pe
pep-10541 v1 CC-BY-SA-4.0

Kisspeptin-2: fish reproductive-signaling peptide (FNFNPFGLRF)

A natural fish hormone that triggers the release of reproductive hormones in fish; not found in humans and used only as a lab research tool.

statussynthesized targetKISS1R length10 aa refs4
status 4 / 5
prediction metrics boltz-2 2.2.1
ipTM0.919
pTM0.890
avg pLDDT70.0
ranking score0.744
STRUCTURE · PEP-10541 × KISS1R
ranking0.744
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
boltz-2 2.2.1 · mmCIF ↓ download
sequence10 aa
1510
FNFNPFGLRF
overview readme

Snapshot

Class: Endogenous fish neuropeptide / reproductive signaling decapeptide
Evidence tier: Animal-only evidence
Status: No approved therapeutic status identified. Research peptide studied in teleost fish models.
Best-supported effect: Stimulation of luteinizing hormone and follicle-stimulating hormone secretion in teleost fish (animal models); greater potency than Kisspeptin-1 in this system
Main caveat: The KiSS-2 gene is absent in placental mammals, including humans. No mammalian or human biology is established for this peptide.


What this is

Kisspeptin-2 is a ten-amino-acid peptide (decapeptide) encoded by the KiSS-2 gene, one of two paralogous kisspeptin genes identified in non-placental vertebrates. It is an endogenous peptide in teleost fish species such as sea bass, where KiSS-2 mRNA is expressed in brain and gonadal tissue. The KiSS-2 gene appears to have been lost in the lineage leading to placental mammals, and Kisspeptin-2 has no established endogenous counterpart in humans. Functional studies in fish indicate that Kisspeptin-2 is more potent than its paralog Kisspeptin-1 in stimulating gonadotropin release, making it a subject of comparative reproductive endocrinology research in non-mammalian vertebrate species.


Evidence map

Evidence layerGradeWhat it supports
HumanNoneNo human evidence is present. The KiSS-2 gene is absent in placental mammals.
AnimalWeakGonadotropin (LH and FSH) secretion stimulated by Kisspeptin-2 in teleost fish (sea bass); comparative potency advantage over Kisspeptin-1 reported in the same fish system
In vitroNoneNo cell or binding assay data are present
ComputationalNoneNo computational or structural prediction data are present
MechanismPlausibleKisspeptin-2 is proposed to act through kisspeptin receptor (Kiss1R / GPR54) in fish; receptor specificity relative to mammalian Kiss1R is not established in the available literature

Animal evidence is based on a single published comparative study in sea bass; independent replication in additional species or systems is not documented.


Claim check

ClaimVerdictEvidence layerConfidence
Stimulates LH and FSH secretion in teleost fishSupported (animal)AnimalMedium — single study; species-limited to teleost fish
Greater gonadotropin-releasing potency than Kisspeptin-1Supported (animal)AnimalMedium — comparative finding within single fish study; not replicated in other systems per source
Relevant to human reproductive biologyNot establishedNoneHigh — the KiSS-2 gene is absent in placental mammals; no human biology basis identified in source
Suitable as a therapeutic candidate in mammalsNot establishedNoneHigh — no mammalian experimental data present in source; gene-loss biology creates a fundamental translation barrier

Experimental exposure

This section reports exposure used in animal experiments. It does not establish human dosing.

ContextSystemExperimental exposureDurationEndpointLimitation
Comparative fish studySea bass (Dicentrarchus labrax)Kisspeptin-2 decapeptide; exact dose and route not individually extracted from sourceNot reported in sourceLH and FSH secretion; comparative potency vs. Kisspeptin-1Single species; no mammalian translation established; exposure details not individually extracted

Preclinical safety signals

No toxicology or safety data are present. The peptide has been studied only in teleost fish comparative experiments. No mammalian safety or tolerability data are identified.


Regulatory status

No approved therapeutic status identified. This card describes a research peptide derived from comparative vertebrate genomics and fish reproductive biology, not an approved medicine. No WADA classification data are present.

Region / bodyStatusNotes
US (FDA)No approved status identifiedNot an approved drug; no IND or clinical program identified in source
EU (EMA)No approved status identifiedNot an approved medicine; source does not report EU regulatory history
WADANot checkedSource does not report anti-doping classification; status not independently verified in this card

Mechanism

Kisspeptin-2 is proposed to act as an agonist at kisspeptin receptors in teleost fish, stimulating the hypothalamic–pituitary–gonadal axis and triggering the release of luteinizing hormone and follicle-stimulating hormone. In the available literature, comparative functional experiments in sea bass demonstrate greater gonadotropin-stimulating activity for Kisspeptin-2 than for Kisspeptin-1, consistent with differential receptor binding or activation potency.

The mammalian kisspeptin system is mediated by Kiss1R (GPR54), encoded by the KiSS-1 gene lineage. Because the KiSS-2 gene has been lost in placental mammals, there is no established endogenous target for exogenous Kisspeptin-2 in humans. Whether Kisspeptin-2 could cross-activate mammalian Kiss1R is not addressed in the available literature.

Target confidence: Inferred from fish comparative studies; not verified in mammalian systems.


Chemistry

FieldValue
Sequence (single-letter)FNFNPFGLRF
Full notationH-Phe-Asn-Phe-Asn-Pro-Phe-Gly-Leu-Arg-Phe-OH
Length10 amino acids
TopologyLinear
ModificationsNone reported; free N-terminus (H-), free C-terminus (-OH)
Molecular weightNot reported in source
FormulaNot reported in source
CASNot reported in source
Sequence confidenceNeeds review — single source (catalog/database entry); no independent sequence verification in available literature

Open questions

  • Mammalian receptor cross-reactivity: Whether Kisspeptin-2 binds or activates the mammalian kisspeptin receptor (Kiss1R / GPR54) has not been established in the available literature. This is a fundamental prerequisite before any mammalian relevance can be assessed.
  • Gene-loss implications: The KiSS-2 gene is absent in placental mammals. Whether any functional analog exists or whether the peptide could have pharmacological activity in mammalian systems via cross-receptor binding remains unstudied per the available literature.
  • Species generalizability: Animal evidence is limited to sea bass in the available literature. Whether the gonadotropin-stimulating effect generalizes to other non-placental vertebrates or to any mammalian species is not established.
  • Quantitative exposure data: the available literature does not individually extract dose, route, or timing for the fish experiments. These parameters are absent from this card.
  • In vitro characterization: No receptor binding assays, cell-based assays, or biochemical characterization data are identified. Receptor affinity and selectivity are unknown from available literature.
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 2026-06-05

Could this naturally fish-specific peptide help control breeding in farmed fish while posing less risk to wild mammals if it leaks into rivers?

Fish farmers use hormone treatments to synchronize breeding, but these chemicals can affect wildlife in nearby waterways. A peptide that only works in fish could make aquaculture more environmentally responsible, benefiting both the industry and ecosystems downstream of fish farms.

The hypothesis
Kisspeptin-2 may have utility in aquaculture as a species-specific gonadotropin-releasing agent for synchronizing spawning in teleost fish species that retain the KiSS-2 gene, exploiting its demonstrated superiority over Kisspeptin-1 in LH and FSH stimulation and its non-mammalian receptor origin to minimize environmental contamination risk from residues that could activate mammalian KISS1R.
Why it’s plausible
Controlled spawning induction is a major challenge in aquaculture for commercially important teleost species. Current agents include GnRH analogs that cross-react with mammalian receptors. Kisspeptin-2 acts upstream of GnRH neurons and is reported more potent than Kisspeptin-1 in sea bass. Because the KiSS-2 gene is absent in placentals, this peptide targets a receptor system effectively absent from mammalian physiology at physiological concentrations, which could reduce ecological hazard relative to GnRH-based spawning agents if it enters aquatic environments.
Why it matters
A KiSS-2 system agonist optimized for aquaculture use could become a safer, species-selective alternative to current GnRH analog spawning agents, with reduced risk of disrupting mammalian reproductive endocrinology in wildlife exposed to aquaculture effluent.
Plausibility.70
Novelty.60
Impact.55
Basis · grounding1 paper · 2 computed/notes
[1]
noteKisspeptin-2 is more potent than Kisspeptin-1 in stimulating LH and FSH secretion in teleost fish (sea bass); KiSS-2 gene is absent in placental mammals.
[2]
paper
Review details the KiSS-2 system in non-mammalian vertebrates and its role upstream of GnRH neurons in gonadotropin regulation.
doi: 10.1016/j.mce.2008.11.017
[3]
sequenceFNFNPFGLRF is a 10 aa peptide with low molecular weight and no known mammalian endogenous counterpart, supporting a potentially selective environmental profile.
openupdated 2026-06-05

Could this fish peptide stimulate the human fertility receptor through a different route than the body's own kisspeptin, avoiding the receptor burnout that limits current treatments?

Treatments that avoid receptor burnout could work over longer periods without losing effectiveness. This would matter greatly for people receiving kisspeptin-based therapies for infertility, potentially reducing the need for complicated dosing regimens.

The hypothesis
Kisspeptin-2 may act as a partial agonist or biased agonist at human GPR54/KISS1R relative to the endogenous mammalian kisspeptin-10, selectively engaging beta-arrestin-mediated signaling over Gq/IP3 mobilization, because its divergent N-terminal extension (FNF, absent in the minimal mammalian Kp-10 pharmacophore) may make receptor-proximal contacts that alter the receptor's active-state conformation.
Why it’s plausible
Biased agonism at KISS1R has been described as a potential route to separating desired (LH pulse) from undesired (receptor desensitization) pharmacology. Kisspeptin-2's extra N-terminal residues FNF relative to the conserved pentapeptide pharmacophore are not required for basic receptor binding but could differentially stabilize receptor conformations. Cross-species ligands with divergent flanking sequences are established probes for biased signaling at GPCRs.
Why it matters
A naturally occurring biased KISS1R agonist could be developed into a pulsatile fertility therapeutic that avoids receptor downregulation, a known limitation of continuous kisspeptin analog dosing in clinical trials.
Plausibility.50
Novelty.70
Impact.75
Basis · grounding2 papers · 1 computed/note
[1]
sequenceKisspeptin-2 (FNFNPFGLRF) carries N-terminal FNF extension beyond the minimal active pentapeptide; these residues could make secondary receptor contacts.
[2]
paper
Review describes divergent kisspeptin biology across vertebrates and notes structural differences between KiSS-1 and KiSS-2 system ligands.
doi: 10.1016/j.mce.2008.11.017
[3]
paper
KISS1R ligand pharmacology review establishes that flanking sequence beyond the core pentapeptide modulates potency and receptor interaction characteristics.
doi: 10.1111/j.1365-2826.2010.02018.x
openupdated 2026-06-05

If scientists close this fish peptide into a ring, could it survive long enough in the bloodstream to work as a once-daily fertility drug?

Current kisspeptin-based treatments break down quickly and need frequent injections. A ring-shaped version could last much longer in the body, potentially allowing simpler dosing for people being treated for infertility or hormone disorders.

The hypothesis
The compact ten-residue length of Kisspeptin-2 (FNFNPFGLRF) places it at the lower size boundary where peptide macrocyclization via head-to-tail or side-chain bridging can be achieved without disrupting the active conformation, and such cyclization would yield a protease-resistant KISS1R agonist with improved plasma half-life relative to linear mammalian kisspeptin-10.
Why it’s plausible
Mammalian kisspeptin-10 (a decapeptide like Kisspeptin-2) is rapidly degraded in plasma by metalloendopeptidases. Kisspeptin-2's sequence already contains the complete pharmacophore in ten residues, making it an attractive template for macrocyclization without adding molecular weight. The presence of Asn residues at positions 2 and 4 provides potential side-chain conjugation sites for lactam bridges that would rigidify the proposed Pro-induced turn and protect the backbone from proteolysis.
Why it matters
A macrocyclic Kisspeptin-2 analog could achieve the extended half-life needed for subcutaneous once-daily dosing in fertility indications, addressing a key unmet need beyond current short-acting kisspeptin analogs in clinical development.
Plausibility.65
Novelty.55
Impact.60
Basis · grounding3 computed/notes
[1]
sequenceFNFNPFGLRF is 10 aa with Asn at positions 2 and 4, providing side-chain handles for lactam macrocyclization; Pro5 pre-organizes a turn geometry suitable for ring closure.
[2]
structurepLDDT=70 indicates partial flexibility; rigidification via macrocyclization is predicted to raise this by constraining backbone.
[3]
notePeptide is a research compound with no approved therapeutic status, indicating engineering space is fully open for analog development.
openupdated 2026-06-05

Does this fish peptide stick specifically to the fertility receptor without also hitting the nearby receptors that control pain and appetite?

If kisspeptin-2 is naturally selective, it would be a cleaner starting point for drugs than other RF-amide peptides that hit multiple receptors. Patients could benefit from fertility treatments with fewer unintended side effects.

The hypothesis
Kisspeptin-2 is selective for KISS1R over RF-amide family receptors NPFFR1, NPFFR2, and QRFPR in teleost fish, and this selectivity is maintained at human orthologs, because the Asn-Phe-Asn N-terminal triplet creates steric exclusion from the narrower binding pockets of the human NPFF receptors that do not accommodate bulky polar N-termini.
Why it’s plausible
Kisspeptin-2 belongs to the broader RF-amide peptide superfamily sharing the C-terminal Arg-Phe motif. Cross-reactivity at NPFF receptors and QRFPR is a concern for any RF-amide-containing peptide, and such off-target activity could produce pain-modulation or orexigenic side effects. The bulkier polar N-terminus of Kisspeptin-2 (F-N-F-N) relative to canonical NPFF peptides (Ser-Leu-Ala-Ala in hNPFF) may create receptor-selectivity by steric clash in NPFF receptor vestibules.
Why it matters
Establishing KISS1R selectivity for Kisspeptin-2 versus NPFF-family receptors would validate it as a clean reproductive probe and therapeutic lead without pain or appetite liabilities.
Plausibility.55
Novelty.65
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
sequenceFNFNPFGLRF shares C-terminal RF with NPFF family but carries bulky polar N-terminal Phe-Asn-Phe-Asn not present in NPFF or QRFP peptides.
[2]
structureipTM=0.919 for KISS1R complex suggests high-quality engagement; comparative modeling against NPFF receptors could reveal differential fit.
[3]
paper
RF-amide family phylogenetic analysis confirms kisspeptins and NPFF peptides share C-terminal motif but diverge substantially in N-terminal extension.
doi: 10.3389/fendo.2012.00173
openupdated 2026-06-05

Does a kink in the middle of this fish peptide force its active end into the right shape to hit its receptor harder than the related peptide?

If confirmed, drug designers could lock this bend in place artificially, creating a more stable, potent molecule that activates fertility-related receptors more efficiently. This could lead to smaller, cheaper reproductive hormone treatments.

The hypothesis
The Phe-Asn-Pro-Phe (FNPF) sub-sequence within Kisspeptin-2 (positions 5-8, PFGLR reading from N-terminus: more precisely the FNPF motif spanning residues 1,2,5,6 as F-N...P-F) constitutes a discontinuous beta-turn pharmacophore that pre-organizes the C-terminal Arg-Phe for KISS1R engagement, and this conformational pre-organization explains the greater potency of Kisspeptin-2 relative to Kisspeptin-1 in teleost fish.
Why it’s plausible
Kisspeptin-2 (FNFNPFGLRF) is reported to be more potent than Kisspeptin-1 in stimulating gonadotropin release in sea bass. The sequence contains a Pro at position 5 that could induce a turn, positioning the terminal RF for receptor contact. A proline-enforced turn creating a compact active conformation, rather than simple sequence differences, may underlie the potency difference. The moderate pLDDT of 70 suggests partial structural flexibility consistent with a turn-based rather than fully helical active conformation.
Why it matters
Understanding the conformational basis of potency differences between Kisspeptin-1 and Kisspeptin-2 could guide design of constrained cyclic or stapled analogs with improved receptor engagement, relevant to any KISS1R-targeted therapeutic program.
Plausibility.60
Novelty.50
Impact.55
Basis · grounding3 computed/notes
[1]
sequenceFNFNPFGLRF contains Pro at position 5, a canonical beta-turn inducer; terminal RF dipeptide is the conserved receptor contact.
[2]
structurepLDDT=70 for the peptide chain indicates moderate local disorder, consistent with a flexible peptide adopting a defined turn only upon receptor binding.
[3]
noteKisspeptin-2 is reported more potent than Kisspeptin-1 in stimulating LH and FSH secretion in teleost fish (sea bass).
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.9193800687789917 boltz-2
ranking score 0.7435304522514343 boltz-2
3-letter notation
Phe-Asn-Phe-Asn-Pro-Phe-Gly-Leu-Arg-Phe
recipeboltz-2 2.2.1
parametervalue
modelboltz-2 2.2.1
weights
hardwarevast_v100_32gb
mlx version
python
random seed1
msa strategycolabfold_local
runtime
predicted by
predicted at2026-05-22
citationbibtex
peptidemodel (2026). Kisspeptin-2: fish reproductive-signaling peptide (FNFNPFGLRF) (pep-10541, v1). PeptideModel. https://peptidemodel.com/card/pep-10541
@peptide{pep10541,
  sequence = {FNFNPFGLRF},
  target   = {kiss1r},
  author   = {peptidemodel},
  year     = {2026},
  status   = {synthesized}
}
related peptides 2 by signal overlap
clinical trials 0 trials · checked 2026-05-09
0
no registered clinical trials as of 2026-05-09; we'll re-check periodically
references 4 papers
discussion no comments
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