer and more comfortable treatment for the patient. We quantified the added value of a patients physics-based digital twin and sketched the future roadmap for implementing such twin-assisted treatment into the clinics. NomenclatureO_ST_ABSSymbolsC_ST_ABSci The concentration of fentanyl in layer i (in the drug uptake model) [ng ml-1] cp The concentration of fentanyl in the central compartment [ng ml-1] cr The concentration of fentanyl in the rapid equilibrated compartment [ng ml-1] cs The concentration of fentanyl in the slow equilibrated compartment [ng ml-1] cg The concentration of fentanyl in the gastrointestinal compartment [ng ml-1] cl The concentration of fentanyl in the hepatic compartment [ng ml-1] ce The concentration of fentanyl in the effect compartment [ng ml-1] Di Diffusion coefficient of fentanyl in layer i (in the mechanistic model) [m2 s-1] D0 Base diffusion coefficient of fentanyl [m2 s-1] DT Diffusion coefficient of fentanyl at temperature T [m2 s-1] D306 Diffusion coefficient of fentanyl at 306[K] [m2 s-1] dpt The thickness of the transdermal patch [{micro}m] dsc The thickness of the stratum corneum [{micro}m] dvep The thickness of the viable epidermis [{micro}m] dEdm The thickness of the equivalent dermis [{micro}m] Ei The intensity of effect i [Formula]The baseline of effect i [Formula]The maximum effect i EC50,i The concentration related to half-maximum effect i [ng ml-1] fu The fraction of unbound fentanyl in plasma ji Fentanyl flux in layer i (in the mechanistic model) Ki/j The partition coefficient of fentanyl between layer i to j (in the mechanistic model) Ki The drug capacity in layer i (in the mechanistic model) kcs Inter-compartmental first-order equilibrium rate constant (central to slow equilibrated) [min-1] kcr Inter-compartmental first-order equilibrium rate constant (central to rapid equilibrated) [min-1] kcg Inter-compartmental first-order equilibrium rate constant (central to gastrointestinal) [min-1] kch Inter-compartmental first-order equilibrium rate constant (central to hepatic) [min-1] ksc Inter-compartmental first-order equilibrium rate constant (slow equilibrated to central) [min-1] krc Inter-compartmental first-order equilibrium rate constant (rapid equilibrated to central) [min-1] khc Inter-compartmental first-order equilibrium rate constant (hepatic to central) [min-1] kgh Inter-compartmental first-order equilibrium rate constant (gastrointestinal to hepatic) [min-1] kmet Metabolization rate constant [min-1] kre Renal clearance rate constant [min-1] ke Inter-compartmental first-order equilibrium rate constant (for effect compartment) [min-1] SI Sensitivity index t Time [h] tD Time lag [h] [Formula]Dependent variable related to xi for sensitivity analysis Vc The apparent volume of the central compartment [L] Vs The apparent volume of the slow equilibrated compartment [L] Vr The apparent volume of the rapid equilibrated compartment [L] Vg The apparent volume of the gastrointestinal compartment [L] Vh The apparent volume of the hepatic compartment [L] xi The independent variable which sensitivity analysis is done based on it {gamma}Hill coefficient {psi}i Drug potential in domain i [ng ml-1]

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Bahrami, F., Rossi, R. M., Defraeye, T.. 2021-01-21. Predicting transdermal fentanyl delivery using physics-based simulations for tailored therapy. https://doi.org/10.1101/2021.01.21.427533

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

PCB-Exposed Gut Microbiota Recapitulate Neurobehavioral Deficits and Reprogram Hippocampal Transcriptomic Signatures

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants associated with developmental neurotoxicity and autism spectrum disorder (ASD). However, whether PCB-induced alterations in gut microbiota contribute to neurodevelopmental toxicity independently of direct chemical exposure remains unclear. Here, we investigated whether transplantation of PCB-associated gut microbiota produces early neurobehavioral alterations and disrupts brain molecular pathways in offspring. Gut microbiota from conventional dams exposed to the Fox River PCB mixture (FRM; 6.0 mg/kg/day) or vehicle were transplanted into germ-free recipient females without direct PCB administration. At postnatal day 7 (P7), offspring underwent ultrasonic vocalization (USV) testing, whole-brain RNA sequencing (n = 4/sex/group), and untargeted serum metabolomics. Untargeted serum metabolomics were also performed in donor dams. PCB-associated fecal microbiota transplantation (FMT) significantly reduced offspring USVs, reproducing effects observed following direct maternal PCB exposure. Brain transcriptomics in offspring identified substantially more differentially expressed genes in males (9,339) than females (1,082), including 512 shared genes. Concordantly regulated genes revealed downregulation of neurotransmitter signaling and ion channel pathways alongside upregulation of RNA processing pathways. Male-associated responses involved altered protein synthesis and neuronal signaling, whereas female-associated responses involved DNA repair and extracellular matrix remodeling. Despite these molecular differences, behavioral responses showed no significant sex-dependent effect. Maternal metabolomics revealed increased bile acids and decreased indole-3-propionic acid, highlighting potential AhR-NF{kappa}B and bile acid-associated signaling mechanisms. Offspring metabolomics further identified alterations in lipid-associated metabolites and metabolic profiles. Collectively, these findings show that transferring PCB-exposed microbiota reproduces early neurobehavioral alterations and induces shared and sex-biased molecular responses, identifying the maternal gut microbiome as a candidate mediator linking PCB exposure to developmental neurotoxicity.

pharmacology and toxicology↗

Cisplatin-triggered sensory dysfunction in NER-defective C. elegans involves GABAergic and cholinergic signaling

Cisplatin (CisPt) is a widely used anticancer drug that causes neurotoxicity as a dose-limiting adverse effect. DNA damage contributes to CisPt-induced neurotoxicity, yet the molecular mechanisms involved remain unclear. Here, we aim to identify pathophysiological mechanisms contributing to DNA damage-driven development of sensory neuronal dysfunction using the 3R-compliant model organism Caenorhabditis elegans. To this end, we employed the nucleotide excision repair (NER)-deficient ercc-1 mutant, which shows enhanced CisPt-induced sensory dysfunction as monitored by the chemotaxis assay, to elucidate drug-induced alterations in neurotransmission and transcriptome. We found that CisPt reduces gamma-aminobutyric acid (GABA) levels in the nematode and that GABA supplementation rescues ercc-1 mutants from CisPt-evoked sensory neurotoxicity, pointing to a neuroprotective function of GABA in the context of our study. Moreover, CisPt impairs the morphological integrity of GABAergic neurons particularly in ercc-1 mutants, which again is rescued by GABA substitution. Conversely, the cholinergic agonist carbachol impairs sensory function and exacerbates the neurotoxic effects of CisPt in ercc-1 mutants, indicating detrimental effects resulting from cholinergic excitation. Transcriptome analysis revealed that CisPt treatment stimulates a broard transcriptional response, including pathways involved in the regulation of neuronal communication, including acetylcholine-mediated neurotransmission, with pronounced effects occurring in the absence of ERCC-1. Based on these finding we suggest impaired GABAergic signaling and the loss of neuronal integrity GABAergic neurons as well as excessive cholinergic excitation as key mechanisms linking CisPt-induced DNA damage in NER defective nematodes to sensory dysfunction. Hence, targeting the balance between GABAergic inhibition and cholinergic excitation is suggested to counteract sensory neurotoxicity triggered by CisPt.

pharmacology and toxicology↗

Mathematical model of phenotypic plasticity predicts interconversion is a drug target for neuroblastoma.

Neuroblastoma is a paediatric cancer arising from the sympathetic nervous system as neural crest cells, made up of noradrenergic (NOR/ADRN/N), mesenchymal like (MES/S), and intermediate (I-type/I) cell types. These cells can interconvert between types, contributing to treatment resistance and relapse. We developed a mathematical model to investigate how interconversion patterns affect the efficacy of phenotype-specific inhibitors. We used three ordinary differential equations to describe the dynamics of the three populations, including logistic growth, interconversion, and drug-induced death. Of the 64 possible interconversion patterns, five reduced the target population: two for N cells and three for S cells. N targeting patterns were more effective with higher interconversion rates, while mesenchymal targeting patterns were more effective with lower interconversion rates. Stability analysis revealed that natural tumour growth was always unstable, but during treatment, N-suppressing patterns combined with an S inhibitor gave the most consistently stable origin. Testing multi-stage and cyclic treatment schedules revealed that N-suppressing patterns with an S inhibitor, followed by an S-suppressing pattern with an N inhibitor, achieved more reliable remission. Three of the five patterns of interest correspond to reported biological plausibility, and known compounds exist to induce most of the required transitions, supporting the clinical relevance of these strategies for improving neuroblastoma treatment outcomes.

pharmacology and toxicology↗