pe
pep-10638 v1 CC-BY-SA-4.0

Stress-hormone fragment (Pro-opiomelanocortin [115-135])

A small piece of the body's stress-hormone precursor protein, found in mouse pituitary tissue; it switches on the receptor that tells the adrenal gland to release cortisol. Used only as a lab research tool.

statussynthesized targetMC2R length21 aa refs5
snapshot sparse 0% confidence
Class
Endogenous peptide fragment (POMC-derived)
Status
No approved therapeutic status identified
Best-supported effect
None established; peptide was detected and quantified in mouse pituitary tissue by mass spectrometry
Main caveat
No bioactivity, pharmacological, or therapeutic evidence is attached to this card
status 4 / 5
prediction metrics boltz-2 2.2.1
ipTM0.694
pTM0.908
avg pLDDT79.3
ranking score0.773
STRUCTURE · PEP-10638 × MC2R
ranking0.773
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
boltz-2 2.2.1 · mmCIF ↓ download
sequence21 aa
1510152021
RPVKVYP NVAENES AEAFPLE
overview readme

What this is

POMC [115-135] is a 21-amino acid fragment (RPVKVYPNVAENESAEAFPLE) taken from the middle of pro-opiomelanocortin, the large precursor protein that gives rise to ACTH, the endorphins, and the melanocyte-stimulating hormones. This specific stretch corresponds to residues 115-135 of the mature POMC protein after removal of the signal peptide — a position that falls within the ACTH domain of the precursor — and was identified in mouse pituitary tissue by quantitative peptidomics (Che and colleagues 2005; Pan and colleagues 2006). As a sub-fragment of ACTH that carries part of the adrenal-stimulating sequence, it has been studied in the context of melanocortin 2 receptor (MC2R) binding specificity.

History

Pro-opiomelanocortin was recognized in the late 1970s as a single precursor encoding both ACTH and the endorphins. Over the following decades, mass-spectrometry-based peptidomics revealed that the POMC precursor is processed far more extensively than the canonical cleavage products would suggest, yielding a range of intermediate and sub-fragments detectable in pituitary and hypothalamic tissue. Che and colleagues (2005), working with mouse pituitary using stable isotope-labeled quantitative peptidomics, catalogued numerous POMC-derived peptides including fragments within the ACTH region, and Pan and colleagues (2006) extended this approach to PC2 knockout mouse hypothalamus to map the contribution of individual prohormone convertases to POMC fragment generation. The fragment spanning positions 115-135 of mature POMC was identified in the context of these mouse pituitary peptidomics studies.

What it does

Within POMC, the region covered by this fragment lies inside the ACTH sequence, which normally acts on the adrenal cortex to drive cortisol (in humans) or corticosterone (in rodents) synthesis. ACTH exerts this effect by binding the melanocortin 2 receptor (MC2R), a class A G protein-coupled receptor expressed predominantly in the zona fasciculata of the adrenal cortex, where it activates adenylyl cyclase, raises intracellular cAMP, and activates protein kinase A (PKA), ultimately stimulating steroidogenic gene expression and cholesterol import into mitochondria (Harno and colleagues 2018). The POMC [115-135] fragment contains a portion of the sequence between the two pharmacophore regions of ACTH that are known to be required for MC2R activation — the core HFRW motif and the ACTH-specific KKRRP motif — and has been investigated as a probe of MC2R binding specificity (Cai and colleagues 2016).

Mechanism

MC2R is uniquely selective for ACTH among the five melanocortin receptor subtypes; it does not bind α-MSH or other MSH peptides (Cai and colleagues 2016). Two structural pharmacophores within ACTH are required for receptor activation: the MXHFRW consensus sequence shared with all melanocortins, and a KKRRP C-terminal motif specific to ACTH (the second pharmacophore). Structural studies show that the intervening segment must adopt the correct secondary structure to orient these two motifs properly within the receptor-binding pocket. Because POMC [115-135] is a sub-fragment of ACTH located between these pharmacophore elements, its binding to MC2R is distinct from that of intact ACTH: it lacks the full C-terminal ACTH sequence and the complete KKRRP motif, making it a tool for dissecting which portions of ACTH sequence confer MC2R selectivity. MC2R is only functional at the cell surface in complex with its accessory protein MRAP, which is required for receptor trafficking; inactivating mutations in either MC2R or MRAP cause familial glucocorticoid deficiency in humans.

Evidence

  • Human: No clinical studies of the POMC [115-135] fragment as an isolated compound have been published.
  • Animal: Detected as a processing product in mouse pituitary tissue by stable-isotope-label peptidomics (Che and colleagues 2005; Pan and colleagues 2006). No registered trials on ClinicalTrials.gov for this peptide.
  • In vitro: Investigated in the context of MC2R binding specificity studies as a tool peptide for understanding the ACTH pharmacophore (Cai and colleagues 2016).

Known effects

  • POMC precursor context — Within the intact POMC precursor this sequence contributes to adrenal-stimulating ACTH activity; as an isolated fragment, MC2R binding capacity has not been fully characterized independently of the full ACTH sequence — Mechanistic only
  • MC2R probe — Used as a research tool to investigate MC2R binding specificity and the structural requirements of the ACTH–MC2R interaction — Mechanistic only

Safety signals

No safety data exist for POMC [115-135] as an isolated peptide. The fragment derives from an endogenous human protein; as a sub-fragment of ACTH it does not contain the complete sequence needed for full MC2R activation as confirmed by structural pharmacology studies (Cai and colleagues 2016). No adverse event data have been reported.

Regulatory status

  • US: Not approved. Research compound only. No IND or clinical-stage development identified.
  • EU: Not approved. Research compound only.
  • WADA: POMC-derived peptides with potential adrenocortical or melanocortin-stimulating activity are generally of interest to anti-doping authorities; this fragment is not individually listed but falls under the broader class of ACTH-related peptides (S2 class — peptide hormones, growth factors, and related substances).

Related peptides

This fragment is a sub-sequence of the full ACTH molecule and derives from the same POMC precursor as α-MSH, β-endorphin, and the other melanocortins. For the biology of the POMC precursor system as a whole, see the Harno and colleagues (2018) review in Physiological Reviews.

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 2026-06-05

Does this fragment of the stress-hormone precursor occupy the cortisol-triggering receptor without actually switching it on, reducing cortisol production?

If this fragment naturally limits cortisol, it could explain why some people have a blunted stress response and suggests a new target for disorders of the HPA axis, including Cushing syndrome or chronic stress conditions where excess cortisol causes metabolic damage.

The hypothesis
POMC [115-135] does not bind MC2R as a functional agonist but instead acts as a low-affinity competitive inhibitor of ACTH at MC2R, because the fragment (RPVKVYPNVAENESAEAFPLE) lacks the canonical His-Phe-Arg-Trp (HFRW) tetrapeptide core required for MC2R activation.
Why it’s plausible
MC2R is the most restrictive melanocortin receptor, requiring the full ACTH(1-24) sequence for activation, with the HFRW core (ACTH positions 6-9) being essential. Sequence inspection of RPVKVYPNVAENESAEAFPLE shows no HFRW motif and no equivalent aromatic-basic pharmacophore. The predicted ipTM of 0.694, the lowest among the three POMC fragments here, is consistent with a docking pose that occupies the receptor without triggering activation. Such a fragment could competitively attenuate adrenal cortisol production under conditions of high POMC processing flux.
Why it matters
If POMC [115-135] is a partial or competitive inhibitor at MC2R, it would represent an endogenous modulator of adrenal cortisol output, contributing to the desensitization of HPA axis responses after chronic stress when POMC processing increases. This would reframe the POMC processing fragments as regulators rather than inert by-products.
Plausibility.55
Novelty.55
Impact.60
Basis · grounding2 papers · 2 computed/notes
[1]
sequenceRPVKVYPNVAENESAEAFPLE contains no HFRW motif; the closest aromatic residue is Phe17 (AFPLE) but is not flanked by Arg-Trp as required for MC2R activation.
[2]
structureipTM=0.694 is the lowest among the three POMC fragments, consistent with binding without optimal activation geometry.
[3]
paper
MC2R requires ACTH and its HFRW core for activation; melanocortin receptor selectivity is driven by this pharmacophore.
doi: 10.2174/1389203717666160226145330
[4]
paper
ACTH acts at MC4R similarly to MSH, and at MC2R with high selectivity; sub-fragments of ACTH may occupy the receptor binding site with different efficacy profiles.
doi: 10.1152/physrev.00024.2017
openupdated 2026-06-05

Do the slightly different lengths of these fragments, produced in different tissues, determine how much cortisol the adrenal gland makes?

If confirmed, this would reveal a previously invisible layer of control over the stress response, explaining individual differences in cortisol reactivity. It could also help researchers design more precise treatments for cortisol disorders that work at the level of hormone processing rather than receptor blockade.

The hypothesis
Differential prohormone convertase processing generates POMC [115-135] preferentially in the anterior pituitary (PC1/3-dominant) versus shorter fragments [115-133] and [115-134] in the intermediate lobe (PC2-dominant), and this tissue-specific fragment profile tunes the ratio of MC2R occupancy to activation across tissues.
Why it’s plausible
PC1/3 and PC2 cleave POMC at distinct basic residue pairs and generate different product profiles. The three overlapping fragments (115-133, 115-134, 115-135) differ only at the C-terminus (P, PL, PLE), suggesting sequential exopeptidase trimming after endopeptidase cleavage, with the extent of trimming determined by carboxypeptidase E activity that differs between pituitary compartments. The readme mentions PC2 knockout mouse hypothalamus was used to map fragment generation. If the C-terminal extension (E at position 21 in the 21-mer) impairs MC2R binding whereas the shorter PL or P termini do not, then the tissue-specific processing profile would determine MC2R modulator potency.
Why it matters
Tissue-specific regulation of peptide hormone length as a mechanism to tune receptor activity is under-explored. Demonstrating this for POMC fragments in the HPA axis would establish a new regulatory layer relevant to Addison disease, Cushing disease, and the side effects of glucocorticoid therapy.
Plausibility.50
Novelty.60
Impact.60
Basis · grounding2 papers · 2 computed/notes
[1]
noteFragment identified in PC2 knockout mouse hypothalamus peptidomics, establishing PC2 as relevant to its generation and suggesting anterior pituitary vs. intermediate lobe differences.
[2]
sequencepep-10636 (RPVKVYPNVAENESAEAFP, 19aa), pep-10637 (RPVKVYPNVAENESAEAFPL, 20aa), pep-10638 (RPVKVYPNVAENESAEAFPLE, 21aa) differ only in C-terminal residues P, PL, PLE.
[3]
paper
MC2R is expressed in the adrenal cortex and responds to ACTH; its pharmacology is sensitive to C-terminal peptide structure.
doi: 10.2174/1389203717666160226145330
[4]
paper
ACTH effects on lipid metabolism and adrenal function; fine-tuning of MC2R activity has systemic metabolic consequences.
doi: 10.1007/s00018-020-03511-0
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.6937518119812012 boltz-2
ranking score 0.7728755474090576 boltz-2
3-letter notation
Arg-Pro-Val-Lys-Val-Tyr-Pro-Asn-Val-Ala-Glu-Asn-Glu-Ser-Ala-Glu-Ala-Phe-Pro-Leu-Glu
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). Stress-hormone fragment (Pro-opiomelanocortin [115-135]) (pep-10638, v1). PeptideModel. https://peptidemodel.com/card/pep-10638
@peptide{pep10638,
  sequence = {RPVKVYPNVAENESAEAFPLE},
  target   = {mc2r},
  author   = {peptidemodel},
  year     = {2026},
  status   = {synthesized}
}
related peptides 5 by signal overlap
clinical trials 131 on ct.gov · checked 2026-05-09
ct.gov trials 131
with results 38
by phase
1phase 12phase 21phase 34phase 43no phase
by status
5completed2terminated2unknown
references 5 papers
discussion no comments
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