ReviewClinical pharmacokinetics2026
Clinical Pharmacokinetics and Disposition of Imrecoxib.
Review in Clinical pharmacokinetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imrecoxib is a cyclooxygenase-2-preferential nonsteroidal anti-inflammatory drug approved in China for the symptomatic treatment of osteoarthritis and is currently marketed only in China. This narrative review evaluates its clinical pharmacokinetics, including disposition, special populations, drug-drug interactions, and evidence for dose adjustment. After oral administration, imrecoxib reaches peak plasma concentrations within 2-3 h, and food increases systemic exposure. It is highly protein bound and extensively metabolised sequentially from imrecoxib (M0) to 4'-hydroxymethylimrecoxib (M1), then to the aldehyde intermediate 4'-formylimrecoxib (M-CHO), and finally to 4'-carboxyimrecoxib (M2). Cytochrome P450 3A4 (CYP3A4) and cytochrome P450 2D6 (CYP2D6) mediate M1 formation, while M2 formation also involves aldehyde oxidase. Both M1 and M2 are pharmacologically active, and M2 is the predominant circulating metabolite. Unchanged urinary excretion is negligible, whereas M1, M2, and their conjugates contribute to renal elimination. Severe renal impairment markedly increases M2 exposure (area under the plasma concentration-time curve from time zero to the last measurable concentration [AUC
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42754736What 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.