# Research progress in electrochemical determination of Janus kinase inhibitors and proposals for amplifying clinical applicability

**Authors:** Peter Mikus, Michal Hanko, Zuzana Zelinkova, Jan Labuda

PMC · DOI: 10.1007/s00604-026-07854-6 · 2026-02-20

## TL;DR

This paper reviews recent advances in electrochemical methods for detecting Janus kinase inhibitors, comparing them to traditional techniques and suggesting ways to improve their clinical use.

## Contribution

The paper introduces electrochemical detection of JAK inhibitors as a novel, sensitive method with potential for real-time point-of-care therapeutic drug monitoring.

## Key findings

- Electrochemical methods achieve detection limits as low as 10−9 M to 10−12 M for JAK inhibitors.
- Modified electrodes with nanomaterials and imprinted polymers enhance sensitivity and specificity.
- Electrochemical approaches show promise for real-time, personalized drug monitoring in clinical settings.

## Abstract

Janus kinase inhibitors (JAKis) represent a class of drugs that treat inflammatory and autoimmune diseases by blocking Janus kinase (JAK) enzymes. Monitoring of precise drug concentration ensures therapeutic effect while minimizing the risk of toxicity. In parallel to conventional methods based on high performance liquid chromatography, liquid chromatography − mass spectrometric or spectrometric methods, sensitive electrochemical methods for the detection of JAKis have been developed in very recent years. The procedures utilize conventional bare glassy carbon electrode or boron-doped diamond electrode and, particularly, chemically modified electrodes incorporating nanomaterials and their composites as powerful catalysts as well as imprinted polymers. The linear concentration ranges and limits of detection achieve very low 10− 9 M to 10− 12 M (µg to ng/mL) values, matching clinically relevant drug levels and are applied to analysis of biological matrices and pharmaceutical products. In this study, the concentration ranges obtained for individual JAKis are presented and compared with those of conventional methods. The manuscript covers the years 2022 to 2025 highlighting the JAKis electrochemical detection as a new topic. The paper aims to address both current trends and future potential in the development of novel sensors and procedures for the JAK inhibitors detection directed to a real-time point-of-care analysis enabling personalized therapeutic drug monitoring. Advantages and disadvantages of electrochemical approaches for the JAKis assay in clinical settings are critically evaluated. To facilitate the development of more reliable, robust and clinically applicable electrochemical methods, a few recommendations that future studies should follow are proposed.

The online version contains supplementary material available at 10.1007/s00604-026-07854-6.

## Linked entities

- **Proteins:** jak (Janus kinase)

## Full-text entities

- **Genes:** JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}, MIP (major intrinsic protein of lens fiber) [NCBI Gene 4284] {aka AQP0, CTRCT15, LIM1, MIP26, MP26}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, JAK3 (Janus kinase 3) [NCBI Gene 3718] {aka JAK-3, JAK3_HUMAN, JAKL, L-JAK, LJAK}, TYK2 (tyrosine kinase 2) [NCBI Gene 7297] {aka IMD35, JTK1}, MUC1 (mucin 1, cell surface associated) [NCBI Gene 4582] {aka ADMCKD, ADMCKD1, ADTKD2, CA 15-3, CD227, Ca15-3}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}, CPE (carboxypeptidase E) [NCBI Gene 1363] {aka BDVS, CPH, IDDHH}
- **Diseases:** Crohn's disease (MESH:D003424), cancer diseases (MESH:D009369), axial spondyloarthritis (MESH:D000089183), COVID-19 (MESH:D000086382), toxicity (MESH:D064420), juvenile idiopathic arthritis (MESH:D001171), RSD (MESH:D010262), inflammatory (MESH:D007249), myeloproliferative disorders (MESH:D009196), metastasis (MESH:D009362), rheumatoid arthritis (MESH:D001172), MOF (MESH:D013651), eczema (MESH:D004485), psoriatic arthritis (MESH:D015535), atopic dermatitis (MESH:D003876), ulcerative colitis (MESH:D003093), alopecia areata (MESH:D000506), IUPAC (MESH:D017759), autoimmune diseases (MESH:D001327), myelofibrosis (MESH:D055728)
- **Chemicals:** Ni (MESH:D009532), poly(vinyl alcohol) (MESH:D011142), MOF (MESH:D000073396), GO (MESH:C000628730), 4-aminobenzoic acid (MESH:D010129), MIPs (MESH:D000082582), 2-hydroxyethyl methacrylate (MESH:C005044), sodium sulfate (MESH:C012036), Deucravacitinib (MESH:C000628674), amino acids (MESH:D000596), nitrogen (MESH:D009584), CNTs (MESH:D037742), uric acid (MESH:D014527), acetazolamide (MESH:D000086), pyrrolopyrimidine (MESH:C527741), polyethylene glycol (MESH:D011092), Cl- (MESH:D002713), zonisamide (MESH:D000078305), selenium (MESH:D012643), Delgocitinib (MESH:C000621572), L-arginine (MESH:D001120), polymer (MESH:D011108), TOF (MESH:C479163), carbon (MESH:D002244), ND (MESH:D058612), Metal (MESH:D008670), MoS2 (MESH:C082964), CuAl2O4 (-), L-methionine (MESH:D008715), graphene (MESH:D006108), Au (MESH:D006046), momelotinib (MESH:C546012), 3-aminophenyl boronic acid (MESH:C028592), iron (II, III) oxide (MESH:D052203), Peficitinib (MESH:C000608065), K+ (MESH:D011188), proton (MESH:D011522), phosphate (MESH:D010710), acid (MESH:D000143), BR (MESH:D001966), UPA (MESH:C000613732), zinc (MESH:D015032), paracetamol (MESH:D000082), Na+ (MESH:D012964), caffeine (MESH:D002110), Pacritinib (MESH:C561234), PBS (MESH:D007854), dopamine (MESH:D004298), Oclacitinib (MESH:C588062), Ag (MESH:D012834), Fedratinib (MESH:C528327), Filgotinib (MESH:C584571), Potassium chloride (MESH:D011189), acetate (MESH:D000085), ferric oxide (MESH:C000499), RITL (MESH:C000614924), Baricitinib (MESH:C000596027), H (MESH:D006859), cellulose (MESH:D002482), MXenes (MESH:C000723374)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12923409/full.md

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Source: https://tomesphere.com/paper/PMC12923409