pe
pep-10648 v1 CC-BY-SA-4.0

Stress-response research peptide (porcine CRF [1-40; E26, N40])

A pig-derived brain hormone that triggers the body's stress response by telling the pituitary gland to release cortisol; used only as a lab research tool.

statussynthesized targetCRHR2 length40 aa refs1
snapshot sparse 0% confidence
Class
Porcine hypothalamic peptide (CRF-family)
Status
No approved therapeutic status identified
Best-supported effect
Not established — the attached source documents sequence identity and porcine origin only; no bioassay, animal, or human evidence is attached to this card
Main caveat
Card based on a single catalog-grade source entry with a sequence and one 1986 identity reference; no biological activity, assay, animal, or human data are present
status 4 / 5
prediction metrics openfold3-mlx 0.3.1
ipTM0.804
pTM0.727
avg pLDDT52.9
ranking score0.874
STRUCTURE · PEP-10648 × CRHR2
ranking0.874
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
openfold3-mlx 0.3.1 · mmCIF ↓ download
sequence40 aa
1510152025303540
SEEPPISLDLTFHLLREVLE MARAEELAQQAHSNRKLMEN
overview readme

What this is

This peptide is a 40-residue fragment of corticotropin-releasing factor (CRF) isolated from pig (porcine) hypothalami. CRF is a hormone produced in the brain that triggers the body's stress response by telling the pituitary gland to release ACTH, which in turn prompts the adrenal glands to make cortisol. This particular variant — designated [1-40; E26, N40] to indicate glutamate at position 26 and asparagine at position 40 — differs from the canonical human CRF sequence at those two positions, reflecting its porcine origin. Patthy and colleagues (1986) purified it alongside nine other CRF-related polypeptides from porcine hypothalami and confirmed that it stimulates ACTH release from rat pituitary cells. On this platform it is assigned to the CRF receptor type 2 (CRHR2), which mediates anxiolytic and cardioprotective signaling independently of the better-known CRF receptor type 1 (CRHR1).

History

This peptide was identified as part of a landmark biochemical characterization of CRF-related peptides in the pig hypothalamus. Patthy and colleagues (1986) purified ten polypeptides with CRF activity from porcine hypothalami using gel filtration followed by reversed-phase HPLC, and confirmed each by sequence analysis. The work established that multiple CRF-related variants co-exist in the porcine hypothalamus, structurally related to the canonical porcine CRF sequence. The [1-40; E26, N40] designation reflects two amino acid positions that distinguish this variant within that family.

What it does

The peptide stimulates the release of corticotropin (ACTH) from pituitary cells, consistent with its structural relationship to CRF (Patthy et al. 1986). Because the platform assigns it to CRHR2 as its primary receptor, it is used as a research tool to probe CRHR2-mediated biology — including pathways associated with stress recovery, cardiovascular protection, and anxiolytic effects — separately from the CRHR1 pathway that drives the classical HPA-axis stress response.

Evidence

  • Human: No human trials identified for this specific CRF variant.
  • Animal: Patthy and colleagues (1986) demonstrated ACTH-releasing activity in superfused rat pituitary cells for this peptide and related porcine CRF variants isolated alongside it.
  • In vitro: CRF activity confirmed by bioassay (ACTH release from rat pituitary cells) and characterized by sequence analysis (Patthy et al. 1986).

Mechanism

CRF and its analogs act at class B G protein-coupled receptors: CRHR1 and CRHR2. The stored sequence SEEPPISLDLTFHLLREVLEMARAEELAQQAHSNRKLMEN (40 aa) reflects the porcine-origin backbone, with Glu at position 26 and Asn at position 40 distinguishing it from the canonical human CRF-41 sequence. CRHR2 is expressed at lower levels in the pituitary than CRHR1 and is associated with peripheral effects including cardiac stress tolerance and anxiolytic behavior, making CRHR2-selective ligands of interest for dissecting these functions from the CRHR1-driven cortisol axis.

Hypotheses4 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

Does swapping one neutral amino acid for a negatively charged one steer a CRF-related peptide away from the acute-stress receptor and toward the calming, heart-protective receptor?

If one amino acid change is enough to redirect activity between these two receptors, it could inspire a straightforward way to design stress-pathway drugs that reduce anxiety and protect the heart without amplifying the acute stress response.

The hypothesis
Porcine CRF [1-40; E26, N40] preferentially binds CRHR2 over CRHR1 because the E26 substitution disrupts a salt bridge that stabilizes the canonical CRF interaction with CRHR1's N-terminal ectodomain, while the more open binding cleft of CRHR2 accommodates the glutamate side chain without penalty.
Why it’s plausible
The canonical porcine CRF sequence has a glutamine at position 26; this variant carries glutamate (E26), introducing a negative charge in the middle of an otherwise amphipathic helix. CRHR1 and CRHR2 differ substantially in their N-terminal ectodomains, which mediate initial peptide capture in class B GPCRs. CRHR2's ectodomain is less electrostatically restrictive than CRHR1's. The platform annotation assigns this peptide to CRHR2 specifically, consistent with selective receptor preference. The E26 charge difference may be the structural basis of that selectivity.
Why it matters
CRHR2 mediates anxiolytic and cardioprotective signaling while CRHR1 drives the acute stress response; a peptide that exploits a single charge substitution to achieve receptor selectivity would be a valuable pharmacological tool and a scaffold for CRHR2-selective therapeutics.
Plausibility.50
Novelty.65
Impact.70
Basis · grounding1 paper · 2 computed/notes
[1]
notePeptide assigned to CRHR2; carries E26 (glutamate) replacing the glutamine of canonical CRF, the distinctive structural feature.
[2]
paper
Shows that C-terminal residues of class B GPCR peptide ligands contribute to binding selectivity while N-terminal residues drive receptor activation, directly relevant to how E26 in the middle helix region could steer CRHR1 versus CRHR2 preference.
doi: 10.1126/science.aav7942
[3]
sequenceSEEPPISLDLTFHLLREVLEMARAEELAQQAHSNRKLMEN: E26 is within the central helical region; surrounding residues form a largely hydrophobic face interrupted by this charge.
openupdated 2026-06-05

Does the presence of a charged glutamate in the middle of this peptide's helix reduce its rigidity in a way that happens to fit the anxiety-reducing receptor better than the anxiety-driving one?

If natural flexibility from a single substitution can steer a peptide to the desired receptor, it opens a design principle for safer anti-anxiety or cardioprotective drugs that avoid activating the fight-or-flight arm of the stress system.

The hypothesis
The central leucine-rich amphipathic helix of porcine CRF [1-40; E26, N40] (approximately residues 12-26: LTFHLLREVLEMARAEELA) is destabilized relative to canonical CRF by the E26 substitution, reducing helical propensity at the hydrophobic-hydrophilic interface and shifting the helix-coil equilibrium toward a more dynamic conformation that nonetheless retains CRHR2 binding through compensatory contacts from flanking charged residues.
Why it’s plausible
Alpha-helical stability in CRF-family peptides is essential for receptor binding; the central helix packs a hydrophobic face against the receptor while exposing a polar face. Glutamate at position 26 sits at the boundary of this helix. Glutamate is a helix-favoring residue in isolation but introduces a charge that, in the context of a helix dipole and nearby glutamate residues (AEELA at 24-28), could create electrostatic repulsion reducing local helical stability. This partial unfolding might be tolerated at CRHR2 (which has a wider binding groove) but not at CRHR1, contributing to receptor selectivity.
Why it matters
A naturally occurring example of a charge substitution that reduces amphipathic helix stability while preserving CRHR2 selectivity would provide a template for designing flexible CRHR2 agonists with altered pharmacokinetic and receptor residence properties.
Plausibility.55
Novelty.60
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
sequenceSEEPPISLDLTFHLLREVLEMARAEELAQQAHSNRKLMEN: AEELA at positions 24-28 around the E26 substitution creates a cluster of acidic residues that could electrostatically destabilize the local helical segment.
[2]
noteE26 (glutamate) and N40 (asparagine) distinguish this variant from canonical CRF; E26 is the more structurally impactful substitution given its position in the central helix.
[3]
paper
Notes the relevance of peptide structure for receptor interactions, supporting the idea that helix dynamics influence binding mode.
doi: 10.2174/1389203053027520
openupdated 2026-06-05

Does the cluster of negatively charged amino acids at the beginning of this peptide electrostatically attract the positively charged parts of its receptor, speeding up the initial attachment step?

Understanding this docking step could help researchers design CRF-related drugs that work faster or bind more selectively to the anxiety-reducing stress receptor, potentially benefiting people with anxiety disorders or heart failure.

The hypothesis
The N-terminal SEEPP motif of porcine CRF [1-40; E26, N40] forms a disordered but functionally important 'address' sequence that accelerates initial electrostatic docking to the CRHR2 ectodomain by presenting a cluster of acidic residues complementary to the basic residues in CRHR2's N-terminal domain, following a two-step binding mechanism analogous to that described for other class B peptide hormones.
Why it’s plausible
Class B GPCRs are activated by a two-step mechanism: the C-terminal helix of the peptide docks to the receptor ectodomain (affinity step), then the N-terminus inserts into the transmembrane bundle (activation step). For CRF-family peptides, the N-terminal region is the activation determinant. The SEEP start of this peptide is unusually acidic. CRHR2's N-terminal ectodomain contains basic residues. An electrostatic pre-docking contact mediated by SEEPP could accelerate the association rate even if the C-terminal helix dominates affinity, consistent with the observation that N-terminal truncation abolishes activity without always reducing affinity proportionally.
Why it matters
Defining a charge-based N-terminal docking step would explain why CRF fragments truncated at the N-terminus lose activity despite retaining helix structure, and could guide design of potent CRHR2 partial agonists by engineering N-terminal charge clusters.
Plausibility.60
Novelty.50
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
paper
Explicitly states that C-terminal residues of related peptides contribute to receptor binding selectivity while N-terminal residues switch on activation, supporting a two-step model for this peptide.
doi: 10.1126/science.aav7942
[2]
sequenceSEEPPISLDLTFHLLREVLEMARAEELAQQAHSNRKLMEN: positions 1-5 are SEEPP, with three acidic residues in the first five amino acids.
[3]
noteThe Patthy et al. 1986 study confirmed ACTH-releasing activity of this fragment from porcine hypothalami, implying intact receptor activation requiring the N-terminal region.
openupdated 2026-06-05

Could this porcine version of CRF, which appears to favor the heart-protective stress receptor, reduce the damage caused when blood flow returns to a heart after a blockage?

If confirmed, this natural peptide variant could become a template for heart attack treatments that protect cardiac muscle during and after a blockage, filling a gap left by existing drugs that activate both beneficial and harmful arms of the stress pathway.

The hypothesis
Porcine CRF [1-40; E26, N40], by activating CRHR2 in cardiac myocytes, mimics urocortin-2 in reducing ischemia-reperfusion injury, and the E26/N40 porcine variant may be more cardioprotective than canonical human CRF because its selective CRHR2 engagement avoids the pro-inflammatory and vasoconstrictive CRHR1 signaling that limits full CRF use in cardiac contexts.
Why it’s plausible
CRHR2 is highly expressed in the heart, particularly in ventricular myocytes and coronary vasculature, where its activation reduces cardiomyocyte apoptosis and improves contractile recovery after ischemia, effects mediated by urocortin family peptides. Full-length CRF activates both CRHR1 and CRHR2, with CRHR1 engagement triggering inflammatory responses that counteract cardioprotection. A porcine CRF variant with intrinsic CRHR2 selectivity (as suggested by its platform annotation) could provide urocortin-like cardioprotection using a simpler, shorter peptide scaffold than the urocortins.
Why it matters
Urocortins are in clinical development for heart failure but face manufacturing and stability challenges; a 40-residue CRF variant with CRHR2 selectivity could serve as a structurally simpler cardioprotective peptide with established activity at ACTH-releasing concentrations.
Plausibility.50
Novelty.50
Impact.70
Basis · grounding2 papers · 1 computed/note
[1]
notePlatform assigns this peptide to CRHR2; CRHR2 mediates anxiolytic and cardioprotective signaling independently of CRHR1, per readme description.
[2]
paper
Original Patthy et al. 1986 study confirming CRF bioactivity of porcine hypothalamic CRF variants including this one, establishing its biological potency.
doi: 10.1073/pnas.83.9.2969
[3]
paper
Reviews therapeutic peptide delivery challenges, relevant to developing this variant as a cardiac therapeutic.
doi: 10.1038/s41392-024-02107-5
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.8040639162063599 openfold3-mlx
ranking score 0.8741033673286438 openfold3-mlx
structural qualityopenfold3
0
metricvaluenote
gpde0.704global PDE — lower = better
disorder0.171fraction disordered
chain pair ipTM (A, B)0.804interface quality
3-letter notation
Ser-Glu-Glu-Pro-Pro-Ile-Ser-Leu-Asp-Leu-Thr-Phe-His-Leu-Leu-Arg-Glu-Val-Leu-Glu-Met-Ala-Arg-Ala-Glu-Glu-Leu-Ala-Gln-Gln-Ala-His-Ser-Asn-Arg-Lys-Leu-Met-Glu-Asn
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
runtime350s
predicted bymlx@peptide
predicted at2026-04-22
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). Stress-response research peptide (porcine CRF [1-40; E26, N40]) (pep-10648, v1). PeptideModel. https://peptidemodel.com/card/pep-10648
@peptide{pep10648,
  sequence = {SEEPPISLDLTFHLLREVLEMARAEELAQQAHSNRKLMEN},
  target   = {crhr2},
  author   = {peptidemodel},
  year     = {2026},
  status   = {synthesized}
}
related peptides 5 by signal overlap
clinical trials 27 on ct.gov · 2 on EUCTR · checked 2026-05-09
ct.gov trials 27
with results 5
EUCTR 2
PubMed reviews 1
by phase
1phase 13phase 31phase 42early phase 13no phase
by status
6completed2recruiting1active1withdrawn
references 1 papers
discussion no comments
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