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Study · Not a test of the peptide alone · 2009

9 results

Overlapping binding site for the endogenous agonist, small-molecule agonists, and ago-allosteric modulators on the ghrelin receptor.

Holst B, Frimurer TM, Mokrosinski J, Halkjaer T, Cullberg KB, Underwood CR, Schwartz TW

Molecular pharmacology15 Oct 2008Cited by 49 (Europe PMC)

PMID18923064 (opens in a new tab)DOI10.1124/mol.108.049189 (opens in a new tab)PepBankPUB-18923064
Publisher pagePubMedAsk about this study
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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: Publisher copyright. Results still quote short attributed sentences.

Results from this study9

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone9

In this study, the peptide was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking the peptide.

  1. 01LabNot a test of GHRP-6 aloneIn vitro (cells)Mechanism

    In mutant receptor assays, the six-agonist set including GHRP‑6 showed its strongest potency decrease after GluIII:09-to-Gln substitution.

    In plain wordsIn lab tests, the agonist set including GHRP‑6 showed its greatest potency decrease with the GluIII:09-to-Gln receptor change.

    Peptide
    GHRP-6
    Outcome
    DecreasePotency after GluIII:09-to-Gln substitution
    Study

    n: not reported in source

    ghrelin receptor mutants
    Comparator
    Unsubstituted receptor
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    The strongest mutational effect with respect to decrease in potency for stimulation of inositol phosphate turnover was for all six agonists the GluIII:09-to-Gln substitution in the extracellular segment of TM-III.

    In this study, GHRP-6 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking GHRP-6.

  2. 02LabNot a test of MK-677 (ibutamoren) aloneIn vitro (cells)Mechanism

    In mutant receptor assays, the six-agonist set including MK‑677 showed its strongest potency decrease after GluIII:09-to-Gln substitution.

    In plain wordsIn lab tests, the agonist set including MK‑677 showed its greatest potency decrease with the GluIII:09-to-Gln receptor change.

    Peptide
    MK-677 (ibutamoren)
    Outcome
    DecreasePotency after GluIII:09-to-Gln substitution
    Study

    n: not reported in source

    ghrelin receptor mutants
    Comparator
    Unsubstituted receptor
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    The strongest mutational effect with respect to decrease in potency for stimulation of inositol phosphate turnover was for all six agonists the GluIII:09-to-Gln substitution in the extracellular segment of TM-III.

    In this study, MK-677 (ibutamoren) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MK-677 (ibutamoren).

  3. 03LabNot a test of GHRP-6 aloneIn vitro (cells)Mechanism

    In mutant receptor assays, the six agonists including GHRP‑6 were affected by substitutions of PheVI:16, ArgVI:20 and PheVI:23.

    In plain wordsIn lab tests, receptor substitutions affected the agonist set including GHRP‑6.

    Peptide
    GHRP-6
    Outcome
    Direction not reportedResponse to TM-VI substitutions
    Study

    n: not reported in source

    ghrelin receptor mutants
    Comparator
    Unsubstituted receptor
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Likewise, all six agonists were affected by substitutions of PheVI:16, ArgVI:20, and PheVI:23 on the opposing face of transmembrane domain (TM) VI.

    In this study, GHRP-6 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking GHRP-6.

  4. 04LabNot a test of MK-677 (ibutamoren) aloneIn vitro (cells)Mechanism

    In mutant receptor assays, the six agonists including MK‑677 were affected by substitutions of PheVI:16, ArgVI:20 and PheVI:23.

    In plain wordsIn lab tests, receptor substitutions affected the agonist set including MK‑677.

    Peptide
    MK-677 (ibutamoren)
    Outcome
    Direction not reportedResponse to TM-VI substitutions
    Study

    n: not reported in source

    ghrelin receptor mutants
    Comparator
    Unsubstituted receptor
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Likewise, all six agonists were affected by substitutions of PheVI:16, ArgVI:20, and PheVI:23 on the opposing face of transmembrane domain (TM) VI.

    In this study, MK-677 (ibutamoren) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MK-677 (ibutamoren).

  5. 05LabNot a test of GHRP-6 aloneIn vitro (cells)Mechanism

    In mutant receptor assays, each agonist including GHRP‑6 was selectively affected by specific mutations.

    In plain wordsIn lab tests, specific receptor mutations selectively affected each agonist, including GHRP‑6.

    Peptide
    GHRP-6
    Outcome
    Direction not reportedSelective mutation effects
    Study

    n: not reported in source

    ghrelin receptor mutants
    Comparator
    Unsubstituted receptor
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Each of the agonists was also affected selectively by specific mutations.

    In this study, GHRP-6 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking GHRP-6.

  6. 06LabNot a test of MK-677 (ibutamoren) aloneIn vitro (cells)Mechanism

    In mutant receptor assays, each agonist including MK‑677 was selectively affected by specific mutations.

    In plain wordsIn lab tests, specific receptor mutations selectively affected each agonist, including MK‑677.

    Peptide
    MK-677 (ibutamoren)
    Outcome
    Direction not reportedSelective mutation effects
    Study

    n: not reported in source

    ghrelin receptor mutants
    Comparator
    Unsubstituted receptor
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Each of the agonists was also affected selectively by specific mutations.

    In this study, MK-677 (ibutamoren) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MK-677 (ibutamoren).

  7. 07LabNot a test of GHRP-6 aloneIn vitro (cells)Mechanism

    In receptor assays, the GHRP‑6 and L-692,429 allosteric modulation map overlapped with the common agonism map but differed from the small-molecule agonism map.

    In plain wordsIn lab tests, the GHRP‑6 and L-692,429 modulation map overlapped with the common activation map but differed from the small-molecule activation map.

    Peptide
    GHRP-6
    Outcome
    Not applicableAllosteric modulation mutational map
    Study

    n: not reported in source

    ghrelin receptor mutants
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    The mutational map of the ability of L-692,429 and GHRP-6 to act as allosteric modulators by increasing ghrelin's maximal efficacy overlapped with the common mutational map for agonism but it was not identical with the map for the agonist property of these small-molecule ligands.

    In this study, GHRP-6 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking GHRP-6.

  8. 08LabNot a test of GHRP-6 aloneIn vitro (cells)Mechanism

    In receptor assays, GHRP‑6 acted as an allosteric modulator by increasing ghrelin maximal efficacy.

    In plain wordsIn lab tests, GHRP‑6 increased the maximum receptor response to ghrelin.

    Peptide
    GHRP-6
    Outcome
    IncreaseGhrelin maximal efficacy modulation
    Study

    n: not reported in source

    ghrelin receptor mutants
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    The mutational map of the ability of L-692,429 and GHRP-6 to act as allosteric modulators by increasing ghrelin's maximal efficacy

    In this study, GHRP-6 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking GHRP-6.

  9. 09Computer modelNot a test of MK-677 (ibutamoren) aloneIn silicoMechanism

    In molecular models, low-energy conformations of nonpeptide agonists including MK‑677 could dock to satisfy many mutational hits.

    In plain wordsIn computer models, nonpeptide agonists including MK‑677 could dock in positions consistent with many mutation results.

    Peptide
    MK-677 (ibutamoren)
    Outcome
    Not applicableNonpeptide agonist docking
    Study

    n: not reported in source

    rhodopsin-based molecular receptor models
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    In molecular models, built over the inactive conformation of rhodopsin, low energy conformations of the nonpeptide agonists could be docked to satisfy many of their mutational hits.

    In this study, MK-677 (ibutamoren) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MK-677 (ibutamoren).

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 3Current

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 2

    14 Oct 2026, 01:46 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 03:13 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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