SYN-AKE (200mg Vial) Dosage Protocol

Quickstart Highlights

SYN-AKE is a small synthetic cosmetic peptide sold under the INCI name Dipeptide Diaminobutyroyl Benzylamide Diacetate (CAS 823202-99-9). PubChem lists it as CID 71465152, molecular formula C₂₃H₃₇N₅O₇, molecular weight 495.6 g/mol^[1]. Vendors describe the structure as β-Ala–Pro–Dab–NHBn · 2 acetate — a beta-alanyl-prolyl-diaminobutyryl chain capped with a benzylamide group, supplied as the diacetate salt^[2]. It is a topical cosmetic ingredient. It is not injected, it is not taken orally, and it has no dose in the sense that word carries elsewhere on this site.

Two names circulate for the same molecule and both are in use: the INCI name calls it a dipeptide, while several suppliers list it as tripeptide-3, because the backbone carries three residues before the benzylamide cap^[2]. Neither name is wrong so much as differently counted, and the practical point is that a search for one will miss product listings under the other. The marketing name comes from the claim underneath it: SYN-AKE is presented as a synthetic mimetic of waglerin-1, a peptide from the venom of the temple pit viper Tropidolaemus wagleri^[3]. That parent toxin is real and well characterised. Whether a three-residue molecule reproduces what it does is a separate question, and one the published record does not answer.

Supplies Needed

SYN-AKE ships as powder in a sealed vial. Three suppliers were checked on 6 August 2026 and all three list the same 200 mg size: Core Peptides (>99% purity, lyophilized, $176), BiotechPeptides ($210, lyophilized, labelled “β-Ala-Pro-Dab-NHBn · 2 Acetate”) and Verified Peptides (99.143% on a batch certificate dated 26 February 2025, $85, out of stock at time of checking)^[2]. Peptide Sciences and Umbrella Labs also list a 200 mg presentation. Presentation is not consistent between them — two describe a lyophilized cake, one describes loose raw powder and states plainly that it is not intended for reconstitution — so the certificate of analysis matters more than the catalogue text.

SYN-AKE Vial

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Protocol Overview

The claim attached to SYN-AKE is a neurotransmitter-inhibitor claim: that it relaxes the small facial muscles whose repeated contraction creates expression lines, by antagonising the nicotinic acetylcholine receptor at the neuromuscular junction in the same way waglerin-1 does^[3]. That is the mechanism the whole category rests on, and it is the mechanism the published literature on this molecule does not test.

What the parent toxin does is documented properly. Waglerin-1 is a 22-amino-acid peptide that competitively antagonises the muscle nicotinic receptor and is strongly selective for the α–ε subunit interface — roughly 3,700-fold higher affinity for the α–ε site than for α–γ^[6]. In adult mouse endplates it suppresses the acetylcholine response with an IC₅₀ near 50 nM, and mice engineered without the ε subunit are resistant to it altogether^[7]. It is a precise, well-mapped pharmacology.

Two features of that pharmacology sit awkwardly under the marketing. First, the activity depends on structure the mimetic does not have: an alanine scan of waglerin-I found the active site sits in the proximity of the disulfide loop, spatially close to His10, and that replacing that residue abolished toxicity entirely^[8]. A three-residue open chain with a benzylamide cap has no disulfide loop to reproduce. Second, the affinity is species-dependent in the wrong direction: waglerin-1 binds the mouse receptor about 100-fold more tightly than the rat or human receptor, and in the human receptor it is polar residues (Ser-187, Thr-189) that confer that lower affinity where the mouse has aromatic ones^[9].

None of that proves SYN-AKE does nothing. It does mean the mechanistic story told on product pages is borrowed from a molecule that is structurally very different and, in humans specifically, markedly less potent — and that no published work bridges the gap. There is also a location problem nobody addresses: the receptor in question sits at the neuromuscular junction, below the dermis, and no percutaneous penetration data for this dipeptide appears in the indexed literature.

Dosing Protocol

Reference conversions only. Each row starts from a concentration of peptide in the finished product, works out how much pure powder a 30 g jar would need, and states what a single 200 mg vial covers. The middle rows are the documented band; the last row is what happens when the supplier’s solution percentage is misapplied to powder.

Dosing & Application

SYN-AKE is applied to intact skin inside a finished formulation. The only quantity that has any documented basis is the concentration of peptide in that formulation, and the single most common mistake with this ingredient is to take a percentage that was written for a diluted commercial solution and apply it to pure powder.

Standard / Gradual Approach

The primary source is unambiguous. The SYN®-AKE Formulation Guidelines published by DSM Nutritional Products, Personal Care (Basel, last updated January 2020) give the composition of the traded product as Dipeptide Diaminobutyroyl Benzylamide Diacetate 0.1–1%, glycerin >50% and water 25–50%, and under “Use level” state: “For skin care preparations a concentration of 1-4% SYN®-AKE is recommended”^[4]. The 1–4% is therefore a percentage of the solution, and the solution is mostly glycerin and water.

Carried through, that gives a finished-product peptide concentration between 0.001% (1% of a 0.1% solution) and 0.04% (4% of a 1% solution). In parts per million that is 10 to 400 ppm. It is a genuinely wide band, and the width is itself informative: the supplier does not pin the peptide content of its own solution to a single figure, so nobody working from a raw powder can claim to be reproducing a specific published concentration.

The practical difference from other cosmetic peptides is worth noting. At 10–400 ppm a 30 g jar needs 0.3 mg to 12 mg of peptide. The upper end of that is comfortably weighable on an ordinary 1 mg-resolution balance; the lower end is not, and would need a stock solution and a micropipette. The table further down works each row out in full.

Storage Instructions

Keep the powder cool, dry, dark and tightly closed, and follow the supplier’s handling guidance for the specific batch. No vendor checked on 6 August 2026 publishes a solubility figure or a recommended solvent for the pure powder, which is a real gap: the only documented handling basis for this ingredient is the commercial solution, and that is a different material.

What the supplier does document is the behaviour of that solution, and it is the closest thing to a handling reference that exists. SYN®-AKE is supplied at pH 4.5–5.5, is miscible with water and insoluble in lipophilic components, and is meant to go into the aqueous phase of a formulation. DSM recommends incorporating it at the end of production below 40 °C, states it has been tested for up to two hours at 70 °C, gives a recommended final formulation pH of 3.0–7.5, and notes compatibility with up to 50% ethanol as the maximum concentration tested^[4].

One accounting point that no supplier states. The 495.6 g/mol figure on every product page is the mass of the diacetate salt^[1]; the free peptide is roughly 375 g/mol, so acetate accounts for about a quarter of the labelled weight. Whether a “200 mg” vial means 200 mg of salt or 200 mg of peptide is not disclosed, and at these concentrations the difference is real arithmetic rather than a rounding question. Ask the supplier which basis the certificate of analysis uses.

Important Notes

The points below are the ones that change how the record on this ingredient should be read. Most of them are not caveats attached to a positive result — they are the reason there is no positive result to attach them to.

• ▪PubMed indexes exactly one article that names Syn-Ake (checked 6 August 2026). It is Gok, Budama-Kilinc and Kecel-Gunduz 2023 in the Journal of Biomolecular Structure & Dynamics^[5], and it is an in-silico study: molecular docking and 50 ns molecular-dynamics simulations against matrix metalloproteinases and SIRT1, plus a DPPH radical-scavenging assay and MTT/Ames safety tests. No skin, no volunteers, no receptor pharmacology.
• ▪That one paper does not test the mechanism the ingredient is sold for. Its docking targets are MMP-1, MMP-8, MMP-13 and SIRT1^[5] — matrix and longevity targets, not the nicotinic acetylcholine receptor that the waglerin-1 story depends on. The only indexed study of the molecule and the marketing claim for the molecule are about different biology.
• ▪No registered clinical trial exists. A ClinicalTrials.gov search for Syn-Ake, the INCI name and waglerin as interventions returned zero studies (checked 6 August 2026).
• ▪The famous numbers come from the supplier, not from a journal. The figures repeated across the internet — 4% applied twice daily to the forehead for 28 days, a smoothing effect on most volunteers, wrinkle reduction “up to 52%” — trace to DSM/Pentapharm’s own product documentation^[4]. They are manufacturer in-vivo data. They may well be accurate; they have not been through peer review, and the underlying study is not published anywhere an independent reader can check its methods.
• ▪The comparison to Argireline is also the supplier’s. The head-to-head that circulates — SYN-AKE versus acetyl hexapeptide-8 versus placebo — comes from the same marketing material, run by the party selling one of the two arms. Our Argireline protocol page carries the same warning in the other direction.
• ▪The mimicry claim has never been measured. No indexed study reports a binding affinity, an IC₅₀ or an electrophysiological effect for this dipeptide at the nicotinic acetylcholine receptor. The claim that it acts like waglerin-1 rests on the design intent, not on a published result.
• ▪Reversibility cuts both ways. Supplier material describes the effect as fully reversible, which is offered as a safety point. It is also a reminder that whatever is being described is transient and cosmetic — an appearance endpoint measured by profilometry, not a change in skin biology.
• ▪Research-use-only material is not a cosmetic ingredient. Vials sold to researchers ship without the solvent, preservative system, pH control or stability testing that the commercial solution has behind it, and every vendor checked states the product is for laboratory use and not for human consumption^[2].

How This Works

The proposed mechanism runs through the neuromuscular junction. Acetylcholine released from a motor nerve terminal binds the muscle nicotinic acetylcholine receptor, the receptor opens, and the muscle fibre contracts. Block that receptor and the contraction weakens. Repeated contraction of small facial muscles is what folds skin into expression lines over years, so a topical agent that damped those contractions would, in principle, soften the lines they create.

Waglerin-1 does exactly that block, and the pharmacology has been mapped in detail. It is one of six waglerin forms that together make up around 38% of the venom protein of Tropidolaemus wagleri and constitute the venom’s main lethal principle^[3]. Its selectivity for the adult α–ε receptor form has been demonstrated genetically: mice lacking the ε subunit resist a dose that kills their wild-type littermates, and neonatal mice, which still express the γ form, resist it too^[7]. Subsequent mutagenesis identified the individual residues — Gly-57, Asp-59, Tyr-111, Tyr-115 and Asp-173 in the ε subunit — that account for the selectivity^[6].

The gap between that and a cosmetic dipeptide is the whole question. Waglerin-1 is a 22-residue peptide whose activity, on the alanine-scan evidence, is carried by a disulfide-constrained loop^[8]. SYN-AKE is a short open chain with a benzylamide cap and no disulfide bridge. Mimetic design of this kind is a legitimate strategy — a small molecule can sometimes reproduce a key contact of a much larger ligand — but whether it succeeded is an empirical question, and here it has not been answered in public.

And even taking the mechanism at face value, there is the species issue. Waglerin-1 binds the human receptor roughly 100-fold more weakly than the mouse receptor^[9]. A mimetic optimised against the mouse pharmacology would inherit that handicap. This is the sort of detail that separates a mechanism story from a mechanism, and it is why the independent literature on topical peptides for ageing skin treats the whole neurotransmitter-inhibitor category as a class under investigation rather than a settled one^[10].

Lifestyle Factors

Because this ingredient acts — if it acts — at the surface, the formulation around it decides more than the peptide count does. The supplier’s own guidance is a useful constraint: aqueous phase, added late, below 40 °C, final pH between 3.0 and 7.5, insoluble in oils^[4]. A peptide put into the wrong phase or cooked at the wrong point in a batch is a peptide that is present on the label and absent in effect, whatever the concentration says.

The confounders that dominate any visible-line endpoint are the ordinary ones, and they are larger than the effect sizes claimed here. Ultraviolet exposure, hydration state, sleep and the base emollient itself all change how skin reads under a profilometer within days. This is why manufacturer appearance studies are hard to interpret without a placebo arm and blinded assessment, and why the absence of independent replication matters more than usual.

Nothing on this page is guidance for use on a person. The concentration arithmetic is documented so that the published figures can be read correctly, not so they can be reproduced — research-grade powder is sold for laboratory work and the vendors say so explicitly^[2].

Potential Benefits & Side Effects

What follows is what has actually been reported, stated at the level it was done. For this ingredient that means separating three things that product pages routinely merge: what the parent toxin does, what a computer simulation predicted, and what a supplier measured in an unpublished appearance study.

How to Apply

The workflow below documents how a cosmetic peptide of this kind is handled and what the documented concentrations are, for reference. It is a description of published practice, not an instruction to apply anything to a person.

Skin Preparation

• ▪Confirm what was actually shipped. The identity to check is CAS 823202-99-9, PubChem CID 71465152, formula C₂₃H₃₇N₅O₇, MW 495.6 as the diacetate^[1]. Ask whether the stated mass is salt or free peptide — the difference is about a quarter of the labelled weight.
• ▪Read the certificate, not the catalogue. Presentation varies between suppliers checked on 6 August 2026: two describe a lyophilized powder, one describes loose raw powder and states it is not for reconstitution^[2]. Purity figures quoted ranged from >99% to 99.143% on a dated batch certificate.
• ▪Note what is missing. No vendor checked publishes a solubility figure or a recommended solvent for the powder. The only documented physical chemistry belongs to the commercial solution: water-miscible, oil-insoluble, supplied at pH 4.5–5.5^[4].

Applying the Product

• ▪Start from the peptide concentration, not the solution percentage. The documented band in a finished product is 0.001–0.04% peptide (10–400 ppm), derived from DSM’s 1–4% use level for a solution that is 0.1–1% peptide^[4]. Everything else follows from that number.
• ▪Work out the mass, then decide whether it can be weighed. A 30 g jar needs 0.3 mg at the bottom of the band and 12 mg at the top. Twelve milligrams is weighable on a 1 mg balance; 0.3 mg is not, and would require a stock solution — for example 200 mg in 20 mL of water gives 10 mg/mL, so 0.3 mg is 30 µL measured with a micropipette.
• ▪Respect the phase and the temperature. The ingredient is water-miscible and oil-insoluble; the supplier directs it into the aqueous phase, added at the end of production below 40 °C, with a final formulation pH between 3.0 and 7.5^[4]. A peptide added to an oil phase or held hot is unlikely to survive the batch intact.
• ▪Do not scale the percentage up because the powder is pure. Applying 4% to raw powder puts 1.2 g into a 30 g jar — between 100 and 4,000 times the documented band, depending which end of the supplier’s own 0.1–1% range you compare against. That single arithmetic slip is the main hazard specific to this ingredient.
• ▪Keep a written record of the basis used. Because the supplier states a range rather than a figure, two batches formulated “the same way” can differ tenfold in peptide content. Documenting which concentration was chosen is the only way any subsequent observation means anything.

After Application

• ▪Store the powder cool, dry, dark and closed, and follow the batch-specific guidance on the certificate. Once in a finished formulation, the product’s own stability and preservative system govern, not the peptide.
• ▪Judge results against an honest baseline. The endpoint claimed for this ingredient is appearance, measured over 28 days, in an unpublished manufacturer study without independent replication^[4]. Any observation made outside those conditions is anecdote sitting on top of data that were never peer reviewed.
• ▪Expect the vehicle to do visible work. Hydration alone changes fine-line appearance within hours. Distinguishing a peptide effect from an emollient effect requires a control formulation identical in everything but the peptide — which is precisely what the public record for SYN-AKE lacks.
• ▪Treat the whole file as preliminary. One computational paper^[5], no registered trial, an unmeasured mechanism and a parent toxin that is weaker at human receptors than at the ones it was characterised in^[9]. That is the honest summary, and it is compatible with the ingredient being harmless and pleasant to use.

Recommended Source

For high-purity research peptides, we point researchers to Prime Lab Peptides for SYN-AKE (200 mg).

References

1. 1
   PubChem CID 71465152 — Dipeptide Diaminobutyroyl Benzylamide Diacetate. National Center for Biotechnology Information.

   Primary chemical record: molecular formula C₂₃H₃₇N₅O₇, molecular weight 495.6 g/mol, IUPAC name identifying the compound as the acetic-acid salt of a beta-alanyl-prolyl-diaminobutyryl benzylamide. CAS 823202-99-9. Retrieved 6 August 2026.

   View Source ↗

2. 2
   Supplier product listings for SYN-AKE 200 mg (Core Peptides, BiotechPeptides, Verified Peptides), retrieved 6 August 2026.

   Three independent research-supplier listings of the same 200 mg presentation: Core Peptides (>99% purity, lyophilized powder, $176), BiotechPeptides ($210, lyophilized, structure given as β-Ala-Pro-Dab-NHBn · 2 acetate) and Verified Peptides (99.143% on batch 01-25-P01A tested 26 February 2025, $85, out of stock). All three state the material is for laboratory research use only and not for human consumption. Cited as evidence that the vial size exists on the market, not as a scientific source.

   View Source ↗

3. 3
   Tan CH, Tan KY, Yap MKK, Tan NH. Venomics of Tropidolaemus wagleri, the sexually dimorphic temple pit viper: unveiling a deeply conserved atypical toxin arsenal. Sci Rep. 2017;7:43237. PMID 28240232.

   Source and standing of the parent toxin: six waglerin forms are identified as the predominant lethal principles of Tropidolaemus wagleri venom, comprising 38.2% of total venom proteins, in a venom otherwise unusual among pit vipers for being neurotoxic rather than haemotoxic.

   View Source ↗

4. 4
   SYN®-AKE Formulation Guidelines. DSM Nutritional Products, Personal Care, Basel, Switzerland. Last updated January 2020.

   The primary source for every concentration figure on this page. Gives the composition of the traded product as Dipeptide Diaminobutyroyl Benzylamide Diacetate 0.1–1%, glycerin >50%, aqua 25–50%; pH as supplied 4.5–5.5; miscible with water, insoluble in lipophilic components; recommended final formulation pH 3.0–7.5; incorporation into the aqueous phase at the end of production below 40 °C, tested up to two hours at 70 °C. Under “Use level”: “For skin care preparations a concentration of 1-4% SYN®-AKE is recommended.” This is a manufacturer document, and the wrinkle-appearance figures attributed to the supplier elsewhere on this page come from the same commercial source rather than from peer-reviewed literature.

   View Source ↗

5. 5
   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.

   The only PubMed-indexed article that names this molecule (checked 6 August 2026). Molecular docking and 50 ns molecular-dynamics simulations against MMP-1, MMP-8, MMP-13 and SIRT1 (best score −9.32 kcal/mol at SIRT1), a DPPH radical-scavenging assay showing concentration-dependent activity, and MTT cytotoxicity plus Ames genotoxicity testing. Entirely computational and bench-chemical: no skin model, no human subjects, and no assay of the nicotinic acetylcholine receptor mechanism the ingredient is marketed on.

   View Source ↗

6. 6
   Molles BE, Tsigelny I, Nguyen PD, Gao SX, Sine SM, Taylor P. 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.

   Maps the pharmacology that the marketing borrows. Waglerin-1, a 22-amino-acid competitive antagonist of the muscle nicotinic receptor, shows 3,700-fold higher affinity for the α–ε binding site than for α–γ, and residues Gly-57, Asp-59, Tyr-111, Tyr-115 and Asp-173 of the ε subunit account for most of that selectivity.

   View Source ↗

7. 7
   McArdle JJ, Lentz TL, Witzemann V, Schwarz H, Weinstein SA, Schmidt JJ. Waglerin-1 selectively blocks the epsilon form of the muscle nicotinic acetylcholine receptor. J Pharmacol Exp Ther. 1999;289(1):543–550. PMID 10087048.

   Genetic demonstration of the target. Adult mice lacking the ε subunit resist the lethal effect of waglerin-1 while heterozygous littermates do not, and neonatal mice (which still express the γ form) are also resistant. In adult wild-type endplates waglerin-1 reduced the acetylcholine response with an IC₅₀ of 50 nM.

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8. 8
   Hsiao YM, Chuang CC, Chuang LC, Yu HM, Wang KT, Chiou SH, Wu SH. Protein engineering of venom toxins by synthetic approach and NMR dynamic simulation: status of basic amino acid residues in waglerin I. Biochem Biophys Res Commun. 1996;227(1):59–63. PMID 8858103.

   The structural objection, from the toxin’s own literature. An alanine scan of seven basic residues found the active site of waglerin I resides in the proximity of the disulfide loop, spatially close to His10, and that the [Ala10] analogue exhibits no toxicity because the loop is twisted relative to the native form. A short open-chain mimetic has no equivalent constraint.

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9. 9
   Molles BE, Rezai P, Kline EF, McArdle JJ, Sine SM, Taylor P. Identification of residues at the alpha and epsilon subunit interfaces mediating species selectivity of Waglerin-1 for nicotinic acetylcholine receptors. J Biol Chem. 2002;277(7):5433–5440. PMID 11724791.

   The species problem stated directly. Waglerin-1 binds the α–ε interface of the mouse receptor about 100-fold more tightly than the rat or human receptor. In the human receptor polar residues Ser-187 and Thr-189 confer the lower affinity, where the mouse has aromatic Trp-187 and Phe-189. Any mimetic designed against the mouse pharmacology inherits this gap.

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10. 10
    Gorouhi F, Maibach HI. Role of topical peptides in preventing or treating aged skin. Int J Cosmet Sci. 2009;31(5):327–345. PMID 19570099.

    The standard independent review of this field, from the Department of Dermatology at the University of California, San Francisco. Categorises cosmetic peptides into signal, enzyme-inhibitor, neurotransmitter-inhibitor and carrier classes — the class SYN-AKE is marketed in — and reviews the controlled ex-vivo and in-vivo efficacy studies that exist for each. Cited here as the academic framing of the category, not as a source of any claim about this specific molecule.

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