ArticleCPT: pharmacometrics & systems pharmacology2019
Evaluating the Role of Janus Kinase Pathways in Platelet Homeostasis Using a Systems Modeling Approach.
Article in CPT: pharmacometrics & systems pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Population pharmacokinetic-pharmacodynamic modelling of platelet time-courses following administration of abrocitinib.British journal of clinical pharmacology · 2022Trial
- Integrated Safety Analysis of Abrocitinib for the Treatment of Moderate-to-Severe Atopic Dermatitis From the Phase II and Phase III Clinical Trial Program.American journal of clinical dermatology · 2021Trial
- Kinetic-Pharmacodynamic Model of Platelet Time Course in Patients With Moderate-to-Severe Atopic Dermatitis Treated With Oral Janus Kinase 1 Inhibitor Abrocitinib.CPT: pharmacometrics & systems pharmacology · 2020Trial
- Upadacitinib enhances platelet procoagulant responses in a subset of healthy individuals and patients with SLE: a pilot study.Lupus science & medicine · 2026Article
- Comparative analysis of hematological changes in patients with rheumatoid arthritis treated with different Janus kinase inhibitors: a real-world study.Journal of rheumatic diseases · 2026Article
- Long-Term Real-World Evaluation of Abrocitinib in Moderate-to-Severe Atopic Dermatitis Across a Diverse Patient Population in a Multi-site Hospital System.American journal of clinical dermatology · 2026Observational
- Review
- Janus kinase inhibitors modify the fatty acid profile of extracellular vesicles and modulate the immune response.Heliyon · 2024Article
- Momelotinib in Myelofibrosis Patients With Thrombocytopenia: Post Hoc Analysis From Three Randomized Phase 3 Trials.HemaSphere · 2023Article
- Quantitative systems pharmacology model of thrombopoiesis and platelet life-cycle, and its application to thrombocytopenia based on chronic liver disease.CPT: pharmacometrics & systems pharmacology · 2021Article
- Janus kinase inhibitors for the therapy of atopic dermatitis.Allergologie select · 2021Review
- JAK Inhibitors in Rheumatoid Arthritis: An Evidence-Based Review on the Emerging Clinical Data.Journal of inflammation research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintaining platelet homeostasis is important to avoid spontaneous bleeding and organ damage. Thrombopoietin, the primary regulator of platelet production, is affected by and acts in part via Janus kinase (JAK)-signal transducer and activator of transcription (STAT)-mediated mechanisms. Interleukin-6 is also partly responsible for inducing thrombopoietin production via the JAK-STAT pathway. Although current understanding suggests that JAK2 is a primary mediator of platelet regulation, the emerging data show that a JAK1-specific inhibitor resulted in the modulation of platelet numbers following dosing. To gain a mechanistic understanding, a model describing platelet regulation based on known physiology and JAK-STAT pathways was built. The model provides a tool to coalesce biological understanding of platelet physiology and an in silico experimental platform to explore drug effects on platelet homeostasis. In this article, we explain the model construction and demonstrate the use of JAK-inhibitor programs as informing probes of the physiology, gaining insights on dosing paradigms that avoid platelet-related safety concerns.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.