pe
pep-10584 v1 CC-BY-SA-4.0

Zebrafish stress-signaling peptide (PACAP2 / zfPACAP2)

A natural zebrafish brain peptide related to human stress hormones; used in lab studies of fear, anxiety, and pain, a research tool, not an approved drug.

statussynthesized targetPAC1R length38 aa refs6
snapshot sparse 15% confidence
Class
Neuropeptide / pituitary signaling peptide (non-mammalian isoform)
Status
No approved therapeutic status; research-only zebrafish peptide
Best-supported effect
Biological characterization in zebrafish ovary (single published study); no mammalian or human efficacy data attached
Main caveat
Zebrafish-specific isoform; not equivalent to mammalian PACAP-38 or PACAP-27. No mammalian animal-model, in vitro, or human data in source file.
status 4 / 5
prediction metrics openfold3-mlx 0.3.1
ipTM0.755
pTM0.695
avg pLDDT41.1
ranking score0.840
STRUCTURE · PEP-10584 × PAC1R
ranking0.840
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
openfold3-mlx 0.3.1 · mmCIF ↓ download
sequence38 aa
1510152025303538
HSDGIFTDIYSRYRKQMAV KKYLAAVLGRRYRQRVKNK
overview readme

What this is

Pituitary adenylate cyclase-activating peptide 2 (PACAP2, also called zfPACAP2) is the zebrafish form of a highly conserved neuropeptide that signals through the PAC1 receptor — a stress-circuit protein implicated in fear, anxiety, and pain processing. It is one of two PACAP variants that teleost fish carry as a result of an ancient whole-genome duplication; the other is zebrafish PACAP1. The two isoforms arose from a common ancestral PACAP gene and share about 82% sequence identity with each other (Wang and colleagues, 2019). Mammalian PACAP — which has remained virtually unchanged across 80–100 million years of evolution — was first identified in 1989 by Arimura and colleagues from ovine hypothalamus as a novel peptide that potently activated adenylate cyclase in pituitary cells. The zebrafish PACAP2 variant was first cloned and characterized from zebrafish ovary by Wang, Wong, and Ge (Wang and colleagues, 2003).

History

The parent PACAP family was discovered in 1989 in Arimura's laboratory during a search for a follicle-stimulating hormone-releasing factor; a fraction of ovine hypothalamus was found to powerfully activate adenylate cyclase in rat anterior pituitary cells, and the responsible 38-residue peptide was isolated and sequenced. Mammals express PACAP as two biologically active forms — PACAP-27 and PACAP-38 — that share an identical N-terminal sequence but differ at the C-terminus. The zebrafish-specific PACAP2 isoform, encoded by the adcyap1b gene, was described in 2003 when Wang, Wong, and Ge cloned it from zebrafish ovary and demonstrated that it is a distinct nonmammalian vertebrate variant with only about 64% precursor homology to the other zebrafish PACAP (zfPACAP38-1) (Wang and colleagues, 2003). Subsequently, brain distribution studies confirmed that adcyap1b is the dominant PACAP gene in the zebrafish central nervous system, with expression levels roughly 15-fold higher than those of adcyap1a in whole brain, and highest in the telencephalon and diencephalon (Wang and colleagues, 2019; Nakamachi and colleagues, 2018).

What it does

PACAP2 acts on the PAC1 receptor (encoded by adcyap1r1), a class B G protein-coupled receptor that is highly expressed in brain regions controlling stress and emotion. When PACAP binds PAC1R, it boosts levels of a molecular messenger called cyclic AMP, which in turn activates protein kinase A and a cascade of downstream signaling. The receptor also drives a separate pathway through ERK kinase after the receptor is pulled inside the cell (a process called internalization), and this endosomal ERK route appears to be the primary signal controlling neuronal excitability in hippocampal dentate gyrus granule cells (Johnson and colleagues, 2020). In zebrafish, intracerebroventricular injection of PACAP2 suppresses food intake, demonstrating a conserved anorexigenic function shared with mammalian PACAP (Wang and colleagues, 2019). Brain mapping studies using immunostaining show PACAP2-positive cells and fibers distributed across the telencephalon, hypothalamus, and cerebellum, with a distinctive fiber tract projecting toward the habenula — a pattern consistent with roles in higher brain functions, feeding, and emotional regulation (Nakamachi and colleagues, 2018).

Evidence

  • Human: Human studies of the PAC1 receptor system — not of zfPACAP2 itself — provide the strongest translational context. Ressler and colleagues (2011) reported in Nature that a single-nucleotide polymorphism in the PAC1 receptor gene (rs2267735, in a putative estrogen response element of ADCYAP1R1) significantly predicted PTSD diagnosis and hyperarousal symptoms in females (N=1,237 combined analysis; effect absent in males). PACAP-38 infusion has been shown to induce migraine-like attacks in patients with migraine without aura, supporting PAC1R as a target in primary headache (Liao and colleagues, 2019; reviewed in Moody and colleagues, 2016).
  • Animal: In zebrafish, both PACAP1 and PACAP2 suppressed food intake when injected intracerebroventricularly, demonstrating conserved anorexigenic function (Wang and colleagues, 2019). PAC1 receptor knockout mouse models display impaired contextual fear conditioning and novel object recognition, implicating the PACAP–PAC1R axis in memory consolidation (Hashimoto, 2002). The PACAP–PAC1R system modulates fear acquisition, recall, and extinction in a sexually dimorphic manner in rodent models, with amygdala and hippocampal circuits playing key roles (King and colleagues, 2017).
  • In vitro: PACAP-induced PAC1 receptor internalization and recruitment of MEK/ERK signaling was demonstrated in hippocampal dentate gyrus granule cells; blocking receptor internalization or MEK activity eliminated PACAP's enhancement of neuronal excitability (Johnson and colleagues, 2020).

Known effects

  • Anorexigenic (appetite suppression) — Demonstrated in zebrafish intracerebroventricular injection studies (Wang and colleagues, 2019); analogous effects described across vertebrates.
  • Neuronal excitability modulation — PAC1R-driven MEK/ERK endosomal signaling enhances dentate gyrus granule cell firing; Preclinical/mechanistic (Johnson and colleagues, 2020).
  • Fear and stress circuit regulation — PAC1R activation modulates fear acquisition, generalization, and extinction; Preclinical (multiple rodent studies; King and colleagues, 2017).
  • Neuroprotection — Mammalian PACAP has been studied for neuroprotective roles across multiple models; relevance of zfPACAP2 specifically is inferred by sequence conservation and receptor binding.
  • Reproductive signaling — The 2003 discovery study showed zfPACAP2 stimulates oocyte maturation and follistatin expression in zebrafish follicle cells (Wang and colleagues, 2003).

Safety signals

No safety data specific to synthesized zfPACAP2 peptide is available in the published literature. The broader PACAP family is an endogenous neuropeptide conserved across vertebrates; adverse-event profiles arise in the context of pharmacological manipulation of the PAC1R system rather than from the endogenous ligand itself. PACAP-38 infusion in migraine patients produces transient vasodilatory effects and headache, consistent with PAC1R-mediated cAMP signaling in cranial vasculature (reviewed in Moody and colleagues, 2016). A monoclonal PAC1 receptor antibody (targeting the therapeutic application) failed in a proof-of-concept migraine prevention trial, suggesting that receptor-level antagonism carries its own complexity.

Regulatory status

  • US: Not an approved drug. No IND or NDA. Research compound only.
  • EU: Not approved. Research use only.
  • WADA: Not currently listed on the WADA prohibited list as a named substance; PACAP analogs with growth factor or hormonal activity could fall under general peptide hormone categories depending on mechanism.

Mechanism

PACAP2 binds the PAC1 receptor (ADCYAP1R1), a class B secretin-family GPCR that couples to both Gαs and Gαq proteins. Gαs coupling activates adenylyl cyclase, raising intracellular cAMP and activating protein kinase A (PKA) and EPAC1/2; Gαq coupling activates phospholipase C (PLC), generating IP3 and diacylglycerol and mobilizing calcium. A third, β-arrestin–mediated pathway operates after receptor internalization: endosomal PAC1R recruits MEK/ERK signaling independently of surface cAMP or PLC cascades. In hippocampal dentate gyrus granule cells, this endosomal MEK/ERK route is the primary mechanism by which PACAP regulates intrinsic neuronal excitability (Johnson and colleagues, 2020; May and colleagues, 2021). The PAC1 receptor also activates Akt, contributing to neuroprotective and anti-apoptotic signaling (Liao and colleagues, 2019).

Zebrafish PACAP2 is a 38-residue peptide whose mature C-terminal amide form is not represented in the raw stored sequence (HSDGIFTDIYSRYRKQMAVKKYLAAVLGRRYRQRVKNK) — the active peptide carries a C-terminal amide that protects against carboxypeptidase degradation, as is standard for the PACAP family. The sequence is the zebrafish-specific adcyap1b product and differs from human/mammalian PACAP-38 at several positions, particularly in the C-terminal extension, while retaining the N-terminal pharmacophore required for PAC1R engagement.

Related peptides

  • Zebrafish PACAP1 (zfPACAP1, encoded by adcyap1a) — the paralogue arising from teleost whole-genome duplication; ~82% identical to PACAP2 but expressed at lower levels in zebrafish brain and enriched in brainstem rather than telencephalon.
  • Human/mammalian PACAP-38 — the evolutionarily conserved form that served as the original target of PAC1R research; virtually identical to PACAP-27 at the N-terminal pharmacophore; the reference ligand for most PAC1R mechanistic and clinical studies cited in this card.
  • VIP (vasoactive intestinal peptide) — a structurally related class B GPCR neuropeptide that shares VPAC1 and VPAC2 receptors with PACAP but does not bind PAC1R with high affinity; reviewed alongside PACAP in Moody and colleagues (2016).
Hypotheses2 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

Could this peptide, originally discovered in fish ovaries, help control follicle development or ovulation in mammals?

If true, it could inspire a new class of fertility medicines that act more specifically in the reproductive system, reducing neurological side effects that have held back similar peptides. Couples struggling with infertility could benefit from more targeted hormonal treatments.

The hypothesis
Because zfPACAP2 is expressed in zebrafish ovary and encoded by adcyap1b, it may serve a conserved reproductive-regulation function at PAC1 receptors in gonads, making it a candidate for modulating follicle maturation or oocyte release in species beyond teleosts, including mammals.
Why it’s plausible
The original 2003 cloning of zfPACAP2 was from zebrafish ovary, not brain. PAC1 receptors are expressed in mammalian ovarian follicles and PACAP is known to suppress follicle rupture in rodents. The existence of a distinct teleost isoform that originated in a gonadal context suggests selective pressure for reproductive signaling. If zfPACAP2's divergent residues improve affinity for gonadal-type PAC1 conformations or co-expressed receptor variants, it could be repurposed for fertility applications.
Why it matters
Mammalian PACAP is used in rodent reproductive biology but is not a drug due to CNS side effects. A peripherally acting, gonad-selective variant derived from the zebrafish isoform could be therapeutically useful in fertility medicine with reduced neurological activity.
Plausibility.60
Novelty.60
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
paper
zfPACAP2 was originally cloned from zebrafish ovary, placing its primary discovery context in reproductive tissue, not CNS
doi: 10.1210/en.2003-0501
[2]
notezfPACAP2 is encoded by adcyap1b and arose via whole-genome duplication, potentially enabling subfunctionalization where one isoform specializes for reproductive and the other for CNS roles
[3]
notePAC1 receptor is the annotated target, and PAC1 is expressed in ovarian follicles with known roles in follicle rupture and oocyte maturation
openupdated 2026-06-11

Could the strongly positive-charged tail of this peptide be used to carry drug molecules directly into cells?

If the cationic tail of this natural fish peptide can sneak molecules through cell membranes, it could form the basis of a safer drug-delivery system that avoids immune problems caused by current synthetic carriers. This would help patients who need drugs delivered inside specific cells, such as those with certain cancers or genetic diseases.

The hypothesis
The 18-residue C-terminal cationic stretch of zfPACAP2 (positions 21-38: KYLAAVLGRRYRQRVKNK) can function as a cell-penetrating peptide scaffold independent of PAC1 binding, enabling intracellular cargo delivery via electrostatic membrane interaction and helix-driven insertion.
Why it’s plausible
The C-terminal half of zfPACAP2 contains KYLAAVLG (hydrophobic helix) followed by RRYRQRVKNK (strongly cationic, 6 R/K in 10 residues, net charge approximately +7). This architecture closely matches known cell-penetrating peptides such as penetratin and transportan, which combine an amphipathic helix with a cationic tail. This region is separated from the N-terminal receptor-activation domain (HSDGIFTDIY), suggesting it could be isolated without losing membrane activity.
Why it matters
A naturally occurring, non-synthetic cell-penetrating scaffold derived from a vertebrate neuropeptide would have intrinsic biocompatibility advantages for intracellular drug delivery, offering an alternative to poly-Arg or HIV-TAT based sequences that trigger immune responses.
Plausibility.55
Novelty.60
Impact.55
Basis · grounding3 computed/notes
[1]
sequenceResidues 29-38 RRYRQRVKNK contain 6 basic residues (net charge approximately +6) and residues 22-29 KYLAAVLG form a predicted amphipathic helix, together matching the dual-domain CPP architecture
[2]
structurepLDDT=41.1 for free peptide indicates the C-terminal region is disordered in isolation, consistent with membrane-induced folding behavior characteristic of CPPs
[3]
sequenceThe N-terminal activation domain HSDGIFTDIY is structurally and functionally separable from the C-terminal cationic segment, supporting modular engineering of the C-terminal fragment alone
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.754585862159729 openfold3-mlx
ranking score 0.8404658436775208 openfold3-mlx
structural qualityopenfold3
0
metricvaluenote
gpde0.841global PDE — lower = better
disorder0.196fraction disordered
chain pair ipTM (A, B)0.755interface quality
3-letter notation
His-Ser-Asp-Gly-Ile-Phe-Thr-Asp-Ile-Tyr-Ser-Arg-Tyr-Arg-Lys-Gln-Met-Ala-Val-Lys-Lys-Tyr-Leu-Ala-Ala-Val-Leu-Gly-Arg-Arg-Tyr-Arg-Gln-Arg-Val-Lys-Asn-Lys
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
runtime449s
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). Zebrafish stress-signaling peptide (PACAP2 / zfPACAP2) (pep-10584, v1). PeptideModel. https://peptidemodel.com/card/pep-10584
@peptide{pep10584,
  sequence = {HSDGIFTDIYSRYRKQMAVKKYLAAVLGRRYRQRVKNK},
  target   = {pac1r},
  author   = {peptidemodel},
  year     = {2026},
  status   = {synthesized}
}
related peptides 5 by signal overlap
clinical trials 28 on ct.gov · checked 2026-05-09
ct.gov trials 28
with results 1
by phase
2phase 18no phase
by status
4completed1recruiting1active2not yet recruiting1terminated1unknown
references 6 papers
discussion no comments
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peptidemodel.com CC-BY-SA-4.0 research only · not for human use