PTD-DBM: what the studies show, status and safety
Summary
PTD-DBM is a lab-built peptide of 25 building blocks, sold as a research chemical. It blocks the contact between a protein called CXXC5 and a second protein called Dishevelled, which lifts a brake on the Wnt signalling pathway. Mouse work on wounds and hair regrowth reports clear effects, but almost always with valproic acid added. Eleven years after the first paper there is no study in people, no safety testing and no assessment by any medicines authority.
Key findings at a glance
- Not one study in people, in eleven years. ClinicalTrials.gov returned no entry on 20 September 2026, while the control search for minoxidil returned 110 studies [1]. Four PubMed entries carry the name, and none of them describes the peptide being given to a person [2].
- 42.8 per cent against 4.9 per cent, in mice. Three days after wounding, that much of the wound surface had regrown under PTD-DBM plus valproic acid, against untreated controls, with 16 animals per group [3].
- On its own it matched a standard comparator, no more. In the same experiment, 100 µM PTD-DBM alone healed wounds about as fast as 100 µM EGF [3].
- The famous hair result is a combination result. 2 mM PTD-DBM with 500 mM valproic acid beat 100 mM minoxidil in C3H mice, measured as hair weight and follicle count [4], [5].
- No authority has ever assessed it. It is absent from the American compounding lists [6], from the Australian Poisons Standard [7], from the 2026 Prohibited List [8] and from the annex to the German anti-doping law [9].
- The inventors moved on to a different molecule. Their own papers describe the small molecule KY19382 as a "mimetic small molecular compound of PTD-DBM" [10].
- The pathway it opens is a cancer pathway. A 2025 review lists off-target activation linked to bowel and liver cancers, and a "narrow therapeutic window", as drawbacks of this approach [11].
What it is
PTD-DBM is not a natural substance and not a medicine. It is a designed chain of 25 building blocks made of three parts, and its name simply describes that construction. The patent that covers it lists the chain as RRRRRRRR-GGGG-RKTGHQICKFRKC [12].
The first part is eight arginines, a stretch known to ferry cargo across cell membranes. The second is a short flexible linker. The third is copied from the human protein CXXC5, positions 284 to 296 of its 322 building blocks [13]. That last piece is the working end; the rest exists to get it inside cells.
No pharmaceutical company developed it. The peptide comes from one academic laboratory, the group of Kang-Yell Choi at Yonsei University in Seoul. That group described the underlying target in 2015 [14] and the construct itself in the same year [3]. The patent claims priority from 12 February 2014 and was granted on 20 February 2019 [12].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Common name | PTD-DBM, also written as the CXXC5-Dvl competing peptide | [12], [4] |
| Class | Lab-made peptide of 25 building blocks that blocks a contact between two proteins | [3] |
| Sequence | RRRRRRRR-GGGG-RKTGHQICKFRKC | [12] |
| Where the working end comes from | Positions 284-296 of human CXXC5, a protein of 322 building blocks | [13] |
| Formula and mass | C124H223N61O28S2, 3080.7 g/mol, for the unlabelled chain | [15] |
| Form used in the papers | The same chain plus a lysine carrying the dye FITC, added to make it visible | [3], [5] |
| How long it lasts in the body | Never measured, in any species | [2] |
| Status | Research chemical, approved nowhere | [6], [7] |
| Developer | Yonsei University, group of Kang-Yell Choi; no company programme for the peptide | [14], [10] |
| CAS registry number | None assigned | [15] |
| Wikidata, PubChem, official drug names | No entry found | [16] |
Two chemical details are open. The chain carries two cysteines, and the mass quoted for traded material only adds up if those two are joined into a ring [15]. The form with free ends would weigh slightly more, and nothing in the papers says which form was used. There is also no pharmacopoeia entry, so purity limits do not exist [2].
How it works
The idea behind PTD-DBM is to release a brake rather than press an accelerator. The Wnt pathway drives repair and regrowth in skin, hair follicles and bone, and the protein CXXC5 damps it down from inside the cell. What follows is drawn from cells in dishes and from mice.
- A brake that the body builds itself. CXXC5 binds to Dishevelled, a relay protein of the Wnt pathway, and the more Wnt signalling runs, the more CXXC5 the cell makes. Two independent groups described that binding in 2009 and 2010 [17], [18], and the feedback loop was worked out in bone cells in 2015 [14].
- A decoy for the same docking site. The peptide carries the exact stretch of CXXC5 that grips Dishevelled, so it may occupy the site first. The docking part of mouse Dishevelled-1 was solved as a crystal structure at 1.76 Å, and the contact with CXXC5 was then modelled onto it rather than crystallised [19]; NMR titrations at ratios from 1:5 to 1:25 show the short motif binding it directly [20].
- Eight arginines as the delivery van. The carrier stretch is meant to pull the peptide through skin and into cells. The evidence for that is a fluorescent glow in tissue rather than a measurement [3], and an independent 2026 paper criticises this class of agents for low bioavailability [21].
- A hair-loss chain of events. In mice, the male hormone DHT raises the messenger prostaglandin D2, which in turn raises CXXC5 and suppresses regrowth. Both genetic removal of CXXC5 and the peptide reversed that suppression [22]. CXXC5 is also raised in shrunken follicles of human balding scalp [4].
- Effects far beyond skin, mostly from other molecules. CXXC5 has been tied to bone formation [14], to growth-plate ageing [23], to diabetic wounds [24], to fatty liver and metabolism [25] and to a mouse model of Alzheimer's disease [26]. Almost all of that work used the small molecules KY19334 and KY19382, not the peptide.
The inventors turned the difference from a direct Wnt activator into their safety argument. Releasing a brake, they wrote, "may further reduce the chance of aberrant activation" linked to cancer [3]. That remains an argument, not a finding.
What the studies found
Every result below comes from a mouse, from isolated tissue or from cells in a dish. No person has ever received PTD-DBM in a study of any kind [1], [2].
Counts as of 20 September 2026. The four PubMed entries are papers whose text carries the name PTD-DBM. Sources [1], [2].
Wound healing
Animal data This is the best evidence the substance has. Seven-week-old male C3H mice received full-thickness wounds of 1.5 cm across and were treated daily for 11 days, with 16 animals per group. On its own, 100 µM PTD-DBM closed wounds about as fast as the active comparator, 100 µM EGF [3].
Animal data The striking number came from the combination. Three days after wounding, 42.8 per cent of the surface had regrown under PTD-DBM with 500 mM valproic acid, against 4.9 per cent in controls. The treated wounds also held more collagen and fewer inflammatory cells [3].
C3H mice, full-thickness wounds 1.5 cm across, daily treatment, 16 animals per group. Source [3].
Cells in a dish
In vitro In human skin fibroblasts and HaCaT skin cells, 2 µM and 10 µM of the peptide on its own raised beta-catenin, alpha-SMA and collagen I, the more so the higher the concentration. Endothelin-1 rose as well, while the cancer-associated markers c-Myc and cyclin D1 did not move. Silencing beta-catenin abolished the effect. The cell work ran on two to three donor preparations and two to three independent repeats per experiment, which is small even for a dish [3].
Hair regrowth
Animal data The 2017 paper is the origin of nearly every marketing claim about this peptide. It reported that CXXC5 is raised in the miniaturised follicles of balding human scalp. The competing peptide, it found, sped up regrowth and new follicle formation in wounded skin [4].
Animal data That paper's full text is not publicly accessible. The figures quoted here come from its abstract and from two later reviews rather than from the original [5].
Animal data The comparison people quote is 2 mM PTD-DBM plus 500 mM valproic acid against 100 mM minoxidil in C3H mice, with hair weight and follicle count as the measures [5]. It is a combination against a single agent, in mice, at a minoxidil concentration of roughly 2 per cent.
Animal data A 2023 study applied 300 µl of a 10 mM solution to shaved mouse backs every second day. A wound model in the same paper used 20 µl daily, with 7 to 10 animals per analysis. It reversed the suppression of regrowth caused by prostaglandin D2, and beta-catenin returned to the cell nucleus (p < 0.005 and p < 0.0005) [22].
Scars and bone
Animal data Hyaluronic acid patches loaded with the peptide, with valproic acid, or with both, reduced scarring in mice and raised markers of regenerative rather than fibrous healing [27]. How much of that came from the peptide rather than the patch or the second drug cannot be read from the report.
Animal data In the study that started the whole programme, mice lacking CXXC5 built denser bone, and a competing peptide pushed bone-cell development along and thickened cultured skull bone [14]. The follow-up work deliberately left the peptide behind in favour of small molecules [20].
What is still unknown
- Whether any of this happens in a person. There is no human study, no case report and no series [1], [2].
- What the body does with the peptide. Uptake, blood levels, half-life, breakdown and excretion are unmeasured in every species [2].
- How much actually crosses skin. The evidence is a fluorescence image, not a concentration [3], [21].
- What the peptide does on its own. The clearest effects came with valproic acid, with Wnt3a or inside a hydrogel patch [3], [27].
- Whether anyone else can reproduce it. The target CXXC5 has been confirmed by independent groups [17], [18], [28], but the peptide itself has never been tested outside the inventing laboratory.
Side effects and safety
There is no side-effect profile, because there is no documented use in people and no safety study in any species. Nothing reported is not the same as nothing happening.
- No safety testing whatsoever. Single-dose toxicity, repeat-dose toxicity, genetic damage, fertility, offspring and cancer risk: not one study exists for any of them [2].
- One long-term observation, in mice. After six months of skin treatment the authors saw no abnormal skin and no rise in c-Myc or cyclin D1, with three animals per group across three experiments [3]. That is two marker proteins, not a cancer study.
- A blood-vessel messenger goes up. The peptide raised endothelin-1 in human skin cells, and 10 µM of the endothelin-receptor blocker bosentan cancelled the rise in alpha-SMA and collagen I that the peptide had produced [3]. Endothelin-1 narrows blood vessels; whether that matters beyond the skin has not been examined.
- The pathway is a cancer pathway. A 2025 review lists "expected off-target effects" tied to bowel and liver cancers and a "narrow therapeutic window" for this class [11]. A paper from the inventing group calls work on this pathway "limited due to its concerning role in cancer" [29].
- CXXC5 is not simply a bad protein. In blood-forming tissue it behaves as a likely tumour suppressor, and its gene sits in a region often lost in myelodysplastic syndrome and acute myeloid leukaemia [30], [31]. Blocking it permanently is not obviously harmless.
- No human safety data of any kind. The American adverse-event database holds no entry for the name [32], which reflects the absence of documented use rather than an absence of risk.
Anyone with a current or past cancer, especially of the bowel or liver, sits squarely against the known biology of this pathway [11]. That is a pharmacological inference, not a finding from a study, because no study exists that could produce one.
Doses used in studies
These are the doses reported in the cited studies, listed for scientific reference. They are not a recommendation and do not translate to human use.
Every line below is an animal experiment or a dish of cells. The figures are concentrations of liquids applied to skin or added to culture medium, not amounts per kilogram of body weight. Nobody has measured how much of any of them enters tissue. Between the wound papers and the hair papers, the concentrations differ a hundredfold without any published dose-finding.
| Study | Model | Dose | Route | Frequency | Duration | Ref |
|---|---|---|---|---|---|---|
| Lee 2015, cell work | Human skin fibroblasts, HaCaT cells | 2 µM and 10 µM | Added to culture medium | Once | 24 to 48 hours | [3] |
| Lee 2015, wound healing | C3H mice, wounds 1.5 cm across, 16 per group | 100 µM alone or with 500 mM valproic acid; comparator 100 µM EGF | Onto the wound | Daily | 11 days | [3] |
| Lee 2015, long-term skin check | Mice, three per group | Not reported separately | Onto the skin | Not reported | 6 months | [3] |
| Lee 2017, hair regrowth | C3H mice | 2 mM with 500 mM valproic acid; comparator 100 mM minoxidil | Onto the skin | Not reported | Not reported | [4], [5] |
| Ryu 2023, regrowth after shaving | C57BL/6N mice, 7 weeks old | 300 µl of a 10 mM solution | Onto shaved back skin | Every second day | Day 8 to day 12 or 20 | [22] |
| Ryu 2023, new follicles in wounds | C57BL/6N mice, 3 weeks old, wounds of 1 cm² | 20 µl of a 10 mM solution | Onto the wound | Daily | Day 7 to day 17 or 25 | [22] |
| Ryu 2023, cell work | HaCaT cells, human dermal papilla cells | 10 µM | Added to culture medium | Once | 72 hours | [22] |
The most quoted results in this table belong to combinations rather than to the peptide by itself [3], [5]. The partner drug, valproic acid at 500 mM, has no sensible counterpart outside an animal experiment.
Development and approval status
PTD-DBM was never withdrawn from development, because development in people never started. Eleven years after its first description it remains a laboratory substance, and its own inventors now work on something else.
From target to abandoned lead
- 2009-2010CXXC5 is found to bind DishevelledTwo independent groups, refs [17], [18]
- 2014Patent priority for the competing peptideYonsei University, 12 February, ref [12]
- 2015Target described in bone cells; the construct is publishedRefs [14], [3]
- 2016The group switches to small moleculesOral candidate tested in a bone-loss model, ref [20]
- 2017Hair regrowth paper and crystal structure of the docking siteRefs [4], [19]
- 2021KY19382 published; the group later calls it a mimetic of the peptideRefs [33], [10]
- 2023Hormone-driven hair loss traced through CXXC5 in miceRef [22]
- 2025An outside group confirms the target, using the small moleculeRef [28]
- 2026Still no registered study in peopleRegistry search on 20 September, ref [1]
- 2009 to 2010 — the binding between CXXC5 and Dishevelled is described twice, independently [17], [18].
- 2014 — the patent claims priority on 12 February, through Yonsei University [12].
- 2015 — the feedback loop is worked out in bone cells, and the construct appears in a wound-healing paper [14], [3].
- 2016 — the same group identifies small-molecule blockers and tests one of them by mouth in mice [20].
- 2017 — the hair regrowth paper appears, and the docking site is solved at 1.76 Å [4], [19].
- 2021 onwards — company development runs through the small molecule KY19382, not the peptide [33], [10].
- 2025 — an outside group confirms that blocking CXXC5 helps diabetic wounds in mice, again with the small molecule [28].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | Never assessed, never nominated for compounding | [6], [32] |
| European Union | Not approved | No authorisation, no development | [1], [34] |
| Germany | Not approved | Not in the anti-doping annex | [9] |
| United Kingdom | Not approved | Register not machine-readable | [34] |
| Australia | Not scheduled | Not named in the Poisons Standard | [7] |
| Canada | Not approved | Register search empty, control search worked | [35] |
| Switzerland | Not approved | Unauthorised medicines may not be traded | [36] |
| South Korea | Not approved | Home of the research; no registered study | [1], [37] |
All entries were checked on 20 September 2026. For Europe, the United Kingdom and Switzerland the register pages could not be queried automatically [34]. Those three lines rest on the complete absence of clinical development rather than on a search result.
Anti-doping
PTD-DBM is not named on the 2026 Prohibited List. A full-text search found no mention of the peptide, of CXXC5 or of Dishevelled, while control searches for ipamorelin and thymosin beta-4 worked as expected [8]. It is likewise absent from the annex to the German anti-doping law [9].
That absence is not a clearance. Class S2 opens by prohibiting the listed substances "and other substances with similar chemical structure or similar biological effect(s)", and section S2.3 catches agents affecting "regenerative capacity" or "vascularisation" [8]. Those are exactly the properties the literature attributes to blocking CXXC5. More on this sits under peptides banned in sport.
Compared with related peptides
| Substance | What it is | Data behind it | Status |
|---|---|---|---|
| PTD-DBM | Peptide of 25 building blocks, decoy for Dishevelled [12] | Mouse and cell work only, from one laboratory [1], [2] | Approved nowhere [6], [7] |
| KY19382 | Small molecule, same target plus GSK-3 beta [33] | Mouse work on hair regrowth [33] and on skin cancer [29] | The candidate a spin-out company pursues [37] |
| KY19334 | Small molecule of the same family [24] | Mouse work on diabetic wounds [24], fatty liver and metabolism [25], memory [26] | Preclinical [24], [25], [26] |
| BMD4722 | Small molecule from an outside group [38] | Binding and cell work only [38] | Preclinical [38] |
| Valproic acid | Not a relative but the usual partner drug [3] | Present in the combinations behind the headline results; on its own it matched the comparator EGF too [3], [5] | A licensed medicine for other conditions, used here only as a pathway activator [3] |
The pattern in that table explains most of the confusion around this substance. Findings on diabetic wounds [24], fatty liver [25], Alzheimer's models [26] and bone loss [20] belong to the small molecules, and attributing them to the peptide inflates its record considerably.
The target itself is in better shape than the peptide. Independent groups described the CXXC5-Dishevelled contact [17], [18], found their own blocker of it [38] and confirmed its role in diabetic wound healing [28]. None of them tested PTD-DBM.
Common misconceptions
- "PTD-DBM has shown clinical efficacy." No clinical study exists. One 2025 review does use that phrase, and the same review elsewhere records "No official approval" and "Majority of work in rodent models" [11], [1].
- "PTD-DBM and KY19382 are much the same thing." One is a peptide, the other a small molecule that also blocks an enzyme. Papers from the inventing group call KY19382 a mimetic of the peptide, not a synonym for it [10], [33].
- "The mouse studies show the peptide grows hair." The headline results came from combinations. Alone, the peptide matched a standard comparator in wounds; the minoxidil comparison involved 500 mM valproic acid as well [3], [5].
- "What is sold is what was studied." The published peptide carried an extra lysine with the dye FITC attached. Traded material is the plain 25-block chain, and the difference has never been tested [3], [15].
- "It is not on any banned list, so it is fine in sport." The list catches substances by similar effect as well as by name, and nobody has ever ruled on this one [8].
- "Releasing a brake instead of pressing the accelerator makes it cancer-safe." That was an argument by the inventors, backed by two unchanged marker proteins and six months of mouse skin [3]. Reviews of the class describe a narrow therapeutic window [11].
Frequently asked questions
Has PTD-DBM ever been tested in humans?
No. A search of the ClinicalTrials.gov registry on 20 September 2026 returned no entry, while the control search for minoxidil returned 110 studies. No published paper describes the peptide being given to a person. Human material appears in the literature only as tissue samples and cell cultures.
Is PTD-DBM approved anywhere?
No country has authorised it, for any use. Register searches in the United States, Canada and Australia returned nothing, each alongside a control search that worked. Unusually, no authority has ever assessed the substance either, so its absence from safety lists says nothing about its safety.
Is PTD-DBM the same as KY19382?
No. KY19382 is not a peptide but a small molecule from the indirubin family, and it also blocks an enzyme called GSK-3 beta. Papers from the inventing group call it a mimetic small molecular compound of PTD-DBM. The company spun out of that laboratory develops the small molecule, not the peptide.
What did the PTD-DBM wound study find?
In mice with full-thickness wounds, 100 µM PTD-DBM on its own sped up healing about as much as the comparator EGF did. Combined with 500 mM valproic acid it went much further. By day three, 42.8 per cent of the wound surface had regrown, against 4.9 per cent in the control group, with 16 animals per group.
Does PTD-DBM grow hair better than minoxidil?
That claim describes mice, not people. The 2017 paper reported that 2 mM PTD-DBM together with 500 mM valproic acid outperformed 100 mM minoxidil in C3H mice, measured as hair weight and follicle numbers. It tested a combination, at a minoxidil concentration far above what people put on their scalp, and no human comparison has ever been run.
How does PTD-DBM work?
It is built from three parts: eight arginines that are meant to carry it into cells, a short flexible linker, and a 13-block stretch copied from the human protein CXXC5. That stretch acts as a decoy that occupies Dishevelled, so the real CXXC5 can no longer bind. The Wnt pathway is not switched on directly; a brake on it is released.
What are the side effects of PTD-DBM?
Nobody knows, because no safety study has ever been run in any species. The only long-term observation is six months of skin treatment in mice, checked against two marker proteins and reported with three animals per group. No report of a side effect exists in the American adverse-event database.
Is PTD-DBM risky because of the Wnt pathway?
The pathway it targets is a well-known cancer pathway, and the literature says so plainly. A 2025 review lists off-target activation linked to bowel and liver cancers, and a narrow therapeutic window, as drawbacks of this whole approach. The reassuring data consist of two unchanged marker proteins in mice.
Why does this page list PTD-DBM doses?
They are facts from published experiments, listed so the evidence can be read as it stands. Every line is a concentration applied to mouse skin or added to cells in a dish. None of them is a dose for a person, and no method exists for turning such a number into one.
Is PTD-DBM banned in sport?
It is not named on the 2026 Prohibited List, and it is not in the annex to the German anti-doping law either. That is not a clearance. Class S2 also covers substances with a similar biological effect, and its wording reaches agents that alter regenerative capacity or the growth of blood vessels.
Sources
- ClinicalTrials.gov, API v2. Queries for "PTD-DBM" and "KY19382" returned 0 studies; "CXXC5" returned 7 records that were checked individually and found to concern unrelated products. Control query "minoxidil": 110 studies. Retrieved 20 September 2026. https://clinicaltrials.gov/
- PubMed and Europe PMC. Searches for "PTD-DBM" (4 records), "CXXC5" (133 records), "CXXC5 AND hair" (7) and "CXXC5 AND wound" (13); no record describes administration to a person, and none reports uptake, breakdown or safety testing. Retrieved 20 September 2026.
- Lee SH, Kim MY, Kim HY, et al. (2015). The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing. Journal of Experimental Medicine 212(7):1061-1080. PMID 26056233. DOI 10.1084/jem.20141601
- Lee SH, Seo SH, Lee DH, Pi LQ, Lee WS, Choi KY (2017). Targeting of CXXC5 by a competing peptide stimulates hair regrowth and wound-induced hair neogenesis. Journal of Investigative Dermatology 137(11):2260-2269. PMID 28595998. DOI 10.1016/j.jid.2017.04.038. Full text not publicly accessible; figures taken from the abstract and from reference 5.
- Fan C, et al. (2026). Overview of short peptides for hair loss. Biomedicines 14(4):864. PMID 42072405. DOI 10.3390/biomedicines14040864
- US Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Page current as of 22 April 2026; full text checked, no mention of PTD-DBM, CXXC5 or Dishevelled. Retrieved 20 September 2026. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
- Therapeutic Goods (Poisons Standard—June 2026) Instrument 2026, F2026L00633. Full text of 811,711 characters searched: "CXXC5", "DISHEVELLED", "PTD" and "DBM" each 0 matches; control terms "IPAMORELIN" 3, "MINOXIDIL" 4. Retrieved 20 September 2026.
- World Anti-Doping Agency. The 2026 Prohibited List, in force since 1 January 2026. Full text searched for "PTD-DBM", "CXXC5", "Dishevelled" and "Wnt" with no match; wording of the S2 introduction and of section S2.3 reviewed; control terms found as expected. Retrieved 20 September 2026.
- Annex to section 2(3) of the German Anti-Doping Act (AntiDopG), Federal Law Gazette 2023 I No. 67, pages 1-5. Full text searched with no match for PTD-DBM, CXXC5, Dishevelled or Wnt; control terms ipamorelin, GHRP-2, GHRP-6, hexarelin and AOD-9604 found as expected. Retrieved 20 September 2026.
- Lee SH, et al. (2025). Molecular signaling pathways in wound-induced hair-follicle neogenesis. Cells 14(6):440. PMID 40136689. DOI 10.3390/cells14060440
- Mehta A, Motavaf M, Raza D, et al. (2025). Revolutionary approaches to hair regrowth: follicle neogenesis, Wnt/beta-catenin signaling, and emerging therapies. Cells 14(11):779. PMID 40497955. DOI 10.3390/cells14110779
- European patent EP 2907520 A1 / B1, "Composition for promoting wound healing". Applicant: Industry Academic Cooperation Foundation of Yonsei University. Inventors Kang-Yell Choi, Soung-Hoon Lee, Hyun-Yi Kim. Priority 12 February 2014, granted 20 February 2019; SEQ ID NO 1 and SEQ ID NO 7. Retrieved 20 September 2026. https://patents.google.com/patent/EP2907520A1/en
- UniProt Knowledgebase, entry Q7LFL8 (CXXC5_HUMAN, 322 amino acids). Sequence checked; the motif RKTGHQICKFRKC sits at positions 284-296. Retrieved 20 September 2026. https://rest.uniprot.org/uniprotkb/Q7LFL8.fasta
- Kim HY, Yoon JY, Yun JH, et al. (2015). CXXC5 is a negative-feedback regulator of the Wnt/beta-catenin pathway involved in osteoblast differentiation. Cell Death and Differentiation 22(6):912-920. PMID 25633194. DOI 10.1038/cdd.2014.238
- Product datasheet for material traded as PTD-DBM, retrieved 20 September 2026. Cited only as evidence of what is traded, not as a scientific reference: formula C124H223N61O28S2, mass 3080.7 g/mol, sequence without the FITC-labelled lysine, no CAS number, sold for laboratory use only. Own recalculation of the formula on 20 September 2026 indicates a ring between the two cysteines.
- Wikidata, wbsearchentities API, query "PTD-DBM", 20 September 2026: no entity. A PubChem check on the same day failed because the interface returned server-busy errors, including for the control query.
- Andersson T, Södersten E, Duckworth JK, et al. (2009). CXXC5 is a novel BMP4-regulated modulator of Wnt signaling in neural stem cells. Journal of Biological Chemistry 284(6):3672-3681. PMID 19001364. DOI 10.1074/jbc.M808119200
- Kim MS, Yoon SK, Bollig F, et al. (2010). A novel Wilms tumor 1 (WT1) target gene negatively regulates the WNT signaling pathway. Journal of Biological Chemistry 285(19):14585-14593. PMID 20220130. DOI 10.1074/jbc.M109.094334
- Lee I, Choi S, Yun JH, et al. (2017). Crystal structure of the PDZ domain of mouse Dishevelled 1 and its interaction with CXXC5. Biochemical and Biophysical Research Communications 485(3):584-590. PMID 27932247. DOI 10.1016/j.bbrc.2016.12.023
- Kim HY, Choi S, Yoon JH, et al. (2016). Small molecule inhibitors of the Dishevelled-CXXC5 interaction are new drug candidates for bone anabolic osteoporosis therapy. EMBO Molecular Medicine 8(4):375-387. PMID 26941261. DOI 10.15252/emmm.201505714
- Ma T, et al. (2026). Hydrogel microneedle delivery of a palmitoylated peptide promotes hair regeneration via dual activation of Wnt/beta-catenin and cAMP-PKA signaling. Journal of Nanobiotechnology 24. PMID 42151987. DOI 10.1186/s12951-026-04542-8
- Ryu YC, Park J, Kim YR, et al. (2023). CXXC5 mediates DHT-induced androgenetic alopecia via PGD2. Cells 12(4):555. PMID 36831222. DOI 10.3390/cells12040555
- Choi S, Kim HY, Cha PH, et al. (2019). CXXC5 mediates growth plate senescence and is a target for enhancement of longitudinal bone growth. Life Science Alliance 2(2):e201800254. PMID 30971423. DOI 10.26508/lsa.201800254
- Kim E, Seo SH, Hwang Y, et al. (2023). Inhibiting the cytosolic function of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair. Experimental and Molecular Medicine 55(8):1770-1782. PMID 37524876. DOI 10.1038/s12276-023-01064-3
- Seo SH, Kim E, Yoon M, et al. (2022). Metabolic improvement and liver regeneration by inhibiting CXXC5 function for non-alcoholic steatohepatitis treatment. Experimental and Molecular Medicine 54(9):1511-1523. PMID 36114279. DOI 10.1038/s12276-022-00851-8. The intervention was the small molecule KY19334, not the peptide.
- Yoon M, Kim H, Shin H, et al. (2023). Inhibition of CXXC5 function rescues Alzheimer's disease phenotypes by restoring Wnt/beta-catenin signalling. Pharmacological Research 194:106836. PMID 37355147. DOI 10.1016/j.phrs.2023.106836. The intervention was the small molecule KY19334, not the peptide.
- Lee SH, An S, Ryu YC, et al. (2023). Adhesive hydrogel patch-mediated combination drug therapy induces regenerative wound healing. Advanced Healthcare Materials 12(18):e2203094. PMID 36854308. DOI 10.1002/adhm.202203094
- Chen Y, Ding X, Ma Z, et al. (2025). CXXC5 function blockade promotes diabetic wound healing through stimulating fibroblast and vascular endothelial cell activation. Cell Communication and Signaling 23(1):108. PMID 40001144. DOI 10.1186/s12964-025-02097-z
- Lee SH, et al. (2025). Novel small molecules downregulate CDK1 expression and inhibit Wnt/beta-catenin signaling in cutaneous squamous cell carcinoma. Experimental and Molecular Medicine 57:1996-2009. PMID 40887499. DOI 10.1038/s12276-025-01532-y
- An Z, et al. (2025). Signal integrator function of CXXC5 in cancer. Cell Communication and Signaling 23(1):25. PMID 39806388. DOI 10.1186/s12964-024-02005-x
- Astori A, et al. (2022). The epigenetic regulator RINF (CXXC5) maintains SMAD7 expression in human immature erythroid cells. Haematologica 107(1):268-283. PMID 33241676. DOI 10.3324/haematol.2020.263558
- openFDA. Label API and adverse-event API (FAERS), queried 20 September 2026: no record for PTD-DBM or CXXC5; control query "MINOXIDIL" returned records. DailyMed API v2 on the same day: 0 entries for PTD-DBM, 323 for the control term.
- Ryu YC, Lee DH, Shim J, et al. (2021). KY19382, a novel activator of Wnt/beta-catenin signalling, promotes hair regrowth and hair follicle neogenesis. British Journal of Pharmacology 178(12):2533-2546. PMID 33751552. DOI 10.1111/bph.15438
- Query attempts at the European Medicines Agency, the MHRA product database and Swissmedic, 20 September 2026: HTTP 401, a page shell without results for both the search term and the control term, and HTTP 404 respectively. No result count could be obtained from these three registers.
- Health Canada, Drug Product Database API, queried 20 September 2026: no entry for PTD-DBM; control query "minoxidil" returned 19 entries.
- Swiss Federal Office for Customs and Border Security, Swissmedic and Swiss Sport Integrity. Joint action "Peptide 2026", notice of 22 June 2026, stating that trading or drop-shipping unauthorised medicines in Switzerland is illegal.
- Google Patents, query "CXXC5 dishevelled peptide", retrieved 20 September 2026. Filings by CK Biotech Inc. (US 2021/0323918 A1, US 2024/0425457 A1, priority 15 October 2018) and by CK Regeon (KR 102784482 B1, priority 4 November 2019) cover the small molecules rather than the peptide.
- Ma S, Choi J, Jin X, et al. (2018). Discovery of a small-molecule inhibitor of Dvl-CXXC5 interaction by computational approaches. Journal of Computer-Aided Molecular Design 32(5):643-655. PMID 29627878. DOI 10.1007/s10822-018-0118-x
Cite this page
The facts on this page were checked on 20 September 2026, and every register search behind the status table was run on that date. Because nothing about this substance has moved for years, the checking date matters more than the publication date.
myPeptides Research & Editing. (2026). PTD-DBM: what the studies show, status and safety. Version 1.0, 20 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/ptd-dbm
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Note |
|---|---|---|
| 1.0 | 20 September 2026 | Initial publication |