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database / metabolic

Leptin fragment (116-130)

preclinical metabolic metabolicendocrine sequence not characterised

Research reference only. The observations below are recorded in the cited literature. Nothing here is advice or a recommendation, and no dosing information is published on this site.

Sequence

Primary structure not characterised in the public records this index draws on. Nothing is shown rather than something invented.

Molecular data

Chemical fields come from the PubChem compound record; computed values are derived from the sequence shown above.
molecular formulanot characterised
molecular weightnot characterised
computed backbone massnot characterised
lengthnot characterised
net charge (pH 7.4)not characterised
mean hydropathynot characterised
half-lifenot characterised
delivery routenot characterised
PubChem CIDnot characterised
PDBnot characterised
UniProt parentP41159

Mechanism

Fragment of leptin investigated for metabolic signalling; primary structure varies by construct in the literature, so the field is left uncharacterised here.

Reported targets: LEPR

Experimental structure

No experimental structure of this peptide is deposited in the PDB. Nothing is rendered here — a predicted fold would not be a structure, and this site does not draw one.

Parent protein

Adipocyte-derived satiety hormone. UniProt P41159 · 167 aa

Reported effects

Each row is an outcome described in the literature indexed for this peptide. Reported in the cited work — not a claim, not a recommendation.

Reported observations and the corpus they are drawn from.
reported outcomewhere it appears
food intake modulationThe leptin fragment Lep116-130 attenuates hedonic consumption and sucrose-se… Frontiers in pharmacology 2026

Literature (6)

The leptin fragment Lep116-130 attenuates hedonic consumption and sucrose-seeking in mice — Frontiers in pharmacology 2026

BackgroundIncreased hedonic intake of palatable and high-calorie foods is one of the leading causes of obesity and is present in eating disorders. Thus, identifying new tools to manipulate hedonic intake could open new treatments for disorders of hunger and energy balance. Leptin 116-130 (Lep116-130) is a biologically active fragment of leptin, an anorectic hormone essential for controlling energy balance. Lep116-130 can reduce the intake of standard food in rodents, but its mechanism of action remains poorly understood, and whether it reduces hedonic intake has not been tested.MethodsIn silico molecular docking was performed to determine the binding of Lep116-130 to the long isoform of leptin receptor (LepRb). In vitro cellular assays were performed to determine whether Lep116-130 increased intracellular calcium levels. Behavioral feeding tests were used to characterize the intake of st…

open access ↗ · PMID 41953200 · DOI 10.3389/fphar.2026.1748508

Leptin-based hexamers facilitate memory and prevent amyloid-driven AMPA receptor internalisation and neuronal degeneration — Journal of neurochemistry 2023

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 36444683 · DOI 10.1111/jnc.15733

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin — Cerebral cortex (New York, N.Y. : 1991) 2017

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 27600840 · DOI 10.1093/cercor/bhw272

Hair cycle control by leptin as a new anagen inducer — Experimental dermatology 2014

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 24237265 · DOI 10.1111/exd.12286

The effects of human leptin fragment(126-140) on pituitary functions in man — European journal of endocrinology 2003

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 14585086 · DOI 10.1530/eje.0.1490407

Hematopoietic stem cell expansion caused by a synthetic fragment of leptin — Peptides 2013

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 24090593 · DOI 10.1016/j.peptides.2013.09.012

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