Evidence mapPaperPMID 29236753Full record

ArticlePloS one2017

Effects of genetic polymorphisms on the OCT1 and OCT2-mediated uptake of ranitidine.

Marleen Julia Meyer, Tina Seitz, Jürgen Brockmöller, Mladen Vassilev Tzvetkov

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Pharmacogenetics and Molecular Ancestry ofPharmaceuticals (Basel, Switzerland) · 2025
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Overview of Drug Transporters in Human Placenta.International journal of molecular sciences · 2021
    Review
  12. OCT1 Polyspecificity-Friend or Foe?Frontiers in pharmacology · 2021
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Expansion of Knowledge on OCT1 Variant ActivityFrontiers in pharmacology · 2021
    Article
  18. Article
  19. Molecular and cellular physiology of organic cation transporter 2.American journal of physiology. Renal physiology · 2019
    Review
  20. 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

4 authors at 1 institution in 1 country.

Marleen Julia MeyerInstitute of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany.
Tina SeitzInstitute of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany.
Jürgen BrockmöllerInstitute of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany.
Mladen Vassilev TzvetkovInstitute of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany.ORCID http://orcid.org/0000-0003-1670-5534
Universitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRanitidine (Zantac®) is a H2-receptor antagonist commonly used for the treatment of acid-related gastrointestinal diseases. Ranitidine was reported to be a substrate of the organic cation transporters OCT1 and OCT2. The hepatic transporter OCT1 is highly genetically variable. Twelve major alleles confer partial or complete loss of OCT1 activity. The effects of these polymorphisms are highly substrate-specific and therefore difficult to predict. The renal transporter OCT2 has a common polymorphism, Ala270Ser, which was reported to affect OCT2 activity.

aimIn this study we analyzed the effects of genetic polymorphisms in OCT1 and OCT2 on the uptake of ranitidine and on its potency to inhibit uptake of other drugs. METHODS AND

resultsWe characterized ranitidine uptake using HEK293 and CHO cells stably transfected to overexpress wild type OCT1, OCT2, or their naturally occurring allelic variants. Ranitidine was transported by wild-type OCT1 with a Km of 62.9 μM and a vmax of 1125 pmol/min/mg protein. Alleles OCT1*5, *6, *12, and *13 completely lacked ranitidine uptake. Alleles OCT1*2, *3, *4, and *10 had vmax values decreased by more than 50%. In contrast, OCT1*8 showed an increase of vmax by 25%. The effects of OCT1 alleles on ranitidine uptake strongly correlated with the effects on morphine uptake suggesting common interaction mechanisms of both drugs with OCT1. Ranitidine inhibited the OCT1-mediated uptake of metformin and morphine at clinically relevant concentrations. The inhibitory potency for morphine uptake was affected by the OCT1*2 allele. OCT2 showed only a limited uptake of ranitidine that was not significantly affected by the Ala270Ser polymorphism.

conclusionsWe confirmed ranitidine as an OCT1 substrate and demonstrated that common genetic polymorphisms in OCT1 strongly affect ranitidine uptake and modulate ranitidine's potential to cause drug-drug interactions. The effects of the frequent OCT1 polymorphisms on ranitidine pharmacokinetics in humans remain to be analyzed.

Indexed as

Polymorphism, GeneticAnimalsCHO CellsCricetulusHEK293 CellsHistamine H2 AntagonistsHumansOrganic Cation Transporter 1Organic Cation Transporter 2RanitidineHistamine H2 AntagonistsOrganic Cation Transporter 1Organic Cation Transporter 2Ranitidine

Identifiers

PMID29236753
PMCPMC5728534
OpenAlexW2773567783

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.