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Emerging Research

PTD-DBM

Skin, Hair & Beauty · ['PTD-Dishevelled Binding Motif peptide', 'CXXC5-Dvl disrupting peptide']

A synthetic cell-penetrating peptide investigated in preclinical models for its ability to disrupt the CXXC5-Dishevelled (Dvl) interaction and de-repress Wnt/beta-catenin signaling in hair-follicle and wound-healing research.

🔬 Research use only — not for human or veterinary use. K4 Elite does not provide dosing instructions.
Molecular Formula
C124H225N61O28S2
Molecular Weight
3082.6 g/mol
PubChem
CID 176453931 ↗
Research Level
Emerging Research
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PTD-DBM chemical structure

PTD-DBM is a laboratory research peptide engineered by fusing a protein transduction domain (PTD), which promotes cellular uptake, to a dishevelled binding motif (DBM). It was reported by the Choi laboratory at Yonsei University in work published in the Journal of Investigative Dermatology (2017) as a tool for studying the CXXC5-Dishevelled interaction in skin and hair-follicle biology.

The compound emerged from the 2015 identification of CXXC5 as a negative-feedback regulator of the Wnt/beta-catenin pathway. Because CXXC5 binds Dishevelled (Dvl) and suppresses downstream canonical Wnt activity, PTD-DBM was designed as a competitive peptide to occupy that binding interface in cell and animal studies.

Published work on PTD-DBM is preclinical, using cultured cells and mouse models. As of this writing there are no completed, peer-reviewed human efficacy trials. All information here is reported from published research and is provided for reference only.

In the canonical Wnt/beta-catenin pathway, Dishevelled (Dvl) is a scaffolding protein required for signal transduction. CXXC5 acts as a negative-feedback inhibitor by binding Dvl and dampening pathway output. PTD-DBM was designed to competitively disrupt the CXXC5-Dvl protein-protein interaction, thereby relieving the CXXC5-mediated brake on Wnt/beta-catenin signaling in the reported models.

The protein transduction domain component is intended to facilitate delivery of the disruptor motif across cell membranes. In mouse studies, disruption of this interaction was associated with increased Wnt pathway activity and reported effects on hair-follicle neogenesis and cutaneous wound repair.

  • Wnt/beta-catenin pathway modulation: Studies characterizing CXXC5 as a negative regulator of Wnt signaling and PTD-DBM as a disruptor of the CXXC5-Dvl interaction (Kim et al., J Invest Dermatol 2017; Lee et al., 2015).
  • Hair-follicle neogenesis: Mouse-model research reporting hair regrowth and follicle formation associated with the peptide, often examined alongside valproic acid as a Wnt activator.
  • Cutaneous wound healing: Preclinical investigation of the CXXC5-Dvl axis in skin repair and re-epithelialization.
  • Dermal papilla / keratinocyte cell biology: In vitro studies of Wnt-responsive markers in follicular and skin cell cultures.
  • CXXC5 target biology: Broader research into CXXC5 as a regulatory node relevant to bone, skin, and other Wnt-dependent tissues.
📋 How published studies were conducted — a research reference summarizing study designs from the literature. This is not usage, dosing, or administration guidance. K4 Elite does not provide dosing instructions; determining any research protocol is the sole responsibility of the qualified researcher.

Kim et al., Journal of Investigative Dermatology (2017): Reported that topical application of PTD-DBM, alone and in combination with valproic acid, was associated with increased hair follicle neogenesis in a mouse model, framed as evidence that disrupting the CXXC5-Dvl interaction can de-repress Wnt/beta-catenin signaling. Reported for reference only.

Lee et al. (2015), CXXC5 negative-feedback study: Identified CXXC5 as a Dishevelled-binding negative regulator of the Wnt pathway and provided the mechanistic rationale later used to design PTD-DBM. This foundational study used cell-based and biochemical assays.

Wound-healing model reports: Follow-up preclinical work examined the CXXC5-Dvl axis in murine cutaneous wound repair, describing changes in re-epithelialization and Wnt-target expression. These are animal-model observations and are not human recommendations.

Combinations examined in the research literature. Descriptive only — not a recommendation to combine compounds.

Valproic acidSynergistic
Studied together in mouse hair-neogenesis models as a Wnt/beta-catenin pathway activator; reported additive effects in preclinical work only.
Wnt pathway inhibitorsCaution
Compounds that suppress Wnt/beta-catenin signaling would be expected to oppose the peptide's proposed mechanism in research contexts.
GSK-3beta inhibitorsSynergistic
Both act to increase canonical Wnt output through different nodes; a theoretical convergence noted in pathway literature.
Other CXXC5-targeting tool compoundsNeutral
Share the same molecular target; comparative data are limited to preclinical research.

References are being compiled for this entry.

What is PTD-DBM designed to do in research?
It is a cell-penetrating peptide designed to disrupt the CXXC5-Dishevelled protein interaction, which in turn de-represses Wnt/beta-catenin signaling in cell and animal studies of hair follicles and skin.
Has PTD-DBM been tested in humans?
No completed, peer-reviewed human efficacy trials have been published. The available evidence is from cultured cells and mouse models.
What is the relationship between PTD-DBM and CXXC5?
CXXC5 is a negative-feedback regulator that binds Dishevelled and suppresses Wnt signaling. PTD-DBM was engineered to competitively interfere with that binding in research models.
Why is PTD-DBM studied alongside valproic acid?
In published mouse studies the two were combined because valproic acid activates Wnt/beta-catenin signaling, and researchers examined whether the combination affected follicle neogenesis.
Is PTD-DBM approved or intended for personal use?
No. PTD-DBM is a research-use-only compound. It is not approved by any regulatory agency for human or veterinary use, diagnosis, or treatment, and nothing here should be taken as medical guidance.
Disclaimer: This profile summarizes published preclinical and laboratory research for reference only. It is not medical advice and makes no claim of safety or efficacy in humans. Determining any research protocol is the sole responsibility of the qualified researcher. Products are sold strictly for in-vitro research and have not been evaluated by the FDA.