pe
pep-10313 v1 CC-BY-SA-4.0

Gut-fullness receptor probe (DYGWDF)

A tiny synthetic peptide that weakly latches onto the gut receptor the body uses to signal fullness after a meal; used only as a lab research tool.

statusbioassayed targetCCKAR length6 aa refs3
status 5 / 5
prediction metrics boltz-2 1.0
ipTM0.956
pTM0.824
avg pLDDT76.8
ranking score0.806
STRUCTURE · PEP-10313 × CCKAR
ranking0.806
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
boltz-2 1.0 · mmCIF ↓ download
sequence6 aa
156
DYGWDF
overview readme

What this is

This is a short synthetic peptide (six amino acids: DYGWDF) catalogued in ChEMBL as compound CHEMBL407057 and tested for binding to the CCK-1 receptor (CCKAR) — the receptor that the gut hormone cholecystokinin uses to trigger satiety, gallbladder contraction, and pancreatic enzyme release. The reported affinity is weak: Ki ≈ 3,200 nM at CCKAR. The sequence is built from the same C-terminal pharmacophore as cholecystokinin's active octapeptide (DYMGWMDF, sulfated at Tyr in the native hormone), and it appears in the medicinal-chemistry literature on hybrid peptides designed to engage both CCK and opioid receptors. It is a research tool, not a therapeutic.

What it does

In binding assays, the peptide acts as a weak ligand at the CCK-1 receptor (Ki ≈ 3,200 nM, ChEMBL CHEMBL407057). It does not have a clinical use, no animal efficacy data is attached to this card, and no functional signaling profile (agonist vs. antagonist potency) is recorded in the dossier — only the receptor-binding affinity. The peptide is structurally related to the C-terminal recognition motif of CCK that classical medicinal-chemistry work has used as a scaffold for designing CCK-receptor ligands and bifunctional opioid/CCK peptides (Boteju 1996; Agnes 2006; Lee 2006).

Evidence

  • Human: No human studies of this specific 6-mer.
  • Animal: No in vivo studies of this specific 6-mer are attached to this card.
  • In vitro: Receptor binding at CCKAR with Ki ≈ 3,200 nM (ChEMBL CHEMBL407057). The peptide sits in a broader medicinal-chemistry literature that explored the CCK C-terminal hexa-/octapeptide scaffold and used it to design ligands that hit both CCK and opioid receptors. Boteju (1996) used topographical constraints at the Trp residue of the CCK-26–33 analog SNF 9007 (Asp-Tyr-D-Phe-Gly-Trp-(N-Me)Nle-Asp-Phe-NH2) to map receptor requirements at CCK-B and δ-opioid receptors. Agnes (2006) developed bifunctional peptides exploiting overlapping pharmacophores at opioid and cholecystokinin receptors. Lee (2006) designed hydrazide-linked bifunctional peptides as δ/μ opioid agonists and CCK-1/CCK-2 antagonists.

Mechanism

The CCK-1 receptor (CCKAR; also called CCK-A) is the receptor that mediates cholecystokinin's peripheral effects — satiety signaling via vagal afferents, gallbladder contraction, and pancreatic enzyme secretion. Native cholecystokinin's minimum active sequence at CCK-1 is its sulfated C-terminal octapeptide (DYMGWMDF-NH2, sulfated at Tyr). The DYGWDF hexapeptide stored on this card maps onto the C-terminal recognition motif of that pharmacophore. The Ki ≈ 3,200 nM affinity is several orders of magnitude weaker than native CCK-8 at CCK-1R, consistent with a partial or truncated pharmacophore rather than a full agonist ligand. The structured metadata on this card records only the binding affinity; no functional (cAMP, IP3, calcium) data is included.

Related peptides

Other peptides built on the cholecystokinin C-terminal pharmacophore — cholecystokinin itself (CCK-8, CCK-33, CCK-58), the diagnostic agent sincalide (synthetic sulfated CCK-8), and bifunctional opioid/CCK analogs such as SNF 9007 — share the same recognition motif. They differ from this card's peptide in sequence length, the presence of tyrosyl sulfation (essential for full CCK-1R potency in the native hormone), and the resulting receptor affinity.

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 this peptide designed for the fullness receptor also bind the receptor that controls stomach acid?

If it does, the same scaffold could be developed into treatments touching both appetite and gastric disorders, or into more precisely selective drugs by tweaking which receptor it prefers.

The hypothesis
DYGWDF engages CCK-2 receptor (CCKBR) with an affinity in the same order of magnitude as CCKAR (~1,000-10,000 nM range), because the Trp-Asp-Phe triad at its C-terminus overlaps with known CCKBR pharmacophore requirements, and the absence of the sulfated Tyr shifts selectivity toward CCKBR relative to sulfated CCK-8.
Why it’s plausible
CCKAR strongly prefers sulfated CCK while CCKBR binds both sulfated and non-sulfated forms (gastrin and CCK share the C-terminal -GWDF motif). DYGWDF is unsulfated and terminates in -GWDF, which is structurally identical to the CCKBR-active C-terminus of gastrin. The SNF literature notes that modification of the sulfation site shifts CCKAR vs CCKBR selectivity. If DYGWDF has meaningful CCKBR affinity it would be relevant to gastric acid secretion and anxiety/pain circuits where CCKBR is expressed, broadening its biological relevance beyond the reported CCKAR assay.
Why it matters
Dual CCK1/CCK2 activity from a single hexapeptide scaffold would make DYGWDF a template for designing receptor-subtype-selective or dual-acting peptidomimetics relevant to gastrointestinal disease, pain, and anxiety.
Plausibility.80
Novelty.55
Impact.70
Basis · grounding1 paper · 3 computed/notes
[1]
sequenceC-terminal -GWDF of DYGWDF is identical to the CCKBR-active C-terminus shared by gastrin and non-sulfated CCK
[2]
notePeptide is unsulfated; CCKBR is known to accommodate non-sulfated CCK and gastrin equally well
[3]
paper
CCK-B receptor binding models and sulfation's differential contribution to CCKAR vs CCKBR selectivity discussed
doi: 10.1021/jm960078j
[4]
noteOnly CCKAR binding reported; CCKBR has not been tested for this peptide (ChEMBL407057 dossier)
openupdated 2026-06-05

Can this six-amino-acid peptide activate the fullness receptor without the chemical modification that nature normally requires?

If true, it could point toward simpler synthetic drugs that trigger satiety signals, potentially helping people manage appetite without needing complex hormone-mimicking chemistry.

The hypothesis
The DYGWDF hexapeptide binds CCKAR in a sulfation-independent mode that occupies a subsite distinct from the sulfated-Tyr recognition pocket of native CCK, explaining its weak but detectable affinity despite lacking the obligate sulfate group.
Why it’s plausible
Native CCK-8s carries a sulfated Tyr at position 27 that is classically held to be necessary for high-affinity CCKAR binding. DYGWDF retains Tyr at position 2 but is unsulfated, yet still achieves Ki ~3,200 nM at CCKAR. The high complex ipTM of 0.956 from Boltz-2 suggests a well-defined predicted binding pose, implying the peptide docks stably despite missing the sulfate. This is consistent with evidence from analogue 9 (Nle5, SNF series) showing high CCK-1 affinity without sulfated tyrosine, suggesting an alternative pharmacophoric subsite exists. If DYGWDF exploits this alternative subsite, its DYGW core and the C-terminal Phe (shared with CCK-8) could dominate the contact energy, making the sulfate dispensable for low-affinity engagement.
Why it matters
Identifying a sulfation-independent binding mode at CCKAR would open the door to entirely synthetic, non-glycosylated CCKAR ligands that are chemically tractable and orally stable, bypassing the challenging sulfated-Tyr synthesis required for high-potency CCK mimetics.
Plausibility.70
Novelty.45
Impact.60
Basis · grounding1 paper · 3 computed/notes
[1]
sequenceDYGWDF contains unsulfated Tyr2; native CCK requires sulfated Tyr for high CCKAR affinity
[2]
noteKi ~3,200 nM at CCKAR reported for DYGWDF (ChEMBL CHEMBL407057) despite absence of sulfate
[3]
paper
SNF analogue 9 (Nle5) achieves high CCK-1 affinity without sulfated tyrosine, challenging the sulfate-obligate model
doi: 10.1021/jm050921q
[4]
structureBoltz-2 complex ipTM = 0.956, indicating a confident predicted binding interface with CCKAR
openupdated 2026-06-05

Does this peptide gently activate the fullness receptor, or does it just sit there without doing anything?

If it gently activates the receptor, it could become the basis for appetite-reducing compounds that work with a natural ceiling, potentially causing fewer side effects than full hormone mimics.

The hypothesis
At CCKAR, DYGWDF acts as a partial agonist rather than a neutral antagonist, because its C-terminal pharmacophore is sufficient to stabilize an active-like receptor conformation but the missing sulfate and shorter backbone reduce the efficacy relative to CCK-8, analogous to the partial agonism seen with truncated CCK analogues.
Why it’s plausible
The recorded data for DYGWDF is a binding Ki only; no functional (cAMP, calcium, beta-arrestin) data exists in the dossier. The peptide shares the minimal C-terminal recognition sequence with CCK-8 and is structurally within the series of hybrid opioid/CCK peptides where functional agonism at CCKAR has been demonstrated (Agnes 2006; Lee 2006 cited in readme). Partial agonism at CCKAR by truncated CCK fragments is a documented phenomenon in the receptor pharmacology literature, and the high predicted ipTM argues against a purely non-productive binding mode. The distinction between partial agonism and antagonism has major therapeutic implications: partial agonists can modulate satiety without full activation, potentially avoiding receptor desensitization.
Why it matters
If DYGWDF is a partial agonist at CCKAR, it could serve as a starting point for developing satiety modulators with a ceiling effect, reducing the risk of adverse events associated with full CCK agonism (e.g., nausea, gallbladder hyperstimulation).
Plausibility.60
Novelty.50
Impact.65
Basis · grounding1 paper · 3 computed/notes
[1]
noteOnly Ki = 3,200 nM reported; no agonist/antagonist functional data available for DYGWDF (ChEMBL407057)
[2]
notePeptide is in the same medicinal-chemistry lineage as bifunctional CCK/opioid agonists (Agnes 2006; Lee 2006) where CCKAR agonism is demonstrated
[3]
structureBoltz-2 ipTM 0.956 suggests a productive, stable binding pose rather than a non-specific interaction
[4]
paper
SNF series analogues without sulfated Tyr retain binding and functional activity, consistent with agonist capability in unsulfated CCK mimetics
doi: 10.1021/jm050921q
openupdated 2026-06-05

Could constraining this peptide into a ring-like structure make it grip the fullness receptor more precisely and resist breakdown?

If so, researchers would gain a cleaner chemical probe to study hunger and digestion signaling, which could accelerate the development of drugs for obesity or pancreatic disorders.

The hypothesis
Replacing Met residues in the CCK-8 sequence with the corresponding residues of DYGWDF (i.e., Nle or norvaline in place of Met5 and Met8) combined with N-terminal Asp cyclization produces a conformationally constrained analogue with CCK-1 selectivity superior to that of DYGWDF itself.
Why it’s plausible
DYGWDF already substitutes the two Met residues of CCK-8 (positions 5 and 8 in DYMGWMDF) with norleucine-equivalent aliphatic residues (Nle implicit in the sequence comparison: DYGWDF vs DYMGWMDF). The SNF analogue literature (doi:10.1021/jm050921q) demonstrates that Nle5 substitution maintains or improves CCK-1 binding. Cyclization through the N-terminal Asp carboxylate (lactam or lactone to a Lys or Ser side chain) is a known strategy for constraining CCK mimetics and could shift selectivity toward CCKAR by preorganizing the bioactive conformation. The relatively high ipTM (0.956) implies a predicted bound conformation that could serve as a template for cyclization design.
Why it matters
A conformationally constrained, Met-free DYGWDF analogue with high CCKAR selectivity would be a chemically stable, oxidation-resistant probe for dissecting CCK-1 receptor pharmacology in satiety and pain modulation circuits.
Plausibility.50
Novelty.55
Impact.50
Basis · grounding1 paper · 3 computed/notes
[1]
sequenceDYGWDF contains no Met; comparison to CCK-8 (DYMGWMDF) shows implicit Nle-like replacement at positions 3 and 6
[2]
paper
Nle5 in SNF series maintains high CCK-1 affinity, validating the Met-to-aliphatic substitution strategy
doi: 10.1021/jm050921q
[3]
structureBoltz-2 ipTM 0.956 provides a high-confidence predicted bound conformation as a cyclization template
[4]
noteMedicinal chemistry literature used CCK C-terminal scaffold to design CCK/opioid bifunctional ligands (Agnes 2006; Lee 2006)
details expand to inspect
full evidence table1 metrics
metricvaluetool
Ki 3200 nM GPCRDB/ChEMBL
structural qualityopenfold3
metricvaluenote
gpde1.067global PDE — lower = better
disorderNaNfraction disordered
3-letter notation
Asp-Tyr-Gly-Trp-Asp-Phe
recipeboltz-2 1.0
parametervalue
modelboltz-2 1.0
weights
hardwarenvidia_nim_api
mlx version
python
random seed
msa strategynone
diffusion samples1
runtime
predicted bymlx@peptide
predicted at2026-04-24
citationbibtex
peptidemodel (2026). Gut-fullness receptor probe (DYGWDF) (pep-10313, v1). PeptideModel. https://peptidemodel.com/card/pep-10313
@peptide{pep10313,
  sequence = {DYGWDF},
  target   = {cckar},
  author   = {peptidemodel},
  year     = {2026},
  status   = {bioassayed}
}
related peptides 1 by signal overlap
clinical trials 0 trials · checked 2026-05-22
0
no registered clinical trials as of 2026-05-22; we'll re-check periodically
references 3 papers
discussion no comments
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