PTD-DBM

PTD-DBM peptide, protein transduction domain–Dishevelled binding motif, CXXC5-Dvl interfering peptide, "Wnt hair peptide"

Skin & cosmetic

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Synthetic fusion peptide: a cell-penetrating "protein transduction domain" sequence joined to a short motif copied from the protein CXXC5 that normally binds Dishevelled
Mechanism: Blocks CXXC5 from binding Dishevelled, removing a natural brake on Wnt/β-catenin signalling in hair follicles and skin, which in mice re-activates follicle growth and wound-induced hair formation
Routes studied: Topical application to shaved or wounded mouse skin; applied to cultured human dermal papilla cells and follicle tissue. No human clinical route studied
Dose range reported: Mouse studies: topical solutions in the tens-to-hundreds of micromolar range applied daily, often together with valproic acid. Community: topical solutions reportedly 0.5–1 mg/ml applied daily to the scalp, sometimes after microneedling; no validated human dose exists
Half-life: Not characterised. Peptides of this type are degraded in hours by skin and serum proteases
Storage: Lyophilised: refrigerate or freeze, protect from light. Reconstituted: refrigerate, community practice is use within weeks
Regulatory status: Not approved anywhere; not a permitted cosmetic ingredient in any listing we are aware of †. A research chemical

Doses are as reported in studies or by the community — never recommendations.

1What it is

PTD-DBM is a laboratory-made peptide from Kang-Yell Choi's group at Yonsei University in South Korea. The group had shown that a protein called CXXC5 acts as a negative-feedback regulator of the Wnt/β-catenin pathway in skin, by binding to Dishevelled (Dvl), a protein that relays the Wnt signal (Lee 2015, J Exp Med). Wnt/β-catenin signalling is central to starting a new hair-growth cycle, and in bald scalp it is dampened. The team designed a peptide containing the exact piece of CXXC5 that grips Dishevelled (the "DBM"), stuck it to a short cell-penetrating sequence (the "PTD") so it could get inside cells, and showed that it freed Wnt signalling and regrew hair in mice (Lee 2017, J Invest Dermatol).

It is entirely synthetic. It has never been tested in a human clinical trial. It reached the community through press coverage of the 2017 paper and is now sold as a research chemical for topical scalp use, which this profile neither endorses nor assumes works.

2How it's thought to work

Wnt signals stabilise β-catenin, which switches on genes that push a resting follicle into the growth (anagen) phase and that drive the dermal papilla cells at the follicle base.

CXXC5 sits on Dishevelled and dampens this signal. In human bald scalp and in mouse models, CXXC5 is raised and Wnt activity is low.

PTD-DBM competes with CXXC5 for Dishevelled, so the brake is released and β-catenin accumulates.

In mice the effect was larger when combined with valproic acid, which separately activates the pathway by inhibiting GSK-3β (the enzyme that normally destroys β-catenin), and when applied to wounded skin, where "wound-induced hair neogenesis" (new follicles forming in a healing wound) was increased.

Proposed: a peptide carrying a cell-penetrating sequence, aimed at the protein that holds Wnt signalling back rather than at Wnt itself. Prising the brake off its partner lets the follicle's own growth signal run. Animal work only.Schematic — not to scale

This is a plausible, well-described mechanism in animals. Whether a topical peptide reaches dermal papilla cells several millimetres deep in human scalp is unknown.

3What the research shows

Hair regrowth and new follicle formation in mice

Topical PTD-DBM on shaved mouse skin accelerated hair regrowth, and on wounded skin increased the number of newly formed follicles; the combination with valproic acid was more effective than either alone (Lee 2017, J Invest Dermatol). The same paper reported that PTD-DBM increased β-catenin and proliferation markers in cultured human dermal papilla cells and in human hair follicle tissue, which is the only human-derived evidence. [1]

CXXC5 as a Wnt brake in skin and wound healing

Mice lacking CXXC5 heal wounds faster with more collagen, and PTD-DBM mimicked this (Lee 2015, J Exp Med). Supporting background, not hair data. [2]

Alopecia in humans

No clinical trial, case series or published case report. Community reports of topical use are mixed, typically from people also using minoxidil, finasteride or microneedling, so attribution is impossible.

Follow-up and development

The Yonsei group has published related work on CXXC5-targeting small molecules and on a commercial development path for hair loss; no PTD-DBM human trial result is public as of this review †.

4Reported side effects and interactions

Literature-reported

No toxicity reported in mice in the published work; no human safety data of any kind.

Community-reported

scalp irritation or itching (often after microneedling), redness; a few report shedding in early weeks that they attribute to a new growth cycle, which is unverifiable. Many report no change.

Theoretical. this is the important part. Wnt/β-catenin is a growth pathway: constitutive activation drives several tumours, including pilomatricoma and some skin and gut cancers. A compound designed to remove a brake on it has an obvious theoretical oncogenic concern with long-term or systemic use. Nothing is known about absorption from human scalp. Combining with valproic acid, as in the mouse study, adds a known teratogen and liver-toxic drug applied off-label to skin.

Interactions. valproic acid (pharmacological synergy in mice; safety untested); minoxidil and finasteride are commonly co-used by community members with no interaction data.

Markers researchers commonly monitor

No compound-specific markers are established and there is no human data. For a topical scalp protocol members commonly discuss:

Marker	Why it's watched
Standardised scalp photographs and, ideally, a fixed-area hair count or trichoscopy image every 4–8 weeks	hair outcomes are slow and otherwise unmeasurable.
Skin examination of the treated area	any new or changing growth, nodule or pigmented lesion in the application zone deserves a clinician's look, given the Wnt mechanism.
CBC and CMP	general baseline only if systemic exposure is suspected; there is no data on absorption.
If valproic acid is being used topically alongside: liver enzymes and a clear understanding that it is a teratogen; this is a clinician conversation

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Typically sold as powder in milligram vials, for topical use. Community practice is to dissolve in sterile or , sometimes with a penetration-enhancing vehicle, and apply to the scalp; it is never studied by injection and injecting it has no rationale. Keep reconstituted solution refrigerated and protected from light; peptides of this type lose activity over weeks. If using the calculator for a topical dilution, note it computes concentration only — no validated dose exists.

Open in calculator, pre-loaded →

6Commonly studied alongside

Valproic acid (the only published combination, in mice); GHK-Cu (#5) and TB-500 (#2), both with mouse hair-growth data; minoxidil and finasteride (standard-of-care, community co-use); microneedling, which is itself a mild wound stimulus and the subject of community "wound-induced neogenesis" speculation.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved; no IND or trial on record for PTD-DBM †. Not on FDA's compounding bulk lists. Sold as a research chemical
European Union	Not authorised; not a listed cosmetic ingredient †
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Not specifically listed by WADA; as a non-approved pharmacological substance it would fall under S0 if used systemically †

8Open questions

Does topical PTD-DBM reach dermal papilla cells in human scalp at all?
Safety of chronic Wnt pathway activation in skin — the central unanswered question.
Any human efficacy data — none exist.
Peptide stability in topical vehicles and how quickly skin proteases destroy it.

9References

1Lee SH et al. (2017). Targeting of CXXC5 by a competing peptide stimulates hair regrowth and wound-induced hair neogenesis. J Invest Dermatol. PubMed · DOI
2Lee SH et al. (2015). The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing. J Exp Med. PubMed · DOI
3Kim HY et al. (2010). CXXC5 is a transcriptional activator of Flk-1 and mediates bone morphogenic protein-induced endothelial cell differentiation and vessel formation. FASEB J (background on CXXC5). PubMed
4Choi BY (2020). Targeting Wnt/β-catenin pathway for developing therapies for hair loss. Int J Mol Sci. PubMed · DOI
5Ito M et al. (2007). Wnt-dependent de novo hair follicle regeneration in adult mouse skin after wounding. Nature (background on wound-induced hair neogenesis). PubMed · DOI

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

forum threads →

community protocols include this →

Threads and protocols are visible to members. Joining is free.

Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

26 Oct 2026Profile published — awaiting medical review

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