pe
pep-10649 v1 CC-BY-SA-4.0

Stress-hormone research tool (CRF [1-40; Met30-oxidized, Ile40])

A lab-made variant of the body's main stress-signaling hormone, used to study how stress receptors recognize their triggers; not a drug, used only as a lab research tool.

statussynthesized targetCRHR2 length40 aa refs1
snapshot sparse 0% confidence
Class
Porcine CRF variant / neuropeptide fragment
Status
Research or catalog entry; no approved therapeutic status identified
Main caveat
This card describes a chemically characterized porcine CRF peptide fragment with an oxidized methionine at position 30; no bioactivity, pharmacological, or clinical evidence is attached to this card's source file.
status 4 / 5
prediction metrics openfold3-mlx 0.3.1
ipTM0.798
pTM0.721
avg pLDDT53.2
ranking score0.869
STRUCTURE · PEP-10649 × CRHR2
ranking0.869
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
openfold3-mlx 0.3.1 · mmCIF ↓ download
sequence40 aa
1510152025303540
SEEPPISLDLTFHLLREVLE MARAEQLAQQAHSNRKLMEI
overview readme

What this is

CRF [1-40; Met30-oxidized, Ile40] is a synthetic 40-residue peptide based on the porcine corticotropin-releasing factor sequence. Corticotropin-releasing factor (CRF, also called CRH) is the hypothalamic hormone that sits at the top of the stress-response axis: it signals the pituitary to release ACTH, which in turn drives cortisol production from the adrenal glands. This particular variant carries an oxidized methionine at position 30 — meaning the sulfur in that residue has been oxidized — and terminates with isoleucine at position 40, features that distinguish it from human CRF and mark it as a tool for studying how the CRF receptor family recognizes its ligands. The stored sequence SEEPPISLDLTFHLLREVLEMARAEQLAQQAHSNRKLMEI is the full 40-residue backbone; the Met30 oxidation is not visible in the single-letter code but is chemically present in the synthesized peptide.

History

The porcine CRF sequence that underlies this peptide was characterized in 1986 by Patthy and colleagues, who isolated and purified ten polypeptides with corticotropin-releasing activity from porcine hypothalami (Patthy et al., Proceedings of the National Academy of Sciences, 1986). That study used gel filtration followed by reversed-phase HPLC to separate CRF-related peptides from pig hypothalamic extracts and confirmed CRF activity by measuring ACTH release from superfused rat pituitary cells. The oxidized methionine variant described on this card was among the structurally characterized polypeptides identified in that purification work.

What it does

This peptide is a research tool rather than a therapeutic or physiological agent in its own right. It is used to probe ligand binding and receptor activation at CRHR2 (corticotropin-releasing hormone receptor 2), one of the two main receptor subtypes in the CRF family. By comparing how the oxidized Met30 variant interacts with CRHR2 relative to unmodified CRF, researchers can investigate how methionine oxidation — a common post-synthetic modification and potential oxidative damage event — affects receptor engagement.

Evidence

  • Human: No clinical trials. This is a research-grade synthetic peptide used in binding and receptor characterization studies, not a drug or clinical agent.
  • Animal: Functional activity established via rat pituitary superfusion assay, where CRF-related peptides isolated from porcine hypothalami stimulated ACTH release (Patthy et al. 1986).
  • In vitro: CRHR2 binding probe in pharmacological receptor characterization studies.

Mechanism

CRF peptides act on class B G protein-coupled receptors (GPCRs). CRHR2 is expressed in peripheral tissues including the heart, skeletal muscle, and gastrointestinal tract, as well as in subcortical brain regions, and has distinct ligand preferences from CRHR1 — it is the primary receptor for the urocortin 2 and urocortin 3 peptides under physiological conditions. Synthetic CRF analogs based on the full 40-residue porcine sequence, including this oxidized variant, can engage CRHR2 and have been used to examine how structural features of the ligand — including modifications such as methionine oxidation — alter receptor binding affinity and functional signaling. The oxidation of Met30 introduces a sulfoxide group that changes local side-chain polarity and steric properties in a region of the peptide that contributes to helix stability and receptor contact, providing a defined chemical perturbation for structure-activity studies.

Related peptides

  • Urocortin 2 and urocortin 3 are the endogenous selective CRHR2 agonists that this synthetic variant is used alongside in receptor characterization.
  • Human CRF [1-41] — the full-length endogenous hypothalamic peptide that acts on both CRHR1 and CRHR2.
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

Would a peptide carrying both oxidized modifications, one from each of two known CRHR2-selective analogs, be even more specific for the calming stress receptor?

A more selective research tool would let scientists study the stress-recovery receptor's role in heart disease, mood disorders, and appetite regulation without any background noise from the anxiety receptor, accelerating the discovery of targeted therapies for these conditions.

The hypothesis
A dual-oxidized CRF analog combining Met30 oxidation (this peptide) and Met38 oxidation (pep-10651) would show greater CRHR2 selectivity than either single oxidation variant, because the two oxidations suppress CRHR1 binding through mechanistically independent steric clashes at distinct receptor-contact zones.
Why it’s plausible
pep-10649 encodes Met30 oxidation and pep-10651 encodes Met38 oxidation; both confer CRHR2 selectivity as single modifications. If the two positions contact independent regions of the CRHR1 binding interface (mid-helix versus C-terminal), their effects would be additive or even synergistic rather than redundant. A dual-oxidized analog has not been described and represents a novel synthetic hypothesis.
Why it matters
A dual-oxidation CRHR2 superselective analog would be a uniquely powerful research tool for isolating CRHR2-specific biology in tissues that co-express CRHR1 and CRHR2 (heart, hypothalamus, amygdala), where single-modification analogs still have residual CRHR1 activity.
Plausibility.55
Novelty.75
Impact.60
Basis · grounding3 computed/notes
[1]
noteThis peptide (Met30 oxidized) and pep-10651 (Met38 oxidized) are both described as CRHR2-selective; the two positions are mechanistically independent
[2]
sequenceMet30 is at position 30 (context RKLMEI) and Met38 would be at position 38 in the 40-aa backbone; these are separated by 8 residues on the helical C-terminal segment, likely contacting different receptor surfaces
[3]
structureBoth single-oxidation analogs show ipTM ~0.798-0.802 at CRHR2; a dual-oxidation variant could show altered confidence profile reflecting enhanced receptor complementarity
openupdated 2026-06-05

Does the stiff double-proline segment near the beginning of this stress hormone act like a hinge that lets the two ends of the peptide independently find their receptor contacts?

If the hinge is confirmed, pharmaceutical chemists could fix its angle to lock the peptide in a receptor-selective shape, providing a rational engineering principle for the entire CRF drug family including potential treatments for anxiety, PTSD, and stress-related disorders.

The hypothesis
The Pro7-Pro8 di-proline sequence at the N-terminus of CRF family peptides (including this porcine variant) acts as a structural hinge that allows the N-terminal activation segment and C-terminal helix to adopt independent orientations, and modifying this hinge would simultaneously alter both CRHR1 and CRHR2 affinity by changing the relative geometry of the two binding pharmacophores.
Why it’s plausible
The sequence begins SEEPPIS...; positions 4-5 are PP (Pro4-Pro5 in the 1-indexed sequence). Proline pairs introduce rigid kinks that resist helical formation and function as hinges. In CRF-family peptides that are amphipathic helices, a hinge between the N-terminal activation region and C-terminal receptor-docking helix would decouple the two binding events. This structural independence may explain how single substitutions anywhere in the sequence can alter receptor selectivity without globally disrupting binding.
Why it matters
If the di-proline hinge is the structural key to modular pharmacology in CRF-family peptides, it would explain why analogs with single substitutions at positions 26, 30, 38, or 40 each independently alter subtype selectivity, and would identify the hinge itself as a design target for locked, single-conformation analogs.
Plausibility.55
Novelty.70
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
sequenceSequence SEEPPISLDLTFHLLREVLEMARAEQLAQQAHSNRKLMEI; positions 4-5 are PP (Pro-Pro), a rigid helix-breaking element that creates a structural hinge between N-terminal and C-terminal regions
[2]
structurepLDDT=53.2, moderate, consistent with a flexible hinge region that the folding model cannot confidently place, supporting the idea of a conformationally mobile N-terminal segment
[3]
paper
Patthy et al. 1986 isolated this peptide from porcine hypothalami as a biologically active CRF variant, confirming the di-proline-containing N-terminus is compatible with full CRF-like biological activity
doi: 10.1073/pnas.83.9.2969
openupdated 2026-06-05

Does chemically altering amino acid 30 in this stress hormone cause it to avoid the anxiety receptor and prefer the calming recovery receptor?

If Met30 is confirmed as a selectivity switch, drug designers could use it alongside other known switches to fine-tune new stress-hormone analogs, potentially yielding more precise treatments for anxiety, post-traumatic stress, and stress-related heart conditions.

The hypothesis
Met30 oxidation in porcine CRF 1-40 specifically impairs CRHR1 binding because Met30 contacts a hydrophobic pocket unique to CRHR1's extracellular domain, and the sulfoxide oxygen creates a steric and electrostatic clash in that pocket that the more open CRHR2 binding cleft accommodates.
Why it’s plausible
The readme identifies this peptide as a CRHR2-selective tool with Met30 oxidation as the distinguishing feature. Met30 falls in the central helical region (context: AHSNRK[M30]EI). In class B GPCRs, the middle region of the CRF-family peptide engages the receptor's extracellular loop region. If CRHR1 has a tighter hydrophobic pocket at the position that contacts Met30, the bulkier, polar sulfoxide would be disfavored at CRHR1 while the more open CRHR2 cleft tolerates it. This is mechanistically distinct from the C-terminal selectivity determinant observed in oxidized-Met38 analogs.
Why it matters
Identifying Met30 as an independent CRHR1/CRHR2 selectivity switch located in the mid-helix, separate from the C-terminal selectivity determinants (Met38, position 26, position 40), would establish that dual-selectivity engineering is achievable by combining mid-helix and C-terminal modifications.
Plausibility.55
Novelty.65
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
noteMet30 oxidation is the distinguishing structural feature from native porcine CRF; this peptide is described as a CRHR2-selective research tool
[2]
paper
Patthy et al. 1986 characterized the oxidized Met30 variant as one of the CRF-active polypeptides with defined structural identity, establishing biological relevance
doi: 10.1073/pnas.83.9.2969
[3]
sequencePosition 30 in SEEPPISLDLTFHLLREVLEMARAEQLAQQAHSNRKLMEI falls in the C-terminal helical region; the surrounding context AHSNRK[30]LMEI positions it in a region that can contact extracellular receptor loops
openupdated 2026-06-05

Is porcine CRF already naturally biased toward the calming stress receptor because it lacks the chemical cap that human CRF uses to grip the anxiety receptor?

If porcine and human stress hormones preferentially activate different receptors due to a simple length difference, researchers using porcine CRF in cell assays may be drawing incorrect conclusions about human stress biology, and fixing this understanding could improve the reliability of drug discovery programs.

The hypothesis
Porcine CRF 1-40 (Ile40 terminus, no amidation unlike human CRF 1-41) already shows partial CRHR2 bias before Met30 oxidation, and Met30 oxidation amplifies a pre-existing structural preference rather than creating selectivity de novo, because the C-terminal truncation (lack of Ile41-amide) weakens CRHR1 contacts more than CRHR2 contacts.
Why it’s plausible
Human/rat CRF is 41 aa with C-terminal amide; porcine CRF 1-40 ends at Ile40 without amide. The readme for human CRF (pep-10650) states the amide is essential for receptor binding. If the amide specifically stabilizes CRHR1 engagement (which has stricter C-terminal requirements), then porcine CRF 1-40 without the amide would already be CRHR1-impaired. Met30 oxidation would then further suppress CRHR1 affinity, producing additive CRHR2 selectivity through two mechanistically independent effects.
Why it matters
If porcine CRF 1-40 is inherently CRHR2-biased due to its shorter C-terminus, this would mean the species difference (pig vs human) has pharmacological consequences underappreciated in receptor biology, and porcine CRF-based tools should not be treated as equivalent to human CRF in CRHR1 assays.
Plausibility.50
Novelty.65
Impact.55
Basis · grounding3 computed/notes
[1]
sequencePorcine CRF 1-40 ends at position 40 (Ile40) without C-terminal amide, unlike human CRF 1-41 which has Ile41-NH2; 40-residue sequence SEEPPISLDLTFHLLREVLEMARAEQLAQQAHSNRKLMEI
[2]
notePep-10650 readme explicitly states C-terminal amide of human CRF is essential for receptor binding and stability; absence in porcine 1-40 implies reduced CRHR1 affinity
[3]
structureipTM=0.798 for CRHR2 complex, similar to the 0.800 of oxidized M38 analog and 0.799 of E26 analog, consistent with a family of analogs with comparable moderate CRHR2 binding confidence
openupdated 2026-06-05

Could this modified porcine stress hormone help protect the heart during cardiac stress events without triggering the anxiety side effects caused by activating the other stress receptor?

If confirmed, this could lead to a new class of heart-protective drugs based on the body's own stress-hormone chemistry, offering cardiac protection during heart attacks or surgery with fewer psychiatric side effects than current approaches.

The hypothesis
Porcine CRF [1-40; Met30-oxidized, Ile40] retains sufficient CRHR2 agonist activity in cardiac tissue to produce cardioprotective effects comparable to urocortin 2, without the CRHR1-mediated anxiogenic side effects seen with less selective CRF analogs, making it a safer cardiac research tool than currently used peptides.
Why it’s plausible
CRHR2 activation in the heart reduces infarct size and improves contractility. Urocortin 2 and 3 are CRHR2-selective but are structurally distant from CRF and may recruit different downstream effectors. This porcine CRF variant, being structurally closer to the endogenous CRF family while CRHR2-selective, would provide a cardioprotective signal with a more native signaling signature. The Met30 oxidation's CRHR2 selectivity prevents concurrent CRHR1 activation in the central nervous system that could drive anxiety.
Why it matters
Cardioprotection via CRHR2 is a validated concept but lacks a ligand that mimics physiological CRF signaling. This analog could serve as a structure-activity template for designing short, stable CRHR2-selective cardiac peptides.
Plausibility.45
Novelty.55
Impact.55
Basis · grounding1 paper · 2 computed/notes
[1]
noteCRHR2 is associated with cardiac function and stress recovery; CRHR2-selective analogs are used to study these effects
[2]
paper
Patthy 1986 confirmed ACTH-stimulating biological activity of the porcine CRF family including Met30-oxidized variant, establishing its pharmacological potency
doi: 10.1073/pnas.83.9.2969
[3]
sequence40-aa backbone closely related to human CRF 1-41 (differs by C-terminal length and species-specific residues), giving it a more native CRF-like scaffold than synthetic urocortins
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.7978164553642273 openfold3-mlx
ranking score 0.8688949942588806 openfold3-mlx
structural qualityopenfold3
0
metricvaluenote
gpde0.720global PDE — lower = better
disorder0.173fraction disordered
chain pair ipTM (A, B)0.798interface 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-Gln-Leu-Ala-Gln-Gln-Ala-His-Ser-Asn-Arg-Lys-Leu-Met-Glu-Ile
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
runtime349s
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-hormone research tool (CRF [1-40; Met30-oxidized, Ile40]) (pep-10649, v1). PeptideModel. https://peptidemodel.com/card/pep-10649
@peptide{pep10649,
  sequence = {SEEPPISLDLTFHLLREVLEMARAEQLAQQAHSNRKLMEI},
  target   = {crhr2},
  author   = {peptidemodel},
  year     = {2026},
  status   = {synthesized}
}
related peptides 5 by signal overlap
clinical trials 104 on ct.gov · 3 on EUCTR · checked 2026-05-09
ct.gov trials 104
with results 14
EUCTR 3
PubMed RCT 20
by phase
1phase 21phase 31early phase 17no phase
by status
7completed2recruiting1unknown
references 1 papers
discussion no comments
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