pe
pep-10625 v1 CC-BY-SA-4.0

CGRP tail fragment: lab research tool (NVGSEAF)

A tiny piece of the CGRP nerve peptide, used in lab studies to understand how CGRP interacts with the calcitonin receptor; not a drug and has no clinical use.

statussynthesized targetCALCR length7 aa refs7
status 4 / 5
prediction metrics boltz-2 2.2.1
ipTM0.923
pTM0.857
avg pLDDT61.6
ranking score0.677
STRUCTURE · PEP-10625 × CALCR
ranking0.677
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
boltz-2 2.2.1 · mmCIF ↓ download
sequence7 aa
157
NVGSEAF
in the news 11 articles
overview readme

What this is

alpha-CGRP (31-37) is a short seven-amino-acid fragment (NVGSEAF) corresponding to the C-terminal tail of rat, mouse, and canine alpha-CGRP — the full neuropeptide that gives the calcitonin/CGRP family its name. It is not a drug and has no clinical use; it is a research peptide used to ask which parts of the parent CGRP molecule do what. The stored sequence is the unmodified linear heptapeptide and represents only the very C-terminus of the 37-residue parent hormone — the rest of the CGRP molecule, including its N-terminal disulfide ring, is not present in this fragment. The "E" at position 36 distinguishes the rat/mouse/canine alpha form from the human beta-CGRP C-terminus, which carries a lysine at the same position.

What it does

In isolation, the heptapeptide is a much weaker pharmacological tool than intact CGRP. Maton and colleagues (1990) tested C-terminal fragments of CGRP on dispersed acini and pancreatic membranes and reported that short CGRP C-terminal peptides behave as agonists at the cholecystokinin (CCK) receptor rather than as functional CGRP receptor agonists — a reminder that fragments of a peptide hormone often acquire activity at unrelated receptors instead of preserving the parent's pharmacology. The platform attaches this card to the calcitonin receptor (calcr) because the parent peptide alpha-CGRP belongs to the calcitonin/CGRP/amylin receptor family (Hay 2018), but the fragment itself has not been shown to be a selective calcitonin-receptor ligand.

Mechanism

The parent peptide alpha-CGRP acts through class B (secretin-family) GPCRs that are reshaped by accessory proteins called RAMPs: the calcitonin receptor-like receptor (CLR) paired with RAMP1 becomes the canonical CGRP receptor, while the calcitonin receptor (CTR) paired with RAMP1/2/3 forms the amylin (AMY) receptors (Hay 2018, Barwell 2012). The C-terminal portion of CGRP — including the region this heptapeptide is taken from — is generally regarded as contributing to receptor recognition and binding in the parent hormone, whereas the N-terminal disulfide-bonded loop is required to drive G-protein activation; RAMPs further reshape ligand selectivity at these receptors as allosteric modulators (Advances in Pharmacology 2020). Because NVGSEAF lacks the disulfide loop and most of the central helical region of CGRP, it would not be expected to act as a full agonist at the CLR/RAMP1 CGRP receptor, which is consistent with the Maton (1990) observation that C-terminal CGRP fragments instead engage the CCK receptor.

Evidence

  • Human: No human studies of this fragment.
  • Animal/in vitro: Maton and colleagues (1990) reported agonist activity of C-terminal CGRP fragments at the CCK receptor on dispersed pancreatic acini and membranes. Broader pharmacology of the calcitonin/CGRP/amylin receptor family — including the calcitonin receptor that this card is linked to — is reviewed by Hay and colleagues (2018) and by Barwell and colleagues (2012). Mechanistic work on calcitonin/amylin receptor peptide interaction has been carried out by Lee and colleagues (2016), and the role of RAMPs as allosteric modulators of these receptors is reviewed in Advances in Pharmacology (2020). None of these specifically validate NVGSEAF as a calcitonin-receptor ligand; they establish the receptor-family context the parent peptide and its fragments are studied against.

Related peptides

Alpha-CGRP (31-37) is a fragment of the parent peptide alpha-CGRP and shares its receptor-family context with calcitonin, amylin, adrenomedullin, and adrenomedullin-2/intermedin (Hay 2018). These all act through class B GPCRs — the calcitonin receptor (CTR, the target this card is linked to) and the calcitonin receptor-like receptor (CLR) — whose ligand selectivity is reshaped by RAMP1, RAMP2, and RAMP3 accessory proteins (Barwell 2012). The fragment is closest in sequence to the C-terminus of the rat, mouse, and canine alpha-CGRP parent peptide; the equivalent C-terminal region of human beta-CGRP differs by one residue (lysine in place of glutamate at position 36).

Hypotheses3 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 NVGSEAF actually bind to the calcitonin receptor, or does it instead act on a gut hormone receptor as older experiments suggested?

Getting the target right directs research toward the correct disease areas. If the true target is a gut receptor, this fragment could inform drug development for digestive and metabolic conditions rather than migraine or bone disease.

The hypothesis
The calcitonin receptor (calcr) annotation for NVGSEAF is incorrect at the fragment level: the high Boltz-2 complex ipTM (0.923) reflects docking of the fragment into a shallow surface groove rather than the orthosteric CGRP-binding pocket, and the true pharmacologically relevant receptor for isolated NVGSEAF in biological assays is a CCK receptor subtype.
Why it’s plausible
The platform assigns calcr based on the parent alpha-CGRP lineage, but the readme explicitly states the fragment has not been shown to be a selective calcitonin-receptor ligand. The ipTM of 0.923 is high, but pLDDT of 61.6 indicates substantial structural disorder in the complex, consistent with a non-specific or low-confidence binding pose. The CGRP receptor requires RAMP1 co-association for high-affinity binding; a 7-residue fragment lacking the N-terminal ring and helix of CGRP is unlikely to recapitulate that interaction geometry. Maton et al. data directly support CCK-receptor activity in isolated fragment form.
Why it matters
Correct target annotation matters for downstream swarm hypothesis generation. If NVGSEAF is a CCK-receptor ligand, hypotheses about calcr-mediated bone metabolism or migraine biology are misdirected, while hypotheses about pancreatic secretion and satiety signaling become relevant.
Plausibility.55
Novelty.45
Impact.60
Basis · grounding1 paper · 2 computed/notes
[1]
structureBoltz-2 complex ipTM=0.923 but pLDDT=61.6 indicates low confidence in the modeled conformation despite favorable interface score; consistent with non-specific or disordered docking.
[2]
noteReadme explicitly states the fragment has not been shown to be a selective calcitonin-receptor ligand and that CGRP receptor requires RAMP1 for high-affinity signaling.
[3]
paper
Pharmacology of the calcitonin/CGRP/AM receptor family shows RAMP-dependent receptor selectivity; small C-terminal fragments are not established CGRP receptor agonists.
doi: 10.1111/bph.14075
openupdated 2026-06-05

Does removing the flexible glycine at position 3 prevent this fragment from activating its receptor?

If a single amino acid controls the shape needed for receptor activation, chemists could design rigid versions of this fragment that lock in the active shape, potentially making more potent or selective research tools.

The hypothesis
The glycine at position 3 (G in NVGSEAF) acts as a conformational pivot that allows the peptide to adopt a bent backbone geometry, and substitution of G3 with alanine or alpha-aminoisobutyric acid would abolish CCK-receptor agonism by locking the fragment in an extended conformation incompatible with receptor engagement.
Why it’s plausible
Glycine is the only natural amino acid without a side-chain, conferring unique backbone flexibility. In a seven-residue peptide, a central glycine at position 3 divides the sequence into an N-terminal tripeptide (NVG) and a C-terminal tetrapeptide (SEAF). The tetrapeptide carries the pharmacophoric elements proposed for CCK engagement (the acidic E). A bend at G3 could position the C-terminal pharmacophore optimally. This is a testable structural hypothesis distinct from any existing CGRP fragment structure-activity data.
Why it matters
Defining the role of G3 would establish the minimal geometric requirements for CCK-receptor engagement by this scaffold, potentially enabling the design of conformationally constrained peptidomimetics with improved receptor selectivity.
Plausibility.50
Novelty.55
Impact.45
Basis · grounding2 computed/notes
[1]
sequenceSequence NVGSEAF confirmed; G at position 3 is the sole residue lacking a side chain, providing unique backbone flexibility in this 7-residue peptide.
[2]
noteFragment is an unmodified linear heptapeptide; no cyclization or conformational constraint is present, making backbone geometry entirely governed by residue identity.
openupdated 2026-06-05

Does the glutamate at position 6 of NVGSEAF explain why rat CGRP fragments activate gut hormone receptors instead of their parent's target?

If true, this tiny peptide could become a clean, non-sulfated research tool for studying gut hormone receptors, which are targets for obesity and digestive disease drugs. It would also explain why rat and human versions of the same fragment behave differently.

The hypothesis
The CGRP C-terminal heptapeptide NVGSEAF engages the CCK receptor (CCK-A or CCK-B) with measurable affinity through a non-classical binding mode, and the glutamate at position 6 (E36 of parent CGRP) is the primary determinant of CCK-receptor selectivity over the calcitonin receptor.
Why it’s plausible
Maton et al. (1990) showed that short CGRP C-terminal fragments act as agonists at CCK receptors rather than CGRP/calcitonin receptors. The heptapeptide ends in -SEAF, where the acidic glutamate at position 6 could mimic the sulfated tyrosine pharmacophore that CCK ligands present for receptor engagement. Human beta-CGRP carries lysine at this position instead of glutamate; the charge reversal at a single residue position distinguishes species variants and could explain differential CCK receptor engagement between alpha and beta C-terminal fragments.
Why it matters
If E36 is the CCK-receptor selectivity determinant, this seven-residue scaffold becomes a minimal, non-sulfated CCK-receptor probe, useful for dissecting the receptor's recognition pharmacophore independently of the bulky, sulfated CCK peptides normally used.
Plausibility.35
Novelty.60
Impact.55
Basis · grounding1 paper · 2 computed/notes
[1]
paper
Literature context describing CGRP fragment pharmacology and the calcitonin gene-related peptide family processing.
doi: 10.1046/j.1365-2613.2000.00176.x
[2]
noteMaton et al. (1990) reported short CGRP C-terminal peptides behave as agonists at CCK receptors, not CGRP receptors; E at position 36 is species-specific to rat/mouse/canine alpha-CGRP versus human beta-CGRP which carries K.
[3]
sequenceSequence NVGSEAF confirmed; position 6 is glutamate (E), an anionic residue absent in the human beta-CGRP C-terminal variant.
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.9233613014221191 boltz-2
ranking score 0.6771465539932251 boltz-2
3-letter notation
Asn-Val-Gly-Ser-Glu-Ala-Phe
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). CGRP tail fragment: lab research tool (NVGSEAF) (pep-10625, v1). PeptideModel. https://peptidemodel.com/card/pep-10625
@peptide{pep10625,
  sequence = {NVGSEAF},
  target   = {calcr},
  author   = {peptidemodel},
  year     = {2026},
  status   = {synthesized}
}
related peptides 5 by signal overlap
clinical trials 19 on ct.gov · checked 2026-05-22
ct.gov trials 19
with results 4
PubMed RCT 92
by phase
3phase 21phase 32phase 44no phase
by status
5completed2recruiting2terminated1unknown
references 7 papers
discussion no comments
sign in to comment
peptidemodel.com CC-BY-SA-4.0 research only · not for human use