F tier · safety concern
A ClinicalTrials.gov search for PTD-DBM returns zero registered studies, and there is no published human experiment of any kind — not a case series, not a pilot, not an ex vivo human scalp study using the peptide. Every PTD-DBM paper comes from Kang-Yell Choi's laboratory at Yonsei University, every in vivo experiment is topical application to mouse skin, and the group's own trajectory has been to abandon the peptide in favour of small molecules (KY19382, KY19334).
ptd-dbm
PTD-DBM is a fusion peptide combining a cell-penetrating protein transduction domain with the Dishevelled-binding motif of CXXC5, a negative regulator of Wnt/beta-catenin signalling. Acting as a decoy, it is intended to occupy Dishevelled and prevent CXXC5 from binding it, thereby de-repressing Wnt signalling in skin; in mice, topical application accelerates hair regrowth and wound-induced hair follicle neogenesis. All published work is preclinical, topical and from a single Korean laboratory; there are no human data and no registered clinical trial.
// we supply this one
available as a research reagent
≥ 98% HPLC · lyophilised powder · batch certificate published. Grade F above is our own and is not adjusted because we stock it.
the explanation
PTD-DBM is a lab-made peptide with a delivery tag stuck on the front so it can get inside skin cells. Once inside it acts as a decoy, soaking up a protein that normally switches off the hair-growth signalling pathway. In mice, rubbing it onto shaved or wounded skin made hair grow back faster and produced new follicles. It has only ever been tested on mouse skin, by one research group, and never on a person.
regulatory status
Unapproved worldwide; preclinical research chemical only
PTD-DBM is not a licensed medicine in the UK, EU, US or any other jurisdiction, is not a prescription-only medicine, and is not a controlled drug; there is no MHRA-authorised product containing it and no cosmetic ingredient listing for it in Great Britain, so it is an unlicensed substance supplied here only as a laboratory research reagent for in vitro and non-human use. A ClinicalTrials.gov search returns zero registered studies, so it has never been an investigational medicinal product in a trial anywhere. The peptide is covered by Yonsei University patent family US20150224167A1 / WO2015122592A1 (priority 12 February 2014), and the programme has been commercialised through the Korean spin-out associated with Kang-Yell Choi, but as small molecules rather than as the peptide. It is not a lawful dietary-supplement or novel-food ingredient in any jurisdiction, and because no government health authority has approved it for human therapeutic use it falls within section S0, Non-Approved Substances, of the WADA Prohibited List.
how it works · proposed mechanism
Wnt/beta-catenin signalling drives hair follicle development and the transition of resting follicles into the growth phase. CXXC5 is a negative feedback regulator that binds Dishevelled (Dvl), an upstream component of the pathway, and suppresses signalling; it is induced by Wnt activity and, in the group's model, by dihydrotestosterone via PGD2 in androgenetic alopecia. PTD-DBM is a decoy that presents the same Dvl-binding motif in trans.
Competitive decoy, not receptor agonism
The peptide carries the Dishevelled-binding motif of CXXC5 itself, so it occupies the Dvl surface that full-length CXXC5 would otherwise use. This is protein-protein interaction disruption from the inside of the cell, which is why a protein transduction domain is required at all. It does not activate a Wnt receptor, does not inhibit GSK-3beta, and does not supply beta-catenin — it removes an inhibitory interaction, and its ceiling is therefore the amount of endogenous Wnt tone present.
Delivery is the whole engineering problem
A 13-residue intracellular decoy has no way into a keratinocyte unaided, hence the cationic transduction domain — octa-arginine in the patent's exemplified construct, with HIV-Tat, Antp, transportan and VP22 claimed as alternatives. This is also the source of the identity problem: the peer-reviewed papers never state which domain or linker was used, so 'PTD-DBM' names a design, not a single defined molecule, and different suppliers can legitimately produce different peptides under the name.
Readouts are follicle-cycle markers in mouse skin
Reported effects are restoration of beta-catenin activation and PCNA expression, recovery of hair shaft elongation in ex vivo vibrissa culture, accelerated anagen re-entry after depilation, and alkaline-phosphatase-positive neogenic follicles in the wound-induced hair neogenesis assay, including in models where dihydrotestosterone or PGD2 had suppressed them. Human involvement extends no further than HaCaT cells, an immortalised human keratinocyte line.
The originators moved to small molecules
Having established the CXXC5-Dvl axis with the peptide, the same laboratory developed KY19382 and KY19334, small molecules that inhibit both CXXC5 function and GSK-3beta, and it is these that appear in the group's later hair-regrowth and diabetic-wound-healing work. That is the clearest available signal about the peptide's own developability: its own inventors replaced it.
what’s reported
evidence shape
7 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
The published evidence for PTD-DBM is topical, in mice, from one laboratory, and frequently entangled with valproic acid — and none of those qualifiers survive into how the peptide is sold. In the 2017 Journal of Investigative Dermatology report the strongest hair regrowth and wound-induced neogenesis are described for topical PTD-DBM combined with valproic acid, an established Wnt activator in its own right, so the peptide's standalone contribution is not cleanly isolated; the group's later Cells 2023 work uses PTD-DBM topically and benchmarks it against valproic acid and the small molecule KY19382 rather than as a systemic agent. There is no human experiment at all — not a trial, not a case series, not even ex vivo human scalp follicles; human involvement stops at HaCaT, an immortalised keratinocyte line. ClinicalTrials.gov returns zero registered studies, and no laboratory unconnected to Kang-Yell Choi has published on the peptide. Most concretely for anyone buying it: no peer-reviewed paper states its sequence, the originating patent claims five different protein-transduction domains as interchangeable, and the exemplified construct is a highly cationic octa-arginine fusion — so a vial labelled PTD-DBM has no verifiable identity, no CAS number, and no published molecular weight against which a certificate of analysis could be checked.
key published findings
- The Dishevelled-binding motif in the originating patent, RKTGHQICKFRKC, matches human CXXC5 residues 284-296 exactly (UniProt Q7LFL8), so the biological premise is verifiable even though the marketed product's composition is not.
- The patent's exemplified construct is SEQ ID NO:7, RRRRRRRRGGGGRKTGHQICKFRKC (octa-arginine + GGGG linker + DBM), but the same patent claims HIV-Tat, Antp, transportan and VP22 as alternative transduction domains, and no peer-reviewed paper says which was used.
- Zero registered clinical trials and zero published human data; the only human material in the entire literature is the immortalised HaCaT keratinocyte line.
- All in vivo work is topical application to mouse skin across depilation-induced anagen, wound-induced hair neogenesis, and dihydrotestosterone/PGD2-driven androgenetic alopecia models; no study has used any systemic route.
- The 2017 paper's strongest results are reported for topical PTD-DBM together with valproic acid, and the 2023 Cells study compares PTD-DBM against valproic acid and KY19382 rather than combining them — so the peptide-alone effect size is not cleanly established.
- The originating laboratory has itself moved on to dual CXXC5/GSK-3beta small molecules (KY19382 for hair, KY19334 for diabetic wound healing), which now carry the programme instead of the peptide.
limitations of the evidence
- No human data of any kind: no trial, no case series, no ex vivo human follicle study, no pharmacokinetics, no dermal penetration measurement in human skin.
- No independent replication — every PTD-DBM publication is authored by Kang-Yell Choi's group at Yonsei University.
- The molecular identity of commercial material is unverifiable: no sequence in the peer-reviewed record, no CAS number, no published molecular formula or mass, and five interchangeable transduction domains claimed in the patent.
- The entire in vivo evidence base is topical to mouse skin; there is no published rationale, pharmacokinetic basis or safety study for any injected or systemic route, which is nonetheless how it is commonly used by consumers.
- Mouse hair follicle biology differs substantially from human — mice cycle synchronously in waves and readily support wound-induced neogenesis, which humans largely do not — so regrowth in a depilated mouse is a weak predictor of effect in human androgenetic alopecia.
- Confounding with valproic acid in the key hair-regrowth report means the peptide's independent contribution is not quantified.
documented safety signals
- No human safety data exist — no adverse-event profile, no local tolerability assessment in human skin, no systemic exposure data, and no published genotoxicity, sensitisation or repeat-dose toxicology study in any species.
- The mechanism is deliberate activation of Wnt/beta-catenin signalling, a pathway with well-established oncogenic potential in skin and colon; chronic pharmacological de-repression of it has no characterised long-term safety profile, and no carcinogenicity study of this peptide has been published.
- Highly cationic cell-penetrating peptides such as octa-arginine fusions are associated in the general literature with concentration-dependent membrane perturbation and cytotoxicity; no such assessment has been published for this construct at all, let alone for systemic administration.
- Because the sequence and composition of commercial material are undisclosed, batch-to-batch and vendor-to-vendor identity cannot be verified, and impurity or counter-ion profiles are unknown.
- Absence of reported harm reflects the complete absence of human study rather than evidence of safety.
identity
| full name | PTD-DBM — a protein-transduction-domain-fused Dishevelled-binding motif peptide derived from CXXC5, used as a decoy to disrupt the CXXC5-Dishevelled interaction |
| category | Cosmetic |
| modality | peptide |
| sequence | Not disclosed in any of the peer-reviewed papers. The originating group's own patent (US20150224167A1, Yonsei University; inventors Kang-Yell Choi, Soung-Hoon Lee, Hyun-Yi Kim) claims the construct as SEQ ID NO:7, RRRRRRRRGGGGRKTGHQICKFRKC — an octa-arginine protein-transduction domain, a tetraglycine linker, and the Dishevelled-binding motif RKTGHQICKFRKC, which corresponds exactly to residues 284-296 of human CXXC5 (UniProt Q7LFL8). Material sold under the name PTD-DBM has not been shown to correspond to this construct, and other protein-transduction domains (HIV-Tat, Antp, transportan, VP22) are claimed as alternatives in the same patent. |
laboratory handling
| storage | Lyophilised powder is stored desiccated at -20 °C and protected from light. Once reconstituted, laboratory practice is refrigeration at 2-8 °C for short-term use, or aliquoting and freezing to avoid repeated freeze-thaw cycles. Handling information only; this material has no approved human use. |
| solubility | Short hydrophilic peptide, readily soluble in sterile or bacteriostatic water and in dilute aqueous buffer. Lot-specific solubility is stated on the certificate of analysis. |
| co-studied with | The only combination with any published basis is topical co-application with valproic acid in mouse hair-regrowth models from the originating laboratory, and even there the peptide's separate contribution is not cleanly quantified. No combination has been studied in humans, and no data exist for co-use with minoxidil, finasteride or any other agent. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
7 citedUnited States Patent and Trademark Office; applicant Industry Academic Cooperation Foundation, Yonsei University · 2015 · official
UniProt Knowledgebase, EMBL-EBI/SIB/PIR · 2026 · official
U.S. National Library of Medicine, ClinicalTrials.gov · 2026 · official
Journal of Investigative Dermatology 137(11):2260-2269 · 2017 · preclinical
Journal of Experimental Medicine 212(7):1061-1080 (PMID 26056233) · 2015 · preclinical
Cells 12(4):555 · 2023 · preclinical
Wikipedia · 2026 · tertiary
Sources marked tertiary or press release are the weakest citations on this page.
others in Cosmetic