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Study · Animal study (in vivo) · mouse · 2015

1 result

NNZ-2566, a novel analog of (1-3) IGF-1, as a potential therapeutic agent for fragile X syndrome.

Deacon RM, Glass L, Snape M, Hurley MJ, Altimiras FJ, Biekofsky RR, Cogram P

Neuromolecular medicine23 Jan 2015Cited by 55 (Europe PMC)

Summary

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Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study1

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In fmr1 knockout mice, NNZ-2566 corrected learning, memory, hyperactivity, social interaction, and macroorchidism and normalized spine density and ERK/Akt signaling.

    In plain wordsIn mice lacking fmr1, NNZ-2566 corrected learning, memory, hyperactivity, social interaction, and testicular abnormalities and normalized spine density and ERK/Akt signaling.

    Outcome
    Not applicableLearning, memory, hyperactivity, social interaction, spine density, ERK/Akt signaling, and macroorchidism
    Study

    mousen: not reported in source

    fmr1 knockout mice
    Outcome group
    Fragile X Syndrome Phenotype · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    was administered to fmr1 knockout mice correcting learning and memory deficits, abnormal hyperactivity and social interaction, normalizing aberrant dendritic spine density, overactive ERK and Akt signaling, and macroorchidism.

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

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:37 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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