ALEMBIC LABS
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distillation №1

Semax — N-terminal acetylation of Met-1 (Ac-Met-Glu-His-Phe-Pro-Gly-Pro)

N-TERMINAL ACETYLATION OF MET-1 (AC-MET-GLU-HIS-PHE-PRO-GLY-PRO)COGNITIVEMay 1, 2026[ REFINED ]
[↓ download report.pdf]
average confidence
80.3%
pTM
0.8509619832038879
ipTM
0.9414758086204529
binding Δ
0.0%
agreement
—
target
Melanocortin-4 receptor (MC4R) / BDNF-TrkB signaling axis
uniprot
P32245
01/

3D structure

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chain A — peptide (plasma red)chain B+ — target / context (white)
02/

AI analysis

tldr

—

detailed analysis

—

03/

research data

A

known activity

// not yet provided by clinical agent

B

biohacker use

// not yet provided by clinical agent

C

mechanism class

// not yet provided by clinical agent

05/

folding metrics

// no per-residue pLDDT trace — Boltz-2 returned summary metrics only

aggregation propensity (window)

3 windows

confidence metrics

pLDDT mean
0.80
pTM
0.85
ipTM
0.94
Boltz ↔ Chai
—
06/

domain annotations

// not yet annotated by clinical / structural agents

07/

structural caption

The predicted complex shows Ac-Met-Glu-His-Phe-Pro-Gly-Pro adopting an extended conformation consistent with native Semax, with the N-terminal acetyl group oriented away from the receptor interface. The His-Phe dyad is positioned toward the orthosteric pocket as expected for melanocortin-like engagement, while the C-terminal Pro-Gly-Pro motif maintains its characteristic kinked geometry. The acetyl cap appears solvent-exposed and does not introduce steric clashes with the receptor surface.

08/

peptide profile

These are sequence-based heuristic estimates, not wet-lab measurements. Real aggregation propensity requires TANGO/Aggrescan, real BBB permeability requires QSAR models, and real half-life requires PK studies. Treat the numbers as ranked indicators — useful for comparing variants, not for absolute claims.

aggregation propensity
heuristic
0.022
● good
Predicted likelihood of self-aggregation. Lower is better.
≤ 0.40 good · ≤ 0.80 moderate
source: Kyte-Doolittle window proxy
stability prediction
heuristic
0.78
● good
Composite stability score. Higher = more stable in solution.
≥ 0.70 good · ≥ 0.40 moderate
source: charge / proline / length composite
BBB penetration
heuristic
0.436
● moderate
Estimated blood-brain barrier permeability. Goal depends on target tissue.
≥ 0.50 high · ≥ 0.20 moderate
source: hydrophobic fraction proxy
half-life estimate
heuristic
short (~15–45 minutes)
● —
In-silico estimated plasma half-life range.
text estimate
source: length-bucket heuristic
09/

known binders

// no ChEMBL binders found for this target

11/

agent findings

4 findingslast updated: 2026-05-01 13:07:56 UTC
researcher: 1literature: 1structural: 1communicator: 1
☿RESEARCHER agentclaude-opus-4-7
2026-05-01 12:52:52 UTC· 13.3s● COMPLETED
N-terminal acetylation of Met-1 (Ac-Met-Glu-His-Phe-Pro-Gly-Pro)
🜍LITERATURE agentclaude-sonnet-4-6
2026-05-01 12:53:06 UTC· 1m 14s● COMPLETED
8 PubMed + 0 bioRxiv synthesised
🜔STRUCTURAL agentclaude-opus-4-7
2026-05-01 12:54:20 UTC· 11m 49s● COMPLETED
N-terminal acetylation is predicted to be structurally well-tolerated, with high-confidence metrics indicating preserved binding geometry at the MC4R interface. Computed properties support a stable, low-aggregation peptide (stability 0.78, aggregation 0.022) with modest BBB penetration (0.44). The half-life estimate remains short in this static profile, but acetylation is mechanistically expected to extend it by blocking aminopeptidase cleavage — an effect not directly captured by the structural
🜄COMMUNICATOR agentclaude-sonnet-4-6
2026-05-01 13:06:09 UTC· 1m 47s● FAILED
// no summary recorded
12/

caveats

  • ─in silico prediction only — requires wet lab validation
  • ─single-run prediction (not ensembled)
  • ─predicted properties may not reflect biological reality
  • ─this is research, not medical advice
  • ─modified peptides have not been synthesized or tested
13/

data

[↓ download fold.json][↓ download structure.pdb][⊘ on-chain unavailable][⎘ copy permalink]
14/

works cited

  1. [1]

    (2025). Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice.

    · PubMed PMID ↗

  2. [2]

    (2021). Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats.

    · PubMed PMID ↗

  3. [3]

    (2026). Therapeutic Peptides in Orthopaedics: Applications, Challenges, and Future Directions.

    · PubMed PMID ↗

  4. [4]

    (2022). Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Membrane Models.

    · PubMed PMID ↗

  5. [5]

    (2010). Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia.

    · PubMed PMID ↗

  6. [6]

    (2017). Semax, an analog of ACTH (transcriptome analysis study)

    · PubMed PMID ↗

  7. [7]

    (2025). Semax, a Copper Chelator Peptide, Decreases the Cu(II)-Catalyzed ROS Production and Cytotoxicity of aβ by Metal Ion Stripping and Redox Silencing.

    · PubMed PMID ↗

  8. [8]

    (2005). Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents.

    · PubMed PMID ↗