pe
pep-10336 v1 CC-BY-SA-4.0

Galanin: natural brain peptide that calms pain and nerve activity

A hormone made naturally in the brain and gut that damps down nerve signals, easing nerve-related pain and helping control seizures; used as a lab research tool, not an approved drug.

statusbioassayed targetGALR1 length30 aa refs9
status 5 / 5
prediction metrics openfold3-mlx 0.3.1
ipTM0.465
pTM0.686
avg pLDDT56.3
ranking score0.599
STRUCTURE · PEP-10336 × GALR1
ranking0.599
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
openfold3-mlx 0.3.1 · mmCIF ↓ download
sequence30 aa
151015202530
GWTLNSAGYLLGPHA VGNHRSFSDKNGLTS
in the news 136 articles
overview readme

What this is

Galanin is a brain and gut signaling peptide that the body makes naturally. Human galanin is 30 amino acids long and is found throughout the central and peripheral nervous system, where it dampens nerve cell activity in regions tied to pain, mood, seizures, memory, and feeding (Webling 2012). The human form differs from the rat and bovine versions in one important chemical detail — where rat and bovine galanin are 29 residues long and amidated at the C-terminus, the human peptide is 30 residues long and is not amidated (Schmidt 1991). Researchers study galanin and its receptors as potential targets for epilepsy, neuropathic pain, anxiety, and metabolic disease (Freimann 2015).

History

Galanin was first identified in 1983 from porcine intestine, and the rat and bovine forms were sequenced soon after from their cDNA. The human sequence was harder to obtain because the peptide is present at low abundance — it took Schmidt and colleagues (1991) extracting 280 postmortem human pituitaries in trifluoroacetic acid and running three successive HPLC purifications, guided by a radioreceptor assay, before they could Edman-sequence the intact peptide. They reported a 30-residue, non-amidated structure, which was confirmed in the same year by molecular cloning of the human galanin precursor (Evans 1991). A second receptor (GalR2) was cloned in 1997 (Wang 1997), and a third (GalR3) in 1998 (Smith 1998), completing the three-receptor family galanin acts through.

What it does

Galanin binds three G-protein-coupled receptors — GalR1, GalR2, and GalR3 — that are coupled mostly to inhibitory Gi/o-type G proteins. The net effect at most synapses is quieter nerve cells: galanin reduces neurotransmitter release and decreases firing in hippocampus, amygdala, and spinal cord neurons, which is why it has anticonvulsant and antinociceptive effects in animal models (Kapur 2011; Freimann 2015). In the pancreas, galanin suppresses insulin release from β cells, an effect mediated through the Gαo2 subtype of Gi/o-family G proteins (Tang 2012). The peptide also influences feeding behavior, learning and memory, and anxiety-related behaviors (Tang 2012; Webling 2012).

Mechanism

The full 30-residue human peptide (hGal 1–30) binds GalR1, GalR2, and GalR3 with low-nanomolar affinity at all three subtypes (Freimann 2015). Most signaling proceeds through Gi/o-family G proteins, lowering cAMP and modulating downstream ion channels — the canonical Gi/o pathway behind the peptide's inhibitory effects on neuronal firing (Webling 2012). The pancreatic β-cell inhibition of insulin release maps specifically onto the Gαo2 subtype rather than the broader Gαi pool, which Tang and colleagues (2012) showed using subtype-selective knockouts. The N-terminal region of galanin carries most of the receptor-binding pharmacophore: truncated fragments such as galanin(2–11) retain binding at GalR3, although with caveats about pharmacological subtype selectivity in transfected cell lines (Lu 2005).

Evidence

  • Human: Galanin's structure, distribution, and receptor pharmacology have been characterized from human tissue (Schmidt 1991; Evans 1991), and galanin-receptor pharmacology has been mapped on cloned human GalR1/2/3 (Wang 1997; Smith 1998; Freimann 2015). No published clinical trials of the native human peptide as a therapeutic.
  • Animal: Anticonvulsant effects in rodent seizure models and a role for galanin receptors in modulating seizure thresholds are reviewed in Kapur (2011). Inhibition of insulin release from pancreatic β cells via Gαo2 demonstrated in genetically modified mice (Tang 2012).
  • In vitro: Binding affinities for GalR1, GalR2, and GalR3 reported in transfected cell lines (Freimann 2015; Webling 2012). GalR3 binding by the galanin(2–11) fragment characterized in transfected lines, with the authors flagging assay-dependent limits on subtype-selectivity claims (Lu 2005).

Known effects

  • Anticonvulsant activity — Preclinical (rodent seizure models, reviewed in Kapur 2011)
  • Antinociceptive activity — Preclinical, primarily through spinal cord GalR1 (Freimann 2015)
  • Suppression of insulin release — Preclinical, Gαo2-mediated in β cells (Tang 2012)
  • Modulation of feeding and metabolism — Mechanistic / preclinical (Tang 2012; Webling 2012)
  • Effects on learning, memory, and anxiety-related behavior — Mechanistic / preclinical (Tang 2012; Webling 2012)

Regulatory status

  • US / EU: Not an approved drug. Galanin and its receptor agonists/antagonists are investigational research tools; no human therapeutic has reached approval.
  • WADA: Not specifically listed as the native peptide.

Open questions

  • Whether any galanin-receptor-selective ligand (rather than the pan-GalR native peptide) can be advanced into clinical development for epilepsy, neuropathic pain, or anxiety (Freimann 2015).
  • The degree of true pharmacological subtype selectivity of galanin fragments in vivo versus in transfected lines (Lu 2005).
  • The relative contribution of GalR1, GalR2, and GalR3 to each of galanin's many physiological effects, given heavy co-expression and overlapping signaling (Webling 2012).
Hypotheses5 directions▾ collapse

Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.

openupdated 2026-06-11

Does galanin really bind the same receptor targeted by diabetes drugs like Ozempic?

If this target annotation is wrong, researchers could avoid wasting resources on a drug design based on a false connection. If it turns out to be real, it could point to a brain peptide with untapped metabolic effects.

The hypothesis
The annotated GLP-1R target for human galanin (GWTLNSAGYLLGPHAVGNHRSFSDKNGLTS) is an artifact of sequence homology curation rather than a genuine functional interaction, and galanin does not meaningfully activate GLP-1R at physiologically relevant concentrations.
Why it’s plausible
The structure prediction ipTM of 0.46 with pLDDT 56.3 indicates low-confidence complex geometry. Galanin's N-terminal Trp-Thr-Leu motif drives GalR binding, while GLP-1R is activated by a structurally unrelated incretin peptide family. The literature snippets reference GalR1/2/3 throughout with no mention of GLP-1R co-activation, making this annotation suspect.
Why it matters
If galanin does not bind GLP-1R, metabolic disease drug programs combining galanin analogs with incretin pathways could be mis-designed. Conversely, confirming the interaction would open a dual-target agonist opportunity for obesity and type 2 diabetes.
Plausibility.85
Novelty.60
Impact.70
Basis · grounding3 computed/notes
[1]
structureipTM=0.46 and pLDDT=56.3 indicate structurally unconvincing galanin-GLP-1R complex prediction
[2]
noteReadme describes GalR1/GalR2/GalR3 as the three receptors galanin acts through, with no mention of GLP-1R
[3]
sequenceN-terminal GWTLN motif characteristic of galanin-family GalR binding lacks structural resemblance to GLP-1 incretin N-terminus
openupdated 2026-06-11

Does the brain's own galanin system break down in people with long-term nerve pain?

If chronic pain patients lose their natural galanin brake, a galanin-based treatment could restore this missing signal and relieve pain through a completely different mechanism than opioids, potentially without addiction risk.

The hypothesis
Galanin co-release with norepinephrine in locus coeruleus projections creates a built-in analgesic circuit in which galanin acts as a negative feedback brake on pain-sensitizing noradrenergic tone, and this endogenous co-transmission mechanism is blunted in chronic neuropathic pain states due to downregulation of galanin expression at injured afferents.
Why it’s plausible
Galanin is co-expressed with norepinephrine in locus coeruleus neurons and with substance P in dorsal root ganglia. In neuropathic pain, galanin expression in DRG is upregulated acutely but then dysregulated. If central noradrenergic co-release of galanin is selectively reduced in chronic pain, the loss of GalR1-mediated autoinhibition would sustain elevated norepinephrine and pain sensitization, making exogenous galanin supplementation a rational therapeutic approach.
Why it matters
Identifying a specific circuit-level deficit in galanin co-transmission during chronic pain would justify intrathecal or intranasal galanin analog delivery as a mechanism-matched treatment, distinct from opioid or NSAID pathways.
Plausibility.70
Novelty.60
Impact.65
Basis · grounding2 papers · 1 computed/note
[1]
paper
Freimann 2015 discusses galanin in pain pathways and neuropathic pain as a therapeutic target
doi: 10.1517/14728222.2015.1072513
[2]
noteReadme states galanin dampens nerve activity in regions tied to pain throughout the peripheral and central nervous system
[3]
paper
Webling 2012 describes galanin interactions with other receptor systems including those relevant to monoamine neurotransmission
doi: 10.3389/fendo.2012.00146
openupdated 2026-06-11

Could joining the active parts of two natural brain peptides create a more powerful anti-seizure candidate?

For patients with drug-resistant epilepsy, a dual-action peptide could in principle provide seizure control that neither component achieves alone, using the brain's own signaling molecules as a starting point.

The hypothesis
A bivalent galanin-neuropeptide Y chimera, linking the GalR1-binding N-terminus of galanin (residues 1-15) to the Y1R-binding C-terminus of neuropeptide Y, would simultaneously suppress hippocampal excitability through two independent inhibitory GPCR pathways and show greater anticonvulsant efficacy than either peptide alone.
Why it’s plausible
GalR1 (Gi, K+ hyperpolarization) and Y1R (Gi, inhibits cAMP) are both expressed in hippocampal interneurons and pyramidal cells. Both peptides are endogenous anticonvulsants but act through separate receptors. The modular GPCR-binding architecture of neuropeptides, where N- or C-terminal segments dictate receptor specificity, makes a chimeric linker-free fusion conceptually tractable. Galanin's N-terminus is the established driver of GalR1 binding.
Why it matters
If a galanin-NPY chimera achieves additive or synergistic hippocampal inhibition, it could be a more potent anticonvulsant than either component, useful for refractory epilepsy where single-target approaches fail.
Plausibility.55
Novelty.70
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
sequenceGWTLNSAGYLLGPH: N-terminal 14 residues include the established GalR1-binding GWTLN motif; modular design is structurally feasible
[2]
paper
Freimann 2015 discusses combination approaches and multi-target strategies in galanin therapeutic development
doi: 10.1517/14728222.2015.1072513
[3]
noteReadme identifies epilepsy as a key therapeutic area and notes three-receptor galanin system, implying multi-receptor targeting is already a concept in the field
openupdated 2026-06-11

Does the small structural difference between human and rat galanin change how the peptide behaves?

If confirmed, pain and epilepsy researchers could design modified galanin drugs that restore the missing chemical feature and test whether they outperform the natural human peptide.

The hypothesis
The non-amidated C-terminus of human galanin (ending in ...KNGLTS-OH) reduces GalR1 binding affinity relative to the amidated bovine/rat forms, and this structural difference is responsible for human-specific differences in galanin's potency at inhibiting pain and neuronal firing.
Why it’s plausible
Rat and bovine galanin are 29 aa and C-terminally amidated, while human galanin is 30 aa and lacks the amide. C-terminal amidation commonly enhances receptor affinity for neuropeptides by neutralizing the negative charge and improving receptor pocket fit. GalR1 is the primary inhibitory receptor linked to analgesia; reduced binding at GalR1 in humans could explain species differences in pain modulation.
Why it matters
Understanding whether the human peptide is intrinsically less potent at GalR1 is critical for translating animal-model pain studies to human therapy, and guides whether amidated galanin analogs would outperform the native human sequence as drug leads.
Plausibility.50
Novelty.55
Impact.55
Basis · grounding1 paper · 2 computed/notes
[1]
noteHuman galanin is 30 aa, non-amidated; rat/bovine are 29 aa and amidated at C-terminus (Schmidt 1991 cited in readme)
[2]
paper
Freimann 2015 review discusses galanin receptor pharmacology and therapeutic development context
doi: 10.1517/14728222.2015.1072513
[3]
sequenceSequence ends in KNGLTS, confirming free carboxyl terminus with no amide modification
openupdated 2026-06-11

Does the chemical difference at the tail of human galanin change how well it calms seizure activity in the brain?

If it holds, epilepsy researchers could design a galanin-based drug with the missing chemical group restored and test it for patients whose seizures resist current medications.

The hypothesis
Galanin's inhibitory effect on seizures operates primarily through GalR1-mediated hyperpolarization of hippocampal pyramidal neurons via Kir3 potassium channel coupling, and the non-amidated C-terminus of human galanin reduces this hyperpolarization magnitude compared to amidated analogs by lowering GalR1 occupancy dwell time.
Why it’s plausible
GalR1 couples to Gi/o, activating Kir3 (GIRK) channels to hyperpolarize neurons. The hippocampus is a key seizure initiation zone and expresses high GalR1. If the non-amidated human C-terminus reduces receptor residence time, the hyperpolarizing current would be shorter and less complete, providing a mechanism linking the human structural variant to its reported (but perhaps underestimated) anticonvulsant potency gap.
Why it matters
If confirmed, this mechanism would directly support developing C-terminally amidated or otherwise stabilized galanin analogs as superior anticonvulsants compared to the native human sequence, potentially benefiting drug-resistant epilepsy patients.
Plausibility.50
Novelty.50
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
noteReadme lists seizure/epilepsy as a key therapeutic area; human galanin is non-amidated unlike rat/bovine forms
[2]
paper
Freimann 2015 reviews galanin and epilepsy, including receptor-mediated inhibitory mechanisms
doi: 10.1517/14728222.2015.1072513
[3]
sequenceFull 30-aa sequence with free C-terminal Ser provides the structural basis for comparing to amidated analogs
details expand to inspect
full evidence table1 metrics
metricvaluetool
Ki 545 nM GPCRDB/ChEMBL
structural qualityopenfold3
0
metricvaluenote
gpde0.921global PDE — lower = better
disorder0.179fraction disordered
chain pair ipTM (A, B)0.465interface quality
3-letter notation
Gly-Trp-Thr-Leu-Asn-Ser-Ala-Gly-Tyr-Leu-Leu-Gly-Pro-His-Ala-Val-Gly-Asn-His-Arg-Ser-Phe-Ser-Asp-Lys-Asn-Gly-Leu-Thr-Ser
recipeopenfold3-mlx 0.3.1
parametervalue
modelopenfold3-mlx 0.3.1
weightsaedd8f3eb814e392…
hardwareapple_m4_base_16gb
mlx version0.31.1
python3.14.3
random seed42
msa strategycolabfold
diffusion samples1
runtime237s
predicted bymlx@peptide
predicted at2026-04-23
python3 openfold3/run_openfold.py predict --query_json {query.json} --runner_yaml examples/example_runner_yamls/mlx_runner.yml --output_dir {output_dir} --num_diffusion_samples 1
citationbibtex
peptidemodel (2026). Galanin: natural brain peptide that calms pain and nerve activity (pep-10336, v1). PeptideModel. https://peptidemodel.com/card/pep-10336
@peptide{pep10336,
  sequence = {GWTLNSAGYLLGPHAVGNHRSFSDKNGLTS},
  target   = {galr1},
  author   = {peptidemodel},
  year     = {2026},
  status   = {bioassayed}
}
related peptides 5 by signal overlap
clinical trials 2 on ct.gov · checked 2026-05-22
ct.gov trials 2
PubMed reviews 4
by phase
2no phase
by status
2completed
references 9 papers
[1]
Galanin receptors as a potential target for neurological disease
Freimann, K. et al. Expert Opinion on Therapeutic Targets 2015
evidence
[2]
Galanin Receptors and Ligands
Webling, K. et al. Frontiers in Endocrinology 2012
evidence
[4] evidence
[5] supporting
[7]
Cloned Human and Rat Galanin GALR3 Receptors
Smith, K. et al. Journal of Biological Chemistry 1998
supporting
[8] supporting
[9] supporting
discussion no comments
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