--- title: "PTD-DBM: Research & Evidence | BodyHackGuide" url: https://www.bodyhackguide.co/compound/ptd-dbm description: "PTD-DBM: mechanism, clinical studies & side effects." lang: en --- Skip to content Compare notes on r/BodyHackGuide (https://reddit.com/r/bodyhackguide) Compare notes with other researchers. Join r/BodyHackGuide (https://reddit.com/r/bodyhackguide) Image: PTD-DBM molecular structure (https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/176453931/PNG?image_size=300x300) # PTD-DBM Skin & Hair (https://www.bodyhackguide.co/wiki#cat-skin-&-hair)Preclinical Also known as: Protein transduction domain-Dishevelled binding motif, PTD-Dvl binding motif peptide, CXXC5-Dvl competitor peptide, Protein transduction domain-Dvl-binding motif PTD-DBM is a synthetic peptide that joins a protein transduction domain, which carries the peptide into cells, to the Dishevelled-binding motif (DBM) of the protein CXXC5, and it was built to block CXXC5 from binding Dishevelled so that Wnt/beta-catenin signalling stays switched on (PMID: 26056233). Kang-Yell Choi's laboratory at Yonsei University in Seoul designed the peptide and published every primary study of it, first in wound healing in 2015 and then in hair regrowth in 2017 (PMID: 26056233; PMID: 28595998). Price check No vendor listings yet We do not track a vendor for PTD-DBM yet. Compare other compounds: https://www.bodyhackguide.co/compare Half-life: No published human value, and no published pharmacokinetic st… Route: Topical MW: 3082.6 g/mol CAS: 1609454-11-6 (PubChem CID 176453931, the record PubChem retur… Last reviewed: Oct 21, 2026 ## Overview ### At A Glance Mechanism The pathway being targeted… Half-Life No published human value, and no published pharmacokinetic study in any species was found. The 2015 report states only that the fluorescein-tagged peptide was delivered into cells in culture and in mouse skin, without plasma or tissue concentrations over time (PMID: 26056233). Routes Topical Potential Benefits Accelerated closure of 1.5 cm full-thickness skin wounds in C3H mice given the peptide topically each day, to about the same degree as epidermal growth factor used as the positive control (PMID: 26056233) Faster wound closure again when topical valproic acid was added to the peptide in the same mouse model (PMID: 26056233) Raised beta-catenin, alpha-smooth muscle actin, collagen I and endothelin-1 in cultured human dermal fibroblasts at 2 and 10 micromolar (PMID: 26056233) Increased fibroblast migration after a scratch and increased collagen gel contraction in human dermal fibroblast cultures (PMID: 26056233) Accelerated hair regrowth and wound-induced hair follicle neogenesis in mice (PMID: 28595998) Reversed the suppression of hair regrowth and of wound-induced hair neogenesis caused by prostaglandin D2 in C57BL/6N mice treated topically (PMID: 36831222) Lowered scar formation and raised collagen III in mouse wounds when loaded with valproic acid into an adhesive hyaluronic acid patch (PMID: 36854308) Safety Notes Common No adverse effect has been reported in any species; the one safety endpoint published is wound histology with c-Myc and cyclin D1 staining six months after wounding, in three mice per group, which showed no abnormality (PMID: 26056233) Serious No human safety data of any kind exist for PTD-DBM The authors checked two oncogenic markers, c-Myc and cyclin D1, and found no increase in cells or mice, which is a narrow check rather than a carcinogenicity study (PMID: 26056233) The peptide raised collagen I and alpha-smooth muscle actin in human dermal fibroblasts about as much as transforming growth factor beta, the mediator of dermal fibrosis (PMID: 26056233) Blocking the same interaction changes bone density, growth plate senescence and fat metabolism in mice (PMID: 25633194; PMID: 30971423; PMID: 35384342) ### Mechanism of Action ### The pathway being targeted Wnt/beta-catenin signalling (the canonical Wnt pathway) controls hair follicle formation and cycling and the proliferative phase of skin wound healing. When a Wnt protein binds the Frizzled receptor, the cytoplasmic protein Dishevelled (Dvl) is recruited to the receptor complex, beta-catenin escapes degradation, accumulates and moves into the nucleus where it acts as a transcriptional cofactor. An independent commentary on this work in the Journal of Investigative Dermatology lays out that sequence and notes that the same pathway is involved in carcinogenesis as well as regeneration (PMID: 28967390). ### CXXC5 is the brake CXXC5 (CXXC-type zinc finger protein 5) was identified as a Dishevelled-binding inhibitor of Wnt signalling by two groups working outside the hair field: in neural stem cells, where bone morphogenetic protein 4 induced it and it interacted with Dvl (PMID: 19001364), and in kidney development, where it was characterized as a Wilms tumour 1 target gene and named WID, for WT1-induced inhibitor of Dishevelled (PMID: 20220130). Choi's group then showed that Wnt3a itself induces CXXC5, making CXXC5 a negative feedback regulator: the pathway turns on its own brake (PMID: 25633194; PMID: 26056233). The binding depends on a short C-terminal Dishevelled-binding motif in CXXC5, and a CXXC5 mutant with that motif deleted neither bound Dvl-1 nor suppressed beta-catenin (PMID: 26056233). The crystal structure of the mouse Dvl1 PDZ domain and modelling of its interaction with CXXC5 were published by the same university's biochemistry group (PMID: 27932247). ### What the peptide is PTD-DBM is that same motif made into a competitor. The 2015 paper describes the synthetic peptide as a protein transduction domain for delivery, a flexible linker, the Dishevelled-binding motif, and a lysine conjugated with fluorescein for visualization, and reports that it entered cells both in culture and in mouse skin (PMID: 26056233). The amino acid sequence is printed in a figure panel of that paper rather than in its text, so it is not quoted here. The chemistry on this page is PubChem's record for the name PTD-DBM, which is the peptide without that fluorescent tag and so is lighter than the molecule the 2015 experiments used. Because the peptide occupies the Dvl site that CXXC5 would use, it lifts the brake rather than pushing the accelerator, which is the stated reason the group pairs it with a separate pathway activator. ### What happens downstream in cells In cultured human dermal fibroblasts, PTD-DBM at 2 and 10 micromolar raised beta-catenin, alpha-smooth muscle actin and collagen I in a concentration-dependent way, increased nuclear beta-catenin, and raised endothelin-1 messenger RNA and protein without changing the oncogenic markers c-Myc and cyclin D1. Silencing beta-catenin abolished the increases in alpha-smooth muscle actin and collagen I, and the endothelin receptor blocker bosentan also blocked them, which places endothelin-1 in the chain (PMID: 26056233). The peptide increased fibroblast migration after a scratch, stress fibre formation and collagen gel contraction, and its effects were additive with Wnt3a or with the glycogen synthase kinase 3 beta inhibitor valproic acid (PMID: 26056233). ### In the hair follicle In the 2017 hair paper, CXXC5 was raised in miniaturized hair follicles and arrector pili muscles in human balding scalp, and in human hair follicle dermal papilla cells CXXC5 suppressed alkaline phosphatase activity and proliferation through its interaction with Dvl-1 (PMID: 28595998). Mice lacking Cxxc5 regrew hair faster, and valproic acid added further regrowth in those mice. Blocking the CXXC5-Dishevelled interaction with the competitor peptide activated Wnt/beta-catenin signalling and accelerated both hair regrowth and wound-induced hair follicle neogenesis (PMID: 28595998). The commentary published alongside it identifies that competitor as the protein transduction domain-Dvl-binding motif peptide and describes the same results (PMID: 28967390), and the group's own 2023 paper names PTD-DBM for the hair work and cites the 2017 paper for it (PMID: 36831222). ### Where CXXC5 sits in the hair-loss cascade The 2023 work put CXXC5 downstream of the two best-known drivers of pattern hair loss in males. Prostaglandin D2 suppressed hair regrowth and wound-induced hair neogenesis in mice, and both effects were reversed by deleting Cxxc5 or by treating with PTD-DBM; dihydrotestosterone acted through prostaglandin D2 in the same chain (PMID: 36831222). That is a mouse result about a human pathway, and the 2017 commentary had already pointed out that a causal link between CXXC5 levels and male pattern hair loss in people had not been tested (PMID: 28967390). ### The small-molecule successors The same laboratory moved from the peptide to small molecules that block the same protein-protein interaction. KY-02061 and the analogue KY-02327 were screened for Dvl-CXXC5 blockade and tested for bone in mice (PMID: 26941261); KY19382 activated Wnt/beta-catenin signalling in human dermal papilla cells, lengthened cultured human hair follicles and mouse vibrissae, and promoted hair regrowth and new follicle formation in mice (PMID: 33751552); and KY19334 was used in mouse models of obesity and insulin resistance (PMID: 36450849; PMID: 35384342). A pharmacophore-based virtual screen from the same university, with Choi as a co-author, identified a separate inhibitor, BMD4722, that binds the Dvl PDZ domain (PMID: 29627878). Anyone reading about PTD-DBM should know that most of the newer work from this group uses those molecules rather than the peptide. ### Overview PTD-DBM is a synthetic peptide that joins a protein transduction domain, which carries the peptide into cells, to the Dishevelled-binding motif (DBM) of the protein CXXC5, and it was built to block CXXC5 from binding Dishevelled so that Wnt/beta-catenin signalling stays switched on (PMID: 26056233). Kang-Yell Choi's laboratory at Yonsei University in Seoul designed the peptide and published every primary study of it, first in wound healing in 2015 and then in hair regrowth in 2017 (PMID: 26056233; PMID: 28595998). The results come from cultured human cells, from mouse skin treated topically, and from mice in which the Cxxc5 gene was deleted; the two strongest findings are faster closure of full-thickness wounds in mice and faster hair regrowth plus new follicle formation in mice (PMID: 26056233; PMID: 28595998; PMID: 36831222). No human trial of PTD-DBM has been published and no trial of it is registered on ClinicalTrials.gov, checked on 20 October 2026. ### Potential Research Fields Hair biology Wound healing Wnt signalling Peptide pharmacology Regenerative medicine ## Chemical Information IUPAC Name Not yet available CAS Number 1609454-11-6 (PubChem CID 176453931, the record PubChem returns for the name PTD-DBM) Molecular Formula C124H225N61O28S2 Molecular Mass 3082.6 g/mol View on PubChem: https://pubchem.ncbi.nlm.nih.gov/compound/176453931 ## Dosing & Protocols ### Unlock the Dosing tab Enter your email to keep reading. It is free, and it opens these tabs on every compound page in this browser. - Route You also get the free peptide cheat sheet by email. Unsubscribe anytime. Have an account? Sign in (https://www.bodyhackguide.co/auth) ## Research ### Unlock the research summary - A summary of the key research - Safety and side effects - A link to the PubMed results ## Interactions ### Interaction Matrix ### Contraindications No product labelling exists for PTD-DBM, so there is no contraindication list. The cautions in the literature are mechanism-based and all of them come from the Wnt/beta-catenin pathway rather than from observed harm. Wnt/beta-catenin signalling is involved in carcinogenesis as well as in regeneration, which the commentary on this work states plainly (PMID: 28967390), and the authors themselves framed their c-Myc and cyclin D1 measurements around the known association between wounds and basal cell carcinoma (PMID: 26056233). The pathway also drives fibrosis. In human dermal fibroblasts the peptide raised collagen I and alpha-smooth muscle actin to a degree comparable with transforming growth factor beta, and the authors list keloid formation, morphea and scleroderma as diseases of exactly that process (PMID: 26056233). Blocking the CXXC5-Dishevelled interaction has effects in bone, growth plate and fat in mice (PMID: 25633194; PMID: 30971423; PMID: 35384342; PMID: 36450849), so a route that reaches the circulation would not be expected to act only on skin. The combined effect that carries most of the published results depends on valproic acid, a drug with its own contraindications in humans. The hair and wound results should not be read as results for the peptide alone where the paper used the combination (PMID: 26056233; PMID: 28595998). Research Disclaimer This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds. No listings found for PTD-DBM. ### Sign in to leave a review Reviews on BodyHackGuide are tied to verified user accounts and moderated before publishing. Sign in (free, no spam) to share your experience with PTD-DBM. ### Related Compounds View All (https://www.bodyhackguide.co/wiki) ### Acetyl Hexapeptide-8 Skin & Hair Marketed topical cosmetic ingredient (INCI: Acetyl Hexapeptide-8 / Argireline). Supported by small human anti-wrinkle studies, including one randomized, placebo-controlled trial; no systemic or injectable clinical development. Not an FDA-approved drug. 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Oral low-dose minoxidil (off-label): 625-5000 mcg/day (0.625-5 mg). Topical minoxidil is dosed by concentration (2% or 5%), not by mcg -- roughly 10-20 mg of minoxidil is delivered per topical application, with only ~1.4% absorbed systemically. Preclinical View Profile https://www.bodyhackguide.co/compound/minoxidil ### Palmitoyl Pentapeptide-4 Skin & Hair Marketed topical cosmetic ingredient with a small set of human cosmetic trials Palmitoyl pentapeptide-4 is the cosmetic ingredient Pal-KTTKS, a five-amino-acid fragment of the type I collagen propeptide with a 16-carbon palmitic acid chain attached, sold to formulators under the trade name Matrixyl (PubChem CID 9897237; PMID: 8486721). t½ No published human value. The relevant measurements are stability in skin rather than plasma. In hairless mouse skin extracts and homogenates both KTTKS and pal-KTTKS were degraded rapidly, with pal-KTTKS the more stable of the two, and adding protease inhibitors improved the stability of both (PMID: 25143811). In rat skin homogenate the free peptide was described as very susceptible to peptide bond cleavage by aminopeptidases present in the skin (PMID: 22921149). 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Not intended as medical advice. Consult a healthcare professional before use. ## Frequently Asked Questions What is PTD-DBM? PTD-DBM is a synthetic peptide built from two parts: a protein transduction domain that carries it into cells and the Dishevelled-binding motif of the protein CXXC5. PTD-DBM works by occupying the site that CXXC5 uses to bind Dishevelled, which stops CXXC5 from shutting down Wnt/beta-catenin signalling (PMID: 26056233). The 2015 paper describes PTD-DBM as a protein transduction domain for delivery, a flexible linker, the Dishevelled-binding motif, and a lysine conjugated with fluorescein for visualization (PMID: 26056233). Who developed PTD-DBM and where does the research come from? PTD-DBM comes from one laboratory, that of Kang-Yell Choi in the Department of Biotechnology at Yonsei University in Seoul. Choi's group published the peptide in the Journal of Experimental Medicine in 2015 for wound healing (PMID: 26056233) and in the Journal of Investigative Dermatology in 2017 for hair regrowth (PMID: 28595998), and has published the follow-up hair and wound work since (PMID: 36831222; PMID: 36854308). From 2017 onward the PTD-DBM papers carry a company affiliation alongside Yonsei University, listed as CK Biotechnology Inc in 2017, CK Biotech Inc in 2021 and CK Regeon Inc in 2023 (PMID: 28595998; PMID: 33751552; PMID: 36831222; PMID: 36854308). Only four PubMed-indexed papers name PTD-DBM, and an independent commentary on the 2017 hair paper came from Johns Hopkins (PMID: 28967390). Has PTD-DBM been tested in people? PTD-DBM has not been tested in people in any published study. Every result is from cultured cells or from mice, and a search of ClinicalTrials.gov on 20 October 2026 found no registered trial of PTD-DBM, of CXXC5 or of the related small molecules KY19382 and KY19334. Two human observations exist without any treatment: CXXC5 protein was lower in acute surgical wounds in five melanoma patients (PMID: 26056233), and CXXC5 was raised in miniaturized follicles and arrector pili muscles in balding human scalp (PMID: 28595998). The commentary published with the 2017 paper raised testing the peptide in human scalp as an open question (PMID: 28967390). What did the hair studies on PTD-DBM actually measure? The hair work on PTD-DBM is mouse work plus human cell work. In human hair follicle dermal papilla cells, CXXC5 suppressed alkaline phosphatase activity and proliferation through Dishevelled-1; in mice, deleting Cxxc5 sped up hair regrowth, and blocking the CXXC5-Dishevelled interaction with the competitor peptide accelerated hair regrowth and wound-induced hair follicle neogenesis (PMID: 28595998). The 2023 paper gives the application detail: the backs of 7-week-old C57BL/6N mice were depilated and treated topically with 300 microlitres of 10 millimolar PTD-DBM every other day, and regrown hair was weighed and measured (PMID: 36831222). No measurement of hair count or hair density in human scalp has been published for PTD-DBM. How does PTD-DBM differ from minoxidil or finasteride? PTD-DBM acts on a different step from either approved drug and has no approval of its own. Finasteride works on androgen metabolism and minoxidil was developed as a vasodilator, while PTD-DBM blocks a protein-protein interaction, CXXC5 with Dishevelled, to keep Wnt/beta-catenin signalling active (PMID: 26056233; PMID: 28595998). Two 2025 reviews group the Dishevelled-CXXC5 interaction with other Wnt targets as a direction beyond minoxidil and finasteride for androgenetic alopecia (PMID: 40924915; PMID: 40497955). The difference that matters is evidence: minoxidil and finasteride carry FDA approvals and human trials, and PTD-DBM has mouse data. What are the known risks of PTD-DBM? PTD-DBM has no human safety data at all, so the risks discussed in the literature are mechanism-based. Wnt/beta-catenin signalling is involved in carcinogenesis as well as regeneration (PMID: 28967390), and the authors measured two oncogenic markers, c-Myc and cyclin D1, which the peptide did not raise in cells or mice (PMID: 26056233). Wnt/beta-catenin signalling also drives fibrosis, and in human dermal fibroblasts PTD-DBM raised collagen I and alpha-smooth muscle actin comparably to transforming growth factor beta (PMID: 26056233), which is why a later paper paired it with a patch aimed at reducing scarring (PMID: 36854308). Mice lacking CXXC5 also differ in bone density, growth plate and fat metabolism (PMID: 25633194; PMID: 30971423; PMID: 35384342). Why do most PTD-DBM experiments add valproic acid? PTD-DBM removes a brake on Wnt signalling rather than activating the pathway directly, so the group pairs it with an activator. Valproic acid inhibits glycogen synthase kinase 3 beta, and topical valproic acid plus topical PTD-DBM accelerated mouse wound closure more than either alone and raised beta-catenin, keratin 14 and collagen I together (PMID: 26056233); the same pairing increased hair regrowth and wound-induced hair neogenesis in the hair work (PMID: 28595998). The commentary on the 2017 hair paper notes that valproic acid also inhibits histone deacetylase, so some of the effect combined with PTD-DBM may be epigenetic rather than Wnt-specific (PMID: 28967390). ## Research Tools ### Peptide Calculator Reconstitution & syringe units https://www.bodyhackguide.co/tools/reconstitution ### Reconstitution Guide How to mix, step by step https://www.bodyhackguide.co/guides/how-to-reconstitute-peptides ### Nasal Spray Calc mL per actuation https://www.bodyhackguide.co/tools/intranasal ### Half-Life Visualizer Decay curves https://www.bodyhackguide.co/tools/halflife ## You may also like ### BPC-157 Injury, Repair & Recovery View product (https://www.bodyhackguide.co/buy/bpc-157) ### PDRN Skin & Hair View product (https://www.bodyhackguide.co/buy/pdrn) ### Minoxidil Skin & Hair View product (https://www.bodyhackguide.co/buy/minoxidil) ### AHK-Cu Skin & Hair View product (https://www.bodyhackguide.co/buy/ahk-cu) ## Related Compounds ### Acetyl Hexapeptide-8 ### AHK-Cu Skin & Hair Preclinical ### Melanotan 2 ### Minoxidil Skin & Hair FDA-Approved ### Palmitoyl Pentapeptide-4 ### PDRN Skin & Hair Phase 4 ## Research Benches Reference pages that put PTD-DBM next to the compounds people pair it with: roles, evidence, overlap and conflicts. No dosing. Research use only. 01 research bench Peptides for Hair Growth GHK-Cu, AHK-Cu, PTD-DBM, thymulin and follistatin-344, measured against minoxidil 6 compounds human data on 4 of 6 https://www.bodyhackguide.co/stack/hair-growth-peptides Free 2026 Peptide Cheat Sheet (PDF) 38 compounds and blends: vial sizes, BAC water volumes, dosing ranges and bloodwork markers. Download Free (https://www.bodyhackguide.co/guides/peptide-cheat-sheet-download) ### Need bloodwork before starting? Full hormone + metabolic panels from Anabolic Insights. Code CHONCH for first-order discount. 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All rights reserved. · Terms (https://www.bodyhackguide.co/terms) · Privacy (https://www.bodyhackguide.co/privacy) ## Structured data ```json [ { "@context": "https://schema.org", "@type": "BreadcrumbList", "itemListElement": [ { "@type": "ListItem", "position": 1, "name": "Home", "item": "https://www.bodyhackguide.co/" }, { "@type": "ListItem", "position": 2, "name": "Compounds", "item": "https://www.bodyhackguide.co/compare" }, { "@type": "ListItem", "position": 3, "name": "PTD-DBM" } ] }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "PTD-DBM", "description": "PTD-DBM is a synthetic peptide that joins a protein transduction domain, which carries the peptide into cells, to the Dishevelled-binding motif (DBM) of the protein CXXC5, and it was built to block CXXC5 from binding Dishevelled so that Wnt/beta-catenin signalling stays switched on (PMID: 26056233). Kang-Yell Choi's laboratory at Yonsei University in Seoul designed the peptide and published every primary study of it, first in wound healing in 2015 and then in hair regrowth in 2017 (PMID: 26056233; PMID: 28595998). The results come from cultured human cells, from mouse skin treated topically, and from mice in which the Cxxc5 gene was deleted; the two strongest findings are faster closure of full-thickness wounds in mice and faster hair regrowth plus new follicle formation in mice (PMID: 26056233; PMID: 28595998; PMID: 36831222). No human trial of PTD-DBM has been published and no trial of it is registered on ClinicalTrials.gov, checked on 20 October 2026.", "lastReviewed": "2026-10-21T06:27:52.916Z", "url": "https://www.bodyhackguide.co/compound/ptd-dbm", "author": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "reviewedBy": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "publisher": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" }, "mainContentOfPage": { "@type": "WebPageElement", "cssSelector": "main" }, "about": { "@type": "Drug", "name": "PTD-DBM", "alternateName": [ "Protein transduction domain-Dishevelled binding motif", "PTD-Dvl binding motif peptide", "CXXC5-Dvl competitor peptide", "Protein transduction domain-Dvl-binding motif" ], "description": "PTD-DBM is a synthetic peptide that joins a protein transduction domain, which carries the peptide into cells, to the Dishevelled-binding motif (DBM) of the protein CXXC5, and it was built to block CXXC5 from binding Dishevelled so that Wnt/beta-catenin signalling stays switched on (PMID: 26056233). Kang-Yell Choi's laboratory at Yonsei University in Seoul designed the peptide and published every primary study of it, first in wound healing in 2015 and then in hair regrowth in 2017 (PMID: 26056233; PMID: 28595998). The results come from cultured human cells, from mouse skin treated topically, and from mice in which the Cxxc5 gene was deleted; the two strongest findings are faster closure of full-thickness wounds in mice and faster hair regrowth plus new follicle formation in mice (PMID: 26056233; PMID: 28595998; PMID: 36831222). No human trial of PTD-DBM has been published and no trial of it is registered on ClinicalTrials.gov, checked on 20 October 2026.", "activeIngredient": "PTD-DBM", "administrationRoute": "Topical", "mechanismOfAction": "The pathway being targeted Wnt/beta-catenin signalling (the canonical Wnt pathway) controls hair follicle formation and cycling and the proliferative phase of skin wound healing. When a Wnt protein binds the Frizzled receptor, the cytoplasmic protein Dishevelled (Dvl) is recruited to the receptor complex, beta-catenin escapes degradation, accumulates and moves into the nucleus where it acts as a transcriptional cofactor. An independent commentary on this work in the Journal of Investigative Dermatology lays out that sequence and notes that the same pathway is involved in carcinogenesis as well as regeneration (PMID: 28967390). CXXC5 is the brake CXXC5 (CXXC-type zinc finger protein 5) was identified as a Dishevelled-binding inhibitor of Wnt signalling by two groups working outside the hair field: in neural stem cells, where bone morphogenetic protein 4 induced it and it interacted with Dvl (PMID: 19001364), and in kidney development, where it was characterized as a Wilms tumour 1 target gene and named WID, for WT1-induced inhibitor of Dishevelled (PMID: 20220130). Choi's group then showed that Wnt3a itself induces CXXC5, making CXXC5 a negative feedback regulator: the pathway turns on its own brake (PMID: 25633194; PMID: 26056233). The binding depends on a short C-terminal Dishevelled-binding motif in CXXC5, and a CXXC5 mutant with that motif deleted neither bound Dvl-1 nor suppressed beta-catenin (PMID: 26056233). The crystal structure of the mouse Dvl1 PDZ domain and modelling of its interaction with CXXC5 were published by the same university's biochemistry group (PMID: 27932247). What the peptide is PTD-DBM is that same motif made into a competitor. The 2015 paper describes the synthetic peptide as a protein transduction domain for delivery, a flexible linker, the Dishevelled-binding motif, and a lysine conjugated with fluorescein for visualization, and reports that it entered cells both in culture and in mouse skin (PMID: 26056233). The amino acid sequence is printed in a figure panel of that paper rather than in its text, so it is not quoted here. The chemistry on this page is PubChem's record for the name PTD-DBM, which is the peptide without that fluorescent tag and so is lighter than the molecule the 2015 experiments used. Because the peptide occupies the Dvl site that CXXC5 would use, it lifts the brake rather than pushing the accelerator, which is the stated reason the group pairs it with a separate pathway activator. What happens downstream in cells In cultured human dermal fibroblasts, PTD-DBM at 2 and 10 micromolar raised beta-catenin, alpha-smooth muscle actin and collagen I in a concentration-dependent way, increased nuclear beta-catenin, and raised endothelin-1 messenger RNA and protein without changing the oncogenic markers c-Myc and cyclin D1. Silencing beta-catenin abolished the increases in alpha-smooth muscle actin and collagen I, and the endothelin receptor blocker bosentan also blocked them, which places endothelin-1 in the chain (PMID: 26056233). The peptide increased fibroblast migration after a scratch, stress fibre formation and collagen gel contraction, and its effects were additive with Wnt3a or with the glycogen synthase kinase 3 beta inhibitor valproic acid (PMID: 26056233). In the hair follicle In the 2017 hair paper, CXXC5 was raised in miniaturized hair follicles and arrector pili muscles in human balding scalp, and in human hair follicle dermal papilla cells CXXC5 suppressed alkaline phosphatase activity and proliferation through its interaction with Dvl-1 (PMID: 28595998). Mice lacking Cxxc5 regrew hair faster, and valproic acid added further regrowth in those mice. Blocking the CXXC5-Dishevelled interaction with the competitor peptide activated Wnt/beta-catenin signalling and accelerated both hair regrowth and wound-induced hair follicle neogenesis (PMID: 28595998). The commentary published alongside it identifies that competitor as the protein transduction domain-Dvl-binding motif peptide and describes the same results (PMID: 28967390), and the group's own 2023 paper names PTD-DBM for the hair work and cites the 2017 paper for it (PMID: 36831222). Where CXXC5 sits in the hair-loss cascade The 2023 work put CXXC5 downstream of the two best-known drivers of pattern hair loss in males. Prostaglandin D2 suppressed hair regrowth and wound-induced hair neogenesis in mice, and both effects were reversed by deleting Cxxc5 or by treating with PTD-DBM; dihydrotestosterone acted through prostaglandin D2 in the same chain (PMID: 36831222). That is a mouse result about a human pathway, and the 2017 commentary had already pointed out that a causal link between CXXC5 levels and male pattern hair loss in people had not been tested (PMID: 28967390). The small-molecule successors The same laboratory moved from the peptide to small molecules that block the same protein-protein interaction. KY-02061 and the analogue KY-02327 were screened for Dvl-CXXC5 blockade and tested for bone in mice (PMID: 26941261); KY19382 activated Wnt/beta-catenin signalling in human dermal papilla cells, lengthened cultured human hair follicles and mouse vibrissae, and promoted hair regrowth and new follicle formation in mice (PMID: 33751552); and KY19334 was used in mouse models of obesity and insulin resistance (PMID: 36450849; PMID: 35384342). A pharmacophore-based virtual screen from the same university, with Choi as a co-author, identified a separate inhibitor, BMD4722, that binds the Dvl PDZ domain (PMID: 29627878). Anyone reading about PTD-DBM should know that most of the newer work from this group uses those molecules rather than the peptide.", "legalStatus": "Not approved for human use (research chemical)", "warning": "For research purposes only. Not for human consumption." } }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "What is PTD-DBM?", "acceptedAnswer": { "@type": "Answer", "text": "PTD-DBM is a synthetic peptide built from two parts: a protein transduction domain that carries it into cells and the Dishevelled-binding motif of the protein CXXC5. PTD-DBM works by occupying the site that CXXC5 uses to bind Dishevelled, which stops CXXC5 from shutting down Wnt/beta-catenin signalling (PMID: 26056233). The 2015 paper describes PTD-DBM as a protein transduction domain for delivery, a flexible linker, the Dishevelled-binding motif, and a lysine conjugated with fluorescein for visualization (PMID: 26056233)." } }, { "@type": "Question", "name": "Who developed PTD-DBM and where does the research come from?", "acceptedAnswer": { "@type": "Answer", "text": "PTD-DBM comes from one laboratory, that of Kang-Yell Choi in the Department of Biotechnology at Yonsei University in Seoul. Choi's group published the peptide in the Journal of Experimental Medicine in 2015 for wound healing (PMID: 26056233) and in the Journal of Investigative Dermatology in 2017 for hair regrowth (PMID: 28595998), and has published the follow-up hair and wound work since (PMID: 36831222; PMID: 36854308). From 2017 onward the PTD-DBM papers carry a company affiliation alongside Yonsei University, listed as CK Biotechnology Inc in 2017, CK Biotech Inc in 2021 and CK Regeon Inc in 2023 (PMID: 28595998; PMID: 33751552; PMID: 36831222; PMID: 36854308). Only four PubMed-indexed papers name PTD-DBM, and an independent commentary on the 2017 hair paper came from Johns Hopkins (PMID: 28967390)." } }, { "@type": "Question", "name": "Has PTD-DBM been tested in people?", "acceptedAnswer": { "@type": "Answer", "text": "PTD-DBM has not been tested in people in any published study. Every result is from cultured cells or from mice, and a search of ClinicalTrials.gov on 20 October 2026 found no registered trial of PTD-DBM, of CXXC5 or of the related small molecules KY19382 and KY19334. Two human observations exist without any treatment: CXXC5 protein was lower in acute surgical wounds in five melanoma patients (PMID: 26056233), and CXXC5 was raised in miniaturized follicles and arrector pili muscles in balding human scalp (PMID: 28595998). The commentary published with the 2017 paper raised testing the peptide in human scalp as an open question (PMID: 28967390)." } }, { "@type": "Question", "name": "What did the hair studies on PTD-DBM actually measure?", "acceptedAnswer": { "@type": "Answer", "text": "The hair work on PTD-DBM is mouse work plus human cell work. In human hair follicle dermal papilla cells, CXXC5 suppressed alkaline phosphatase activity and proliferation through Dishevelled-1; in mice, deleting Cxxc5 sped up hair regrowth, and blocking the CXXC5-Dishevelled interaction with the competitor peptide accelerated hair regrowth and wound-induced hair follicle neogenesis (PMID: 28595998). The 2023 paper gives the application detail: the backs of 7-week-old C57BL/6N mice were depilated and treated topically with 300 microlitres of 10 millimolar PTD-DBM every other day, and regrown hair was weighed and measured (PMID: 36831222). No measurement of hair count or hair density in human scalp has been published for PTD-DBM." } }, { "@type": "Question", "name": "How does PTD-DBM differ from minoxidil or finasteride?", "acceptedAnswer": { "@type": "Answer", "text": "PTD-DBM acts on a different step from either approved drug and has no approval of its own. Finasteride works on androgen metabolism and minoxidil was developed as a vasodilator, while PTD-DBM blocks a protein-protein interaction, CXXC5 with Dishevelled, to keep Wnt/beta-catenin signalling active (PMID: 26056233; PMID: 28595998). Two 2025 reviews group the Dishevelled-CXXC5 interaction with other Wnt targets as a direction beyond minoxidil and finasteride for androgenetic alopecia (PMID: 40924915; PMID: 40497955). The difference that matters is evidence: minoxidil and finasteride carry FDA approvals and human trials, and PTD-DBM has mouse data." } }, { "@type": "Question", "name": "What are the known risks of PTD-DBM?", "acceptedAnswer": { "@type": "Answer", "text": "PTD-DBM has no human safety data at all, so the risks discussed in the literature are mechanism-based. Wnt/beta-catenin signalling is involved in carcinogenesis as well as regeneration (PMID: 28967390), and the authors measured two oncogenic markers, c-Myc and cyclin D1, which the peptide did not raise in cells or mice (PMID: 26056233). Wnt/beta-catenin signalling also drives fibrosis, and in human dermal fibroblasts PTD-DBM raised collagen I and alpha-smooth muscle actin comparably to transforming growth factor beta (PMID: 26056233), which is why a later paper paired it with a patch aimed at reducing scarring (PMID: 36854308). Mice lacking CXXC5 also differ in bone density, growth plate and fat metabolism (PMID: 25633194; PMID: 30971423; PMID: 35384342)." } }, { "@type": "Question", "name": "Why do most PTD-DBM experiments add valproic acid?", "acceptedAnswer": { "@type": "Answer", "text": "PTD-DBM removes a brake on Wnt signalling rather than activating the pathway directly, so the group pairs it with an activator. Valproic acid inhibits glycogen synthase kinase 3 beta, and topical valproic acid plus topical PTD-DBM accelerated mouse wound closure more than either alone and raised beta-catenin, keratin 14 and collagen I together (PMID: 26056233); the same pairing increased hair regrowth and wound-induced hair neogenesis in the hair work (PMID: 28595998). The commentary on the 2017 hair paper notes that valproic acid also inhibits histone deacetylase, so some of the effect combined with PTD-DBM may be epigenetic rather than Wnt-specific (PMID: 28967390)." } } ] }, { "@context": "https://schema.org", "@type": "Organization", "@id": "https://www.bodyhackguide.co#organization", "name": "BodyHackGuide", "alternateName": "BHG", "url": "https://www.bodyhackguide.co", "logo": { "@type": "ImageObject", "url": "https://www.bodyhackguide.co/logo.png", "width": 512, "height": 512 }, "description": "Evidence-based research reference for peptides and nootropics. 273 compound profiles, interactive dosing calculators, vendor price comparisons, and trust-scored vendor reviews scored on a public, reproducible methodology applied to every vendor. 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