PTD-DBM
CXXC5–Dishevelled inhibitor
- Injection
- Oral
- Nasal spray
- Suppository
- Gel or cream
Gel or cream — no established human dose.
No provider we've verified carries PTD-DBM yet
The acronym unpacks into the design. PTD is a protein transduction domain — a carrier sequence that crosses cell membranes on its own, with no needle into the cytoplasm and no liposome wrapper. DBM is a Dishevelled binding motif, modeled on the stretch of a protein called CXXC5 that normally docks onto Dishevelled. That is the whole molecule: a delivery tag fused to a competitive inhibitor. It came out of Kang-Yell Choi’s laboratory at Yonsei University in Seoul, with the first substantial hair-regrowth paper appearing around 2017.
To see what it is inhibiting, start with the follicle. Hair follicles are not static — each one cycles through years of active growth, a brief regression, and months of rest, and then either restarts or, in pattern baldness, fails to. What drives the restart is Wnt signaling: a Wnt protein binds its receptor, the signal travels through Dishevelled, β-catenin accumulates and switches on the genes that tell stem cells to proliferate. Wnt fires, follicles enter growth. Wnt is suppressed, follicles stall.
CXXC5 is the brake, and in balding scalp there is more of it. This peptide does not push the accelerator — it competes for the place the brake grips.
That is a genuinely different idea from the two approved drugs. CXXC5 is a negative feedback regulator: Wnt fires, CXXC5 rises, CXXC5 binds the PDZ domain of Dishevelled and stops the signal propagating. In a healthy follicle the brake comes off when it needs to. In androgenetic alopecia, DHT is upstream of a chain that raises PGD2 and in turn CXXC5, so the brake stays on and follicles miniaturise over successive cycles. Occupy the docking site and the brake cannot grip. In mice, that produced new hair. Nobody has published what it produces in a person. For the study-by-study record and the KY19382 follow-on program, read the deep-dive on PeptideWellness.
Who it's for (or who should avoid)
What it's aimed at
There is no patient group, because there is no human evidence. What the animal work addressed:
- Androgenetic alopecia in mice — the target condition, and where the striking regrowth results come from
- Follicles stalled in rest rather than lost — the mechanism needs something left to restart, which is a real limit on the ambition even in principle
- Cell-culture models of Wnt suppression — where the CXXC5 competition was characterized
- Korean cosmetic formulations — it is already sold in products there, which is a commercial fact and not a clinical one
That is the complete list, and it does not contain a human being. Anything written about what it does to scalps is extrapolation from rodents.
Who should avoid it
- Anyone with a current or past cancer diagnosis — the Wnt pathway is central to stem-cell proliferation throughout the body, and modulating it deserves proper study rather than a shrug
- Anyone pregnant, breastfeeding or planning a pregnancy — no reproductive data of any kind, and Wnt signaling is fundamental to development
- Anyone who would be swapping an approved drug for this — finasteride and minoxidil have decades of human data; this has none, and trading evidence for novelty is the wrong direction
- Anyone self-dosing a research chemical, which is the only form available in the US: no established concentration, no vehicle, no schedule, no monitoring and no batch anyone has tested
Route, dose and course
There is no human protocol to report, and that is the finding rather than an omission on this page.
The animal studies applied it to skin. Korean cosmetic products contain it at concentrations the manufacturers set. No human dose, vehicle or schedule has been established anywhere in the peer-reviewed literature, and there is no US supply route:
- No approved product — nothing to dispense, because nothing is approved
- No compounding route — not on the 503A bulks list, not on the 503B nominated list
- No prescriber — no indication to write for, and no dose to write
- What is sold instead — research-chemical vials and imported cosmetics, with no verified potency, identity or batch testing
The follow-on molecule from the same laboratory, KY19382, is a small molecule hitting both CXXC5 and GSK-3β. It is a different compound with its own record, and its existence is a reasonable sign that the lab considers the peptide a starting point rather than the destination.
The usual arc
Nobody knows, and this page will not pretend otherwise. There is no human timeline because there has never been a human study — no onset, no plateau, no duration, no data on what happens when you stop. Hair-cycle biology alone would put any real effect on a scale of months rather than weeks, since a follicle has to complete a cycle to show anything. Reports circulating from people using imported product are anecdotes about an unverified compound, and they are the weakest kind of evidence for the strongest kind of claim.
No provider we've verified carries PTD-DBM yet
That is the honest answer, and it is not the same as "you can't have it". None of the licensed telehealth providers we track publishes PTD-DBM, so there is no price to quote and no intake to send you to. Whether that changes depends on federal action rather than on us — which is why the next box exists rather than a button that goes nowhere.
Tell me when someone carries it
Questions we get about PTD-DBM
Has it been tested in people?
No. As of mid-2026 every published efficacy study runs on mice or cell culture, there is no IND-stage candidate with publicly registered human trials under this name, and there is no peer-reviewed human safety data. That is a different situation from a drug that failed in humans — nothing has been tried. It also means the mouse results, which are genuinely striking, are the entire basis for everything written about it.
Can I get it in the US?
Not through any regulated route. It is not FDA-approved, and it is not on the 503A bulks list or the 503B nominated substances list, so no compounding pharmacy is sanctioned to prepare it. It is sold in cosmetic formulations in South Korea and as a research chemical online, and neither is a US supply route for something you intend to put on your scalp with an expectation of effect.
See what licensed providers actually carry →How is this different from finasteride and minoxidil?
It aims at a different point in the chain. Finasteride works upstream on DHT; minoxidil acts on the follicle and its blood supply through a mechanism that was found before it was understood. Both are approved, both have decades of human data, and both maintain or thicken existing follicles. PTD-DBM's proposition is further downstream and more ambitious: release the CXXC5 brake and let stalled follicles re-enter the growth phase. Ambition is not evidence — the two approved drugs have it and this does not.
What does releasing the brake actually mean?
Follicles cycle: years of growth, a brief regression, months of rest, then either a restart or, in pattern baldness, a failure to restart. Wnt signaling drives the restart. CXXC5 is the negative feedback that shuts Wnt down once it has fired, and in balding scalp there is more of it, so the brake stays on. This peptide competes for the site where CXXC5 docks. Whether that translates from a mouse to a human scalp is the whole open question.
Is it safe?
Unknown, and the honest version of that is not reassuring. There is no peer-reviewed human safety data at any dose. The Wnt pathway it modulates is central to stem-cell proliferation throughout the body, which is a mechanism that warrants proper study rather than an absence of reports — and an absence of reported harm in a compound nobody has formally studied in people is not a safety record.
We publish no medical reviewer by design. Every claim on this page traces to a source we hold on file, and the reviewed write-up with those citations lives on our hub. Read the full research on PeptideWellness ↗
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