Evidence map›Paper›PMID 32252727›Full record

ArticleBMC pulmonary medicine2020

NTP42, a novel antagonist of the thromboxane receptor, attenuates experimentally induced pulmonary arterial hypertension.

Eamon P Mulvaney, Helen M Reid, Lucia Bialesova, Annie Bouchard, Dany Salvail, B Therese Kinsella

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Evaluation ofFrontiers in pharmacology · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. The thromboxane receptor antagonistFrontiers in cardiovascular medicine · 2022
    Article
  11. Review
  12. Review
  13. 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

6 authors at 1 institution in 1 country.

Eamon P MulvaneyATXA Therapeutics Limited, UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Helen M ReidATXA Therapeutics Limited, UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Lucia BialesovaATXA Therapeutics Limited, UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Annie BouchardIPS Therapeutique Inc., 3035 Boulevard Industriel, Sherbrooke, QC, J1L 2T9, Canada.
Dany SalvailIPS Therapeutique Inc., 3035 Boulevard Industriel, Sherbrooke, QC, J1L 2T9, Canada.
B Therese KinsellaATXA Therapeutics Limited, UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland. therese.kinsella@atxatherapeutics.com.ORCID http://orcid.org/0000-0003-3072-941X
University College Dublin · IE

Funding

Enterprise Ireland CF/2012/2608Enterprise Ireland CFTD/2009/0122Horizon 2020 Framework Programme 822258
6 · The paper itself

Abstract

backgroundNTP42 is a novel antagonist of the thromboxane prostanoid receptor (TP), currently in development for the treatment of pulmonary arterial hypertension (PAH). PAH is a devastating disease with multiple pathophysiological hallmarks including excessive pulmonary vasoconstriction, vascular remodelling, inflammation, fibrosis, in situ thrombosis and right ventricular hypertrophy. Signalling through the TP, thromboxane (TX) A

methodsPAH was induced by subcutaneous injection of 60 mg/kg MCT in male Wistar-Kyoto rats. Animals were assigned into groups: 1. 'No MCT'; 2. 'MCT Only'; 3. MCT + NTP42 (0.25 mg/kg BID); 4. MCT + Sildenafil (50 mg/kg BID), and 5. MCT + Selexipag (1 mg/kg BID), where 28-day drug treatment was initiated within 24 h post-MCT.

resultsFrom haemodynamic assessments, NTP42 reduced the MCT-induced PAH, including mean pulmonary arterial pressure (mPAP) and right systolic ventricular pressure (RSVP), being at least comparable to the standard-of-care drugs Sildenafil or Selexipag in bringing about these effects. Moreover, NTP42 was superior to Sildenafil and Selexipag in significantly reducing pulmonary vascular remodelling, inflammatory mast cell infiltration and fibrosis in MCT-treated animals.

conclusionsThese findings suggest that NTP42 and antagonism of the TP signalling pathway have a relevant role in alleviating the pathophysiology of PAH, representing a novel therapeutic target with marked benefits over existing standard-of-care therapies.

Indexed as

AcetamidesAnimalsAntihypertensive AgentsDisease Models, AnimalHeart VentriclesHemodynamicsHumansHypertrophy, Right VentricularMaleMonocrotalinePulmonary Arterial HypertensionPulmonary ArteryPyrazinesRatsRats, Inbred WKYReceptors, ThromboxaneAcetamidesAntihypertensive AgentsMonocrotalinePyrazinesReceptors, ThromboxaneselexipagSildenafil CitrateMonocrotalineNTP42PAHProstanoidPulmonary arterial hypertensionThromboxaneThromboxane receptor antagonist

Identifiers

PMID32252727
PMCPMC7132963
OpenAlexW3014138887

What OpenQuestion 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 OpenQuestion graph.