Evidence map›Paper›PMID 20361239›Full record

ArticleJournal of computer-aided molecular design2010

Using a homology model of cytochrome P450 2D6 to predict substrate site of metabolism.

Rayomand J Unwalla, Jason B Cross, Sumeet Salaniwal, Adam D Shilling, Louis Leung, John Kao, Christine Humblet

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Article in Journal of computer-aided molecular design, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
7.7field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 38 citations in OpenAlex.

  1. BioMed research international · 2021
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Protein modeling: what happened to the "protein structure gap"?Structure (London, England : 1993) · 2013
    Review
  7. Article
  8. Article
  9. Review
  10. IDSite: An accurate approach to predict P450-mediated drug metabolism.Journal of chemical theory and computation · 2011
    Article
  11. Comparison of the inhibitory profiles of itraconazole and cimetidine in cytochrome P450 3A4 genetic variants.Drug metabolism and disposition: the biological fate of chemicals · 2011
    Article
  12. Review
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

7 authors at 4 institutions in 2 countries.

Rayomand J UnwallaChemical Sciences, Wyeth Research, S-2421, 500 Arcola Road, Collegeville, PA 19426, USA. unwallr@wyeth.com
Jason B Cross
Sumeet Salaniwal
Adam D Shilling
Louis Leung
John Kao
Christine Humblet
McPhee Research (United States) · USWomen's Health Research Institute · CAPfizer (United States) · USPrinceton University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CYP2D6 is an important enzyme that is involved in first pass metabolism and is responsible for metabolizing ~25% of currently marketed drugs. A homology model of CYP2D6 was built using X-ray structures of ligand-bound CYP2C5 complexes as templates. This homology model was used in docking studies to rationalize and predict the site of metabolism of known CYP2D6 substrates. While the homology model was generally found to be in good agreement with the recently solved apo (ligand-free) X-ray structure of CYP2D6, significant differences between the structures were observed in the B' and F-G helical region. These structural differences are similar to those observed between ligand-free and ligand-bound structures of other CYPs and suggest that these conformational changes result from induced-fit adaptations upon ligand binding. By docking to the homology model using Glide, it was possible to identify the correct site of metabolism for a set of 16 CYP2D6 substrates 85% of the time when the 5 top scoring poses were examined. On the other hand, docking to the apo CYP2D6 X-ray structure led to a loss in accuracy in predicting the sites of metabolism for many of the CYP2D6 substrates considered in this study. These results demonstrate the importance of describing substrate-induced conformational changes that occur upon binding. The best results were obtained using Glide SP with van der Waals scaling set to 0.8 for both the receptor and ligand atoms. A discussion of putative binding modes that explain the distribution of metabolic sites for substrates, as well as a relationship between the number of metabolic sites and substrate size, are also presented. In addition, analysis of these binding modes enabled us to rationalize the typical hydroxylation and O-demethylation reactions catalyzed by CYP2D6 as well as the less common N-dealkylation.

Indexed as

Models, ChemicalAmino Acid SequenceBinding SitesCrystallography, X-RayCytochrome P-450 CYP2D6HumansMolecular Dynamics SimulationMolecular Sequence DataProtein BindingProtein ConformationSubstrate SpecificityCytochrome P-450 CYP2D6

Identifiers

PMID20361239
OpenAlexW1992854159

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Registered trials

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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.