SYN-AKE (Dipeptide Diaminobutyroyl Benzylamide Diacetate)
The best-known thing about this ingredient — that it comes from snake venom — is the part that needs the most correction. SYN-AKE contains no venom. It is a small synthetic molecule modelled on a fragment of a venom peptide, and the venom peptide’s pharmacology is not the ingredient’s pharmacology. This page gives verified identity data, separates the two literatures, and states how little has actually been published on the ingredient itself.
What SYN-AKE is
SYN-AKE is a trade name; the INCI name is Dipeptide Diaminobutyroyl Benzylamide Diacetate, and that name, read carefully, describes the whole molecule. The core is a β-alanyl-prolyl dipeptide joined to a 2,4-diaminobutyryl residue whose carboxyl terminus is capped as a benzylamide rather than left free. The material is supplied as the diacetate salt, which is why the formula and molecular weight carry two acetate units.
Calling it a peptide is generous. It is a peptidomimetic — a small molecule built from amino-acid units and designed to reproduce the shape of a natural peptide’s active region, without being that peptide or behaving like one in a formulation.
Where the snake comes in
The natural molecule behind it is waglerin-1, found in the venom of the temple pit viper Tropidolaemus wagleri. Waglerin-1 is a genuinely interesting toxin: Molles et al. (2002, Biochemistry) mapped how residues in the ε subunit of the muscle nicotinic acetylcholine receptor confer its selectivity for the α–ε subunit interface site. Debono et al. (2017, J Mol Evol) — a paper titled, without irony, “Viper Venom Botox” — traced the molecular origin of the waglerin peptides and noted openly that their industrial application is in skin cream products. The venomics of the species has been characterised in detail (Tan et al., 2017, Sci Rep).
All of that is real, and none of it is evidence about SYN-AKE. Waglerin-1 is a 22-residue, disulphide-constrained peptide acting at a specific receptor subunit interface. SYN-AKE is a roughly 496 g/mol synthetic analogue of a fragment of it. Whether the analogue retains the receptor selectivity that the mapping work established for the parent toxin, at concentrations reachable through intact skin, is a question the published literature does not answer — and the ingredient’s own indexed study did not test.
Reference data
Verified against the public chemical record; the deposited structure was inspected and matches the INCI description.
| Property | Value |
|---|---|
| INCI name | Dipeptide Diaminobutyroyl Benzylamide Diacetate |
| Trade name | SYN-AKE (DSM) |
| Class | Peptidomimetic small molecule, supplied as the diacetate salt |
| Structure | β-Alanyl-prolyl joined to 2,4-diaminobutyryl, C-terminally capped as the benzylamide |
| CAS number | 823202-99-9 |
| Molecular formula | C₂₃H₃₇N₅O₇ (diacetate salt) |
| Molecular weight | ≈ 495.6 g/mol (diacetate salt) |
| PubChem CID | 71465152 |
| Modelled on | Waglerin-1, from Tropidolaemus wagleri venom |
| Physical form | White to off-white powder (as supplied) |
| Documented use concentration | Not found in any independently published source |
Note the salt form when reading a certificate: the figure a mass-spectrometry identity check reports is for the free base, not for the diacetate, and a weighed quantity of diacetate salt contains proportionally less of the active molecule. This is an ordinary but easily missed accounting problem when a formula is written against a peptide-salt raw material.
The evidence, stated plainly
The one indexed study of the ingredient
Gok, Budama-Kilinc and Kecel-Gunduz (2024, J Biomol Struct Dyn) is, as far as we can find, the only published study of SYN-AKE as such. It combined molecular docking and 50-nanosecond molecular-dynamics simulation of the molecule against matrix metalloproteinases and SIRT1, a DPPH radical-scavenging assay for antioxidant activity, an MTT cytotoxicity assay and an Ames genotoxicity test. The authors reported stable predicted binding to MMP-13 and SIRT1 and concentration-dependent radical scavenging, and concluded the molecule “may hold promise” in anti-ageing formulations.
Two observations a formulator should make about that paper. First, it is computational plus benchtop chemistry — there is no skin model, no human subject and no permeability measurement in it. Second, and more interesting: the targets it docked against, MMPs and SIRT1, have nothing to do with the nicotinic-receptor mechanism the ingredient is sold on. The one study of SYN-AKE tested a different hypothesis from the one in the marketing.
The combination study
Zhu et al. (2026, Int J Cosmet Sci) is an ex-vivo study plus two clinical studies (n = 50 and n = 42) of a serum containing dipeptide diaminobutyroyl benzylamide diacetate together with acetyl hexapeptide-8, gluconolactone, niacinamide and laminaria extract. Statistically significant improvements were reported for the finished serum. All authors were employed by L’Oréal, and with five actives in the formula nothing in the result is attributable to this ingredient specifically.
What is missing
- No standalone human trial of the ingredient.
- No published measurement of whether it permeates skin, which for a molecule whose proposed target sits at a neuromuscular junction is the whole question.
- No Cosmetic Ingredient Review safety assessment that we could locate, and therefore no independently reviewed maximum use concentration.
- No published demonstration that the analogue retains waglerin-1’s receptor selectivity.
Formulation, stability and storage
Little is published, so this section states only what has a basis.
- Salt form. Supplied as the diacetate. That affects both the weighing calculation and, in a poorly buffered system, the pH of a concentrated premix.
- Water phase. The molecule is polar and salt-forming; the benzylamide cap adds a hydrophobic element, but this is not a lipidated active in the way the palmitoyl peptides are.
- Small, and not a normal peptide backbone. With a capped C-terminus and a β-amino acid in the chain, it is not a straightforward exopeptidase substrate the way a conventional peptide is — which is a plausible reason for the design, though we have found no published stability data confirming it.
- No published pH window or compatibility data. None found in the indexed literature. Any figure a supplier gives is theirs, not the literature’s.
Raw material is stored dry, cold and dark, as any small synthetic powder would be; see how to store peptides.
Verifying identity and purity
Mass spectrometry confirms identity by comparing the measured mass against the expected mass for this specific structure — remembering that the diacetate salt and the free base give different numbers, and a certificate should say which it is reporting. HPLC reports purity as a percentage. For an ingredient with essentially one published study behind it, the certificate is doing more of the work than usual. See how to read a COA; any batch we ship can be checked on verify.
Verify a batch
Every order ships with a per-batch Certificate of Analysis. Have a vial in hand? Enter its lot number to look up the COA for that exact batch.
Sourcing and related ingredients
Supplied as raw material with a per-batch Certificate of Analysis reporting HPLC purity and mass-spectrometric identity confirmation. Not supplied as a finished cosmetic, and not supplied for human use as material; a certificate is not a cosmetic safety assessment.
The other ingredients in this cluster built around the same neuromuscular idea are Acetyl Hexapeptide-8 and Acetyl Octapeptide-3, both of which approach it from peptide chemistry rather than from venom mimicry. The full list is on the cosmetic ingredient hub.
Frequently asked questions
What is the INCI name for SYN-AKE?
Is SYN-AKE actually snake venom?
Is SYN-AKE a peptide?
What does the published research on SYN-AKE show?
What concentration do formulators use?
Literature cited
- Gok B, Budama-Kilinc Y, Kecel-Gunduz S. “Anti-aging activity of Syn-Ake peptide by in silico approaches and in vitro tests.” J Biomol Struct Dyn. 2024;42(10):5015–5029. PMID 37349941. pubmed.ncbi.nlm.nih.gov/37349941. (Docking, molecular dynamics, DPPH, MTT, Ames; no skin model or human subject.)
- Debono J, Xie B, Violette A, Fourmy R, Jaeger M, Fry BG. “Viper Venom Botox: The Molecular Origin and Evolution of the Waglerin Peptides Used in Anti-Wrinkle Skin Cream.” J Mol Evol. 2017;84(1):8–11. PMID 27864608. pubmed.ncbi.nlm.nih.gov/27864608.
- Molles BE, Tsigelny I, Nguyen PD, et al. “Residues in the epsilon subunit of the nicotinic acetylcholine receptor interact to confer selectivity of waglerin-1 for the alpha-epsilon subunit interface site.” Biochemistry. 2002;41(25):7895–7906. PMID 12069578. pubmed.ncbi.nlm.nih.gov/12069578. (About waglerin-1, not about SYN-AKE.)
- Tan CH, Tan KY, Ng TS, et al. “Venomics of Tropidolaemus wagleri, the sexually dimorphic temple pit viper: Unveiling a deeply conserved atypical toxin arsenal.” Sci Rep. 2017;7:43237. PMID 28240232. pubmed.ncbi.nlm.nih.gov/28240232.
- Zhu M, He X, Zhu Z, et al. “The effect of a serum containing acetyl hexapeptide-8, dipeptide diaminobutyroyl benzylamide diacetate and gluconolactone on skin biomarkers, wrinkles and skin texture: Ex vivo and clinical studies.” Int J Cosmet Sci. 2026 (online ahead of print). PMID 41668671. pubmed.ncbi.nlm.nih.gov/41668671. (Five-active formula; all authors employed by L’Oréal.)
- National Center for Biotechnology Information. “PubChem Compound Summary for CID 71465152, Dipeptide diaminobutyroyl benzylamide diacetate.” pubchem.ncbi.nlm.nih.gov/compound/71465152 (structure, formula, mass, CAS).
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