Myristoyl Pentapeptide-17
Lash/brow peptide
Myristoyl Pentapeptide-17 (Lash/brow peptide) is a healing & recovery research compound. Fatty-acid-modified peptide that stimulates keratin production in follicle keratinocytes — used for eyelash and brow growth.
Myristoyl Pentapeptide-17 quick facts
| Reported research dose | Topical, as directed |
| Route | Topical |
| Frequency | 1x Daily (topical) |
| Half-life | N/A (topical) |
| Forms | Topical |
| Evidence level | Cosmetic/topical |
The lash/brow-growth peptide found in serums.
How Myristoyl Pentapeptide-17 works
Fatty-acid-modified peptide that stimulates keratin production in follicle keratinocytes — used for eyelash and brow growth.
Proposed benefits
Eyelash and brow density support (cosmetic).
Where to get Myristoyl Pentapeptide-17
See vetted vendors for Myristoyl Pentapeptide-17 →The evidence for Myristoyl Pentapeptide-17
Graded by what exists behind each claim.
✅ Clinically validated
- No independent randomized trials — the human data is manufacturer-generated, reporting increased eyelash length and density with topical use. That is the weakest kind of clinical evidence there is: unblinded, unpublished in peer review, and produced by the party selling it. Worth reading as a starting point rather than a result.
📊 Correlative data
- Common in over-the-counter lash serums as the non-prostaglandin alternative to bimatoprost. Reported effect is markedly smaller — which is also why it does not carry bimatoprost's iris-pigmentation risk.
🧪 Theoretical / extrapolated
- A myristoylated peptide proposed to upregulate keratin genes in the hair follicle, increasing the structural protein available for the shaft.
- That is a fundamentally different mechanism from bimatoprost, which extends the anagen growth phase. Building a thicker shaft and growing for longer are not the same lever, and the second one is stronger.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Myristoyl Pentapeptide-17 actually does
Start with what cannot be written on this page, because it is the most important thing about the compound. There is no published amino-acid sequence for myristoyl pentapeptide-17. It does not appear in the Cosmetic Ingredient Review’s palmitoyl-oligopeptide report with the palmitoylated peptides in this Vault, it does not appear in the survey of peptides found in marketed facial cosmetics Resende 2021, and a search of the indexed biomedical literature returns no primary paper on it at all — not a cell study, not an animal study, not a chemical characterization. Everything written about this molecule anywhere traces back to the supplier that sells the raw material. That is the finding, and no amount of confident prose changes it.
What can still be computed, without the sequence. The myristoyl group is a 14-carbon acyl chain, C14H26O, adding 210.36 Da. The lightest pentapeptide that exists is five glycines, 303.27 Da, so the absolute floor for a myristoylated pentapeptide is 513.63 Da. A pentapeptide of ordinary composition sits nearer 570–670 Da free, which puts the finished molecule in the 780–880 Da range. Whatever the sequence turns out to be, this compound is over the 500 Da threshold usually quoted for passage through intact stratum corneum Bos 2000 — and it is over it by a margin that no choice of five residues can close.
Why the tail is C14 and not C16, which is the one genuinely interesting design decision here. Every other lipopeptide in this Vault carries palmitic acid, C16. Fourteen carbons is the chain length biology itself uses: N-myristoyltransferase attaches exactly this acyl group to the N-terminal glycine of hundreds of human proteins, and the modification exists to give a soluble protein a weak, reversible grip on a membrane rather than a permanent anchor. Two fewer carbons than palmitate is roughly an order of magnitude less lipid affinity, which is the difference between a molecule that inserts into a membrane and stays and a molecule that samples it and comes off again. This is extrapolation and is labeled as such: nobody has published why this particular ingredient is myristoylated rather than palmitoylated. But if the intent was residence in the follicular canal rather than burial in the stratum corneum, C14 is the chemically sensible choice, and it is the only structural argument in favor of the design that anyone can actually make from what is disclosed.
The mechanism claim, and what it would have to mean. The compound is sold as an upregulator of keratin genes, increasing the structural protein available to the shaft. Keratins are made by the matrix keratinocytes at the base of the follicle bulb, which sit below the skin surface, not in it. So the claim is not a claim about the eyelid at all — it is a claim about reaching a bulb through the follicular opening and changing transcription in a dividing keratinocyte. No published experiment has demonstrated any step of that: not the delivery, not the transcriptional change, not the keratin.
Cell, rodent, human — and where it stops
Cells: nothing. Rodents: nothing. Independent human trials: nothing. That is the entire translation chain for this molecule, and stating it precisely is more useful than dressing it up.
The closest human study, and it is worth reading properly. An eyelash serum built on peptides and glycosaminoglycans was tested in 30 women aged 25 to 65 over 12 weeks, with assessments at baseline, 4 weeks and 12 weeks. At 12 weeks the reported changes were lash length +8.3%, number +5%, width +10.1%, volume +14.1%, arc +13.4% and angle +28.3%, with satisfaction rising from 73.34% at day 28 to 84.33% at day 84 and no adverse effects reported Fernandez-Gonzalez 2024. Three things about that study, in order of importance. It was open-label with no control arm, so every number includes whatever an unblinded participant applying a conditioning liquid to her lashes twice a day would report anyway. Its abstract does not name which peptides were in the serum, so it cannot be cited as evidence for this specific molecule, only for the category. And the effect sizes are ranked in a revealing order: the largest change was in lash angle and the smallest in lash count. Angle is curl, which is exactly what a conditioning film does mechanically and immediately; count is the endpoint that requires new follicles in anagen, and it moved least. If the mechanism were biological, that ranking should be the other way round.
What the field’s own review says. Eyelash serums split into prostaglandin analogs and non-prostaglandin products, and for the non-prostaglandin ingredients the review’s conclusion is that they lack formal evidence in this application; it also notes that over-the-counter products are not required to demonstrate efficacy or safety before sale Baiyasi 2024. This compound sits squarely in that group.
The comparator that shows what a real mechanism looks like. Bimatoprost ophthalmic solution 0.03% was approved in December 2008 for eyelash hypotrichosis, and its mechanism is described: it increases the percentage of lashes in the anagen growth phase, stimulates melanogenesis and enlarges the dermal papilla Cohen 2010. Note that this is a different lever from the one claimed here. Extending anagen makes a lash grow for longer; upregulating keratin would make a lash thicker while it grows. The first produces length and count, the second should produce diameter — and, as the next section argues, it should produce diameter in a specific and visible pattern that nobody has looked for.
The obstacle, named specifically for this site. The lash line is not facial skin. A serum drawn along the lash base can enter the follicular opening directly, and the follicular route is the one path by which a molecule too heavy for the intercellular lipid route Bos 2000 Mortazavi 2022 can reach living tissue. That is the strongest structural argument this compound has and it is never made. It is also unmeasured: no study has quantified delivery of any peptide into a human eyelash follicle, and the only permeation numbers in this family come from full-thickness skin of a hairless mouse, where a comparable lipopeptide reached the layers but never the receptor fluid Choi 2014.
Myristoyl Pentapeptide-17 pharmacokinetics — how much of it actually gets in
The card says N/A (topical). Here is the arithmetic behind the blank, and it is unusually favorable — which is why the absence of evidence here is a failure to look rather than a physical impossibility.
Mass. A myristoylated pentapeptide is at minimum 513.63 Da and realistically 780–880 Da, over the 500 Da rule of thumb Bos 2000. Against skin, that is disqualifying. Against a follicular opening, it is not, because the follicle is a hole rather than a membrane.
Quantity. The lash line is small. Both upper lash lines together are on the order of 1 cm² of application area, so a serum applied at 2 mg/cm² delivers about 2 mg of product per application. At a peptide level of 0.01% that is 200 ng of peptide per application, roughly 0.25 nanomoles. There are on the order of 150 lashes per upper lid, so the dose per follicle is in the picogram range — and a single dermal papilla is a structure of a few thousand cells. Whether picograms per follicle is enough depends entirely on a potency figure that has never been measured for this compound, which is the honest end of that calculation.
What destroys it. The eyelid margin is wet, enzymatically active and continuously washed by tear film; meibomian lipid and blinking both remove applied material mechanically within minutes to hours. Acylating the N-terminus blocks aminopeptidase attack at the front of a peptide, which is the one durable advantage of this class of modification Choi 2014, but nothing published describes the stability of any lash peptide in tear film. No residence time, no clearance, no recovery figure exists for this molecule anywhere.
Systemically: nothing measurable, and for once that is a certainty rather than an assumption. Two hundred nanograms applied to a wet mucocutaneous margin cannot produce a systemic concentration of anything, and there is no blood marker on this site with a route to move on this compound.
What would have to be true, and how you would know it was not
What to watch. A macro photograph of one eye, taken with the same lens at the same distance under the same lighting, with a millimetre rule in frame and the head against a fixed rest, at week 0, week 4 and week 12. From that photograph, three numbers: the length of the three longest lashes, a count within a marked segment of the lid margin, and — the one nobody records — the shaft diameter at the base compared with the diameter halfway up the same lash.
How long before it means anything. Twelve weeks, and the reason is the lash cycle rather than impatience. An eyelash spends a short period growing and a long period resting; a compound acting on the matrix of a follicle that is already in anagen changes only the segment being made from that day forward, so nothing it does can appear at the tip of an existing lash at any point.
What will fool you. Three things, and they are all in the published trial. Unblinded self-assessment, which rose from 73% to 84% satisfaction in a study with no control arm Fernandez-Gonzalez 2024. Conditioning: any oily film increases curl and apparent volume immediately, which is why the largest reported effect in that trial was on lash angle. And synchronized regrowth — anybody starting a lash serum after extensions, an infection or a period of rubbing is watching a recovery that was going to happen.
Prediction 1, and it is the one this page exists to make. If the claimed mechanism is real — more keratin produced by the matrix — then a lash that was already growing when the serum started should end up thicker at its base than along its distal half, because only the newly synthesized segment saw the compound. That is a visible taper reversal on a macro photograph, it distinguishes a shaft-building mechanism from an anagen-extension mechanism Cohen 2010 and from a cosmetic conditioning film, and no lash product of any kind has ever been evaluated this way.
Prediction 2, and it cuts against the compound. Lash count should not change. Nothing in a keratin-production mechanism recruits a resting follicle into growth; that is what the prostaglandin analog does by increasing the anagen percentage Cohen 2010. So a serum of this type that reports a meaningful increase in the number of lashes is either not working by the mechanism claimed for it, or is not working at all and the count is measurement noise. In the published trial the count moved least of all the endpoints Fernandez-Gonzalez 2024, which is consistent with the second reading.
Prediction 3, the one that protects you. Iris color and periorbital contour should not change, ever. Those are prostaglandin effects, not peptide effects. Photograph the iris under fixed lighting at week 0 and week 12: if it darkens, or if the upper lid sulcus deepens, the product contains something other than what is on the label — and over-the-counter lash products are not assessed for efficacy or safety before sale Baiyasi 2024, so that is a real possibility rather than a hypothetical one.
What nobody has tested yet
1. Nobody has published the sequence. Five residues. A single line of text would let anyone compute the mass, the charge, the isoelectric point and the protease susceptibility, and would let this page do for it what it does for every other peptide in this Vault. Its absence is a commercial decision, not a scientific one, and it is why this entry has computed a range instead of a number.
2. Nobody has confirmed the ingredient is what the label says. The analytical chemistry for identifying a cosmetic peptide in a finished cream is established and has been applied to other cosmetic peptides in commercial products Kluczyk 2021. Running it on three commercial lash serums would answer, for the first time, whether myristoyl pentapeptide-17 is present at the level claimed — and, given that these products are not pre-assessed Baiyasi 2024, whether anything else is.
3. There is no keratin experiment. The entire mechanism is a claim about keratin gene expression, and no published study has put this peptide on a keratinocyte and measured a keratin transcript. Cultured human outer root sheath keratinocytes with a quantitative PCR panel is an undergraduate-level experiment and it is the missing foundation of the product.
4. Nobody has measured follicular delivery at the lash line. Follicle-casting and differential tape-stripping methods exist for scalp; the eyelid margin has never been studied this way for any active at all, which means the one route by which any of these serums could work is entirely unquantified Mortazavi 2022.
5. The controlled version of the trial that already exists. The published lash study was open-label with 30 participants and no control Fernandez-Gonzalez 2024. The same protocol run as a randomized, vehicle-controlled, split-eye study — serum on one eye, identical vehicle on the other — would separate the peptide from the conditioning film in one experiment, at a fraction of the marketing budget already spent on the category Gorouhi 2009.
Myristoyl Pentapeptide-17 — its own safety story, not its class's
The class block on this page is written for injectable repair peptides and warns about angiogenesis and systemic exposure. Neither applies to 200 nanograms on an eyelid. What does apply is specific to this site of application.
The eyelid is the highest-risk cosmetic site on the body for contact dermatitis, and this product is applied to it deliberately. Eyelid skin is the thinnest on the body and the most reactive to leave-on ingredients; periorbital dermatitis presents as itching, scaling and swelling that people routinely attribute to allergies rather than to the serum they started six weeks earlier. The practical instruction is to stop for two weeks at the first sign of lid margin redness or itch and see whether it resolves, because a chronically inflamed lid margin causes lash loss — the exact outcome the product was bought to reverse.
The applicator is a real hazard and it is never mentioned. A wand repeatedly drawn along the lash base, recapped into a warm moist tube and used for months is a bacterial and Demodex reservoir, and blepharitis is far more common than any peptide effect. Replace the product on schedule, do not share it, and do not use it on an inflamed lid.
The adulteration question, which is this category’s genuine risk. Over-the-counter lash products are not required to demonstrate efficacy or safety before sale Baiyasi 2024. Prostaglandin analogs produce dramatic, reproducible lash growth Cohen 2010 and peptides do not, which creates an obvious commercial incentive. The signature of that substitution is visible without a laboratory: iris darkening, periorbital skin pigmentation, deepening of the upper lid sulcus and conjunctival redness are prostaglandin effects and cannot be produced by any pentapeptide. If a peptide-labeled serum produces them, the label is wrong. Photographing the iris at the start of a course is a thirty-second precaution that makes that detectable.
What zero reported adverse events means here. The one published trial in this space reported none, in 30 unblinded participants over 12 weeks with no control arm Fernandez-Gonzalez 2024. That is a sample too small to detect anything uncommon and a design that cannot attribute what it does detect. It is not a safety record; it is the absence of one, and for a product applied millimetres from the eye that distinction is worth making explicitly.
Sources read for this page
- Fernandez-Gonzalez P, Trullas C, Granger C, Del Alcazar E, Sola J. Open clinical trial evaluating the efficacy of a novel eyelash growth enhancer with peptides and glycosaminoglycans. J Cosmet Dermatol 2024 · PMID 38572527
- Baiyasi M, Yousif J, Potts G. Eyelash serums: A comprehensive review. J Cosmet Dermatol 2024 · PMID 38475901
- Cohen JL. Enhancing the growth of natural eyelashes: the mechanism of bimatoprost-induced eyelash growth. Dermatol Surg 2010 · PMID 20384750
- Bos JD, Meinardi MM. The 500 Dalton rule for the skin penetration of chemical compounds and drugs. Exp Dermatol 2000 · PMID 10839713
- Mortazavi SM, Moghimi HR. Skin permeability, a dismissed necessity for anti-wrinkle peptide performance. Int J Cosmet Sci 2022 · PMID 35302659
- Choi YL, Park EK, Kim E, Na DH, Shin YH. Dermal Stability and In Vitro Skin Permeation of Collagen Pentapeptides (KTTKS and palmitoyl-KTTKS). Biomol Ther (Seoul) 2014 · PMID 25143811
- Resende DISP, Ferreira MS, Sousa-Lobo JM, Sousa E, Almeida IF. Usage of Synthetic Peptides in Cosmetics for Sensitive Skin. Pharmaceuticals (Basel) 2021 · PMID 34451799
- Gorouhi F, Maibach HI. Role of topical peptides in preventing or treating aged skin. Int J Cosmet Sci 2009 · PMID 19570099
- Kluczyk A, Ludwiczak J, Modzel M, Kuczer M, Cebrat M, Biernat M, Bartosz-Bechowski H. Argireline: Needle-Free Botox as Analytical Challenge. Chem Biodivers 2021 · PMID 33482052
Myristoyl Pentapeptide-17 — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- Repair peptides work by promoting angiogenesis — new blood vessel growth — plus fibroblast migration and growth-factor signaling. That is what makes them useful, and it is the entire basis of the one theoretical concern worth naming: angiogenesis is also what a tumor needs to grow beyond a few millimetres.
- There is no evidence these compounds cause or accelerate cancer. There is a mechanistic reason not to run a pro-angiogenic agent systemically with an active or recently treated malignancy, and that reasoning stands without a trial.
- The second predicted issue is more mundane and more likely: they can mask a signal. Something that reduces pain and inflammation around an injury lets you load a tissue that has not finished healing.
What has actually been reported
- Very well tolerated in reported use. Injection-site reactions and transient light-headedness are the common complaints.
- Human data is thin — most of the literature is rodent — so 'well tolerated' here means 'no signal has emerged from a lot of informal use', which is weaker than a clean trial and stronger than nothing.
How to reduce the risk
Same mechanism as the prediction.
- Stop when the thing you were treating has resolved. There is no mechanism here that demands a clock, and equally no reason to keep running a pro-angiogenic signal once the job is done.
- Do not let reduced pain set your training load. The tissue heals on its own timeline whether or not you can feel it. Reloading early on the strength of feeling better is the most common way people turn a good result into a re-injury.
- Get the diagnosis before the peptide. These accelerate healing of things that heal. A tear that needs surgical repair does not become a tear that does not, and the delay costs you.
- One injury, one compound, long enough to judge it. Otherwise you learn nothing transferable for next time.
What it does to your bloodwork
A fact about the assay.
- Nothing routine tracks these directly. The endpoint is the injury, which means your own honest assessment of function is the measurement.
Don't run this if
- Active or recently treated malignancy — the angiogenesis reasoning.
- Any undiagnosed lump or lesion. Find out what it is first.
The honest unknown
- Long-term systemic exposure in humans has never been characterized. The use case is naturally self-limiting — you stop when the injury resolves — which is why this matters less here than it would elsewhere.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Myristoyl Pentapeptide-17 — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
Applied topically, this has no systemic exposure worth speaking of — so there is nothing to interact with anything you take, and no blood marker it could move. That is the honest answer rather than an empty section. The real interactions for a topical are layering ones: what you put on before and after it, and at what pH.
- How to work up to it, and when not to
- When to take it, and why that window
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Myristoyl Pentapeptide-17 in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Myristoyl Pentapeptide-17
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Baseline inflammation — the thing you're claiming to reduce |
| Complete Blood Count (CBC) with Differential | Infection, anemia and platelet count before anything injectable |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney baseline |
| Vitamin D (25-Hydroxy) | Low D slows soft-tissue and bone healing measurably |
The Inflammation Deep Dive panel covers these in one order — 10 markers, $248.35 with the discount applied.
Check results you already have → · All 103 markers A–Z
Myristoyl Pentapeptide-17 — frequently asked questions
What is Myristoyl Pentapeptide-17?
Myristoyl Pentapeptide-17 (Lash/brow peptide) is a healing & recovery research compound. Fatty-acid-modified peptide that stimulates keratin production in follicle keratinocytes — used for eyelash and brow growth.
Is the full Myristoyl Pentapeptide-17 protocol on this page?
The reported research dose is on this page, along with how Myristoyl Pentapeptide-17 works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Myristoyl Pentapeptide-17?
Myristoyl Pentapeptide-17 has an approximate half-life of N/A (topical), which is part of what determines how often it's dosed.
What's the evidence behind Myristoyl Pentapeptide-17?
Current evidence level: Cosmetic/topical. Myristoyl Pentapeptide-17 is offered for research purposes only and is not an approved medicine.
What Myristoyl Pentapeptide-17 is used for
Myristoyl Pentapeptide-17 appears under 1 goal in the goal router.
Related Healing & Recovery compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.