Evidence map›Paper›PMID 37902256›Full record

ArticlePharmacology research & perspectives2023

The roles of CYP2C19 and CYP3A4 in the in vitro metabolism of β-eudesmol in human liver: Reaction phenotyping and enzyme kinetics.

Nadda Muhamad, Kesara Na-Bangchang

Open access · goldAbstract read
In one paragraph

Article in Pharmacology research & perspectives, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Nadda MuhamadGraduate Studies, Chulabhorn International College of Medicine, Thammasat University, Pathumthani, Thailand.ORCID 0000-0002-0954-9687
Kesara Na-BangchangGraduate Studies, Chulabhorn International College of Medicine, Thammasat University, Pathumthani, Thailand.ORCID 0000-0001-6389-0897
Thammasat University · TH

Funding

Center of Excellence in Pharmacology and Molecular Biology of Malaria and CholangiocarcinomaThailand Science Research and Innovation Fundamental FundThammasat University Research Fund TUFT-FF 48/2565The Thailand Research Fund under the Royal Golden Jubilee Ph.D. Program PHD/0095/2561
6 · The paper itself

Abstract

β-eudesmol is a major bioactive component of Atractylodes lancea (AL). AL has been developed as the capsule formulation of standardized AL extract for treating cholangiocarcinoma (CCA). However, the complex constituents of herbal products increase the risk of adverse drug interactions. β-eudesmol has demonstrated inhibitory effects on rCYP2C19 and rCYP3A4 in the previous research. This study aimed to identify the cytochrome P450 (CYP) isoforms responsible for the metabolism of β-eudesmol and determine the enzyme kinetic parameters and the metabolic stability of β-eudesmol metabolism in the microsomal system. Reaction phenotyping using human recombinant CYPs (rCYPs) and selective chemical inhibitors of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 was performed, and enzyme kinetics and metabolic stability were investigated using human liver microsome (HLM). The results suggest that CYP2C19 and CYP3A4 play significant roles in β-eudesmol metabolism. The disappearance half-life (t

Indexed as

Cytochrome P-450 CYP3ACytochrome P-450 Enzyme SystemCytochrome P-450 CYP2C19HumansKineticsLiverMicrosomes, LiverSesquiterpenes, Eudesmanebeta-eudesmolCYP2C19 protein, humanCYP3A4 protein, humanCytochrome P-450 CYP2C19Cytochrome P-450 CYP3ACytochrome P-450 Enzyme SystemSesquiterpenes, EudesmaneAtractylodes lancea (Thunb.) DCcytochrome P450drug metabolismenzyme kineticsreaction phenotypingβ-eudesmol

Identifiers

PMID37902256
PMCPMC10614204
OpenAlexW4388021690

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.