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Study · Animal study (in vivo) · rodents · 2016

7 results

A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor, RXFP1.

Hossain MA, Kocan M, Yao ST, Royce SG, Nair VB, Siwek C, Patil NA, Harrison IP, Rosengren KJ, Selemidis S, Summers RJ, Wade JD, Bathgate RAD, Samuel CS

Chemical science26 Feb 2016Cited by 63 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC. Results still quote short attributed sentences.

Results from this study7

7 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In rodent heart or lung disease models, B7‑33 prevented or reversed organ fibrosis with potency similar to H2 relaxin.

    In plain wordsIn rodents with heart or lung disease, B7‑33 prevented or reversed organ scarring with potency similar to H2 relaxin.

    Outcome
    DecreaseOrgan fibrosis
    Study

    rodentsn: not reported in source

    three models of heart or lung disease
    Comparator
    H2 relaxin
    Outcome group
    Lung injury and fibrosis · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, this small peptide agonist prevented or reversed organ fibrosis and dysfunction in three pre-clinical rodent models of heart or lung disease with similar potency to H2 relaxin.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rodent heart or lung disease models, B7‑33 prevented or reversed organ dysfunction with potency similar to H2 relaxin.

    In plain wordsIn rodents with heart or lung disease, B7‑33 prevented or reversed organ dysfunction with potency similar to H2 relaxin.

    Outcome
    DecreaseOrgan dysfunction
    Study

    rodentsn: not reported in source

    three models of heart or lung disease
    Comparator
    H2 relaxin
    Outcome group
    Overall treatment effect · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, this small peptide agonist prevented or reversed organ fibrosis and dysfunction in three pre-clinical rodent models of heart or lung disease with similar potency to H2 relaxin.
  3. 03AnimalAnimal study (in vivo)Safety outcome

    In vivo, B7‑33 did not promote prostate tumor growth, in contrast to H2 relaxin.

    In plain wordsIn animals, B7‑33 did not promote prostate tumor growth, in contrast to H2 relaxin.

    Outcome
    No significant changeProstate tumor growth
    Study

    n: not reported in source

    prostate tumor growth model
    Comparator
    H2 relaxin
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, in contrast to H2 relaxin, B7-33 did not promote prostate tumor growth in vivo.
  4. 04AnimalOther designMechanism

    In the reported mechanistic analysis, B7‑33 activated RXFP1-angiotensin II type 2 receptor heterodimers and downstream pERK1/2 signaling.

    In plain wordsIn preclinical tests, B7‑33 activated receptor pairs and downstream pERK signaling.

    Outcome
    IncreaseRXFP1-angiotensin receptor heterodimer signaling
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The molecular mechanism behind the strong anti-fibrotic actions of B7-33 involved its activation of RXFP1-angiotensin II type 2 receptor heterodimers that induced selective downstream signaling of pERK1/2 and the collagen-degrading enzyme, matrix metalloproteinase (MMP)-2.
  5. 05AnimalOther designMechanism

    In the reported mechanistic analysis, B7‑33 activated signaling of the collagen-degrading enzyme MMP-2.

    In plain wordsIn preclinical tests, B7‑33 activated signaling of the collagen-degrading enzyme MMP-2.

    Outcome
    IncreaseMMP-2 signaling
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The molecular mechanism behind the strong anti-fibrotic actions of B7-33 involved its activation of RXFP1-angiotensin II type 2 receptor heterodimers that induced selective downstream signaling of pERK1/2 and the collagen-degrading enzyme, matrix metalloproteinase (MMP)-2.
  6. 06LabIn vitro (cells)Activity measurement

    In cells expressing RXFP1, B7‑33 bound to RXFP1.

    In plain wordsIn cells, B7‑33 bound to the RXFP1 receptor.

    Outcome
    Not applicableRXFP1 binding
    Study

    n: not reported in source

    cells endogenously expressing RXFP1
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we report the design and synthesis of a H2 relaxin B-chain-only analogue, B7-33, which was shown to bind to RXFP1 and preferentially activate the pERK pathway over cAMP in cells that endogenously expressed RXFP1.
  7. 07LabIn vitro (cells)Mechanism

    In cells expressing RXFP1, B7‑33 preferentially activated pERK signaling over cAMP signaling.

    In plain wordsIn cells, B7‑33 activated pERK signaling preferentially over cAMP signaling.

    Outcome
    IncreasePreferential pERK signaling
    Study

    n: not reported in source

    cells endogenously expressing RXFP1
    Comparator
    cAMP signaling
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we report the design and synthesis of a H2 relaxin B-chain-only analogue, B7-33, which was shown to bind to RXFP1 and preferentially activate the pERK pathway over cAMP in cells that endogenously expressed RXFP1.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:25 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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