hBD-3
The salt-tolerant, broad-spectrum defensin that kills resistant staphylococci and may help wounds heal
Human beta-defensin 3 was found in 2001 while looking for the skin's own defences against Staphylococcus aureus. It kills a broad range of microbes, including multi-resistant strains, even at salt levels that disable other defensins, and in mouse and cell studies it promoted wound healing. It is not a medicine.
What is it?
hBD-3 came out of a search for the body's own weapons against Staphylococcus aureus. In 2001 researchers isolated a 5-kDa peptide from psoriatic scales and cloned it from keratinocytes. It killed many potential pathogens, including multi-resistant Staphylococcus, did not damage red blood cells, and kept working at salt concentrations that switch off most other defensins.
Its second role is in repair. Keratinocytes make more hBD-3 when skin is wounded, and platelet-released growth factors, the active ingredients of platelet-rich fibrin dressings, increased its production in human skin cells and in experimental human skin wounds. In mice, hBD-3 sped wound healing by drawing in immune cells and building new blood vessels, and in human fibroblasts it raised growth factors through the FGFR1/JAK2/STAT3 pathway.
hBD-3 also signals to immune cells: with hBD-2 it attracts monocytes and macrophages through the chemokine receptor CCR2. In people, a 2026 proteomics study found its circulating form among the best markers separating patients with psoriasis from healthy volunteers.
None of this has produced a treatment. hBD-3 has not been tested in people as a medicine and has no human dose; research-grade material sold online is untested for human use.
At a Glance
Every value in this table is printed from the Grey Peptides dataset, the same record the compound explorer and comparison tool read, so the three can never disagree.
Published Research
These studies were read from their PubMed abstracts on October 5, 2026.
Discovery: a skin peptide against S. aureus
A novel 5-kDa, non-haemolytic peptide isolated from psoriatic scales and cloned from keratinocytes showed salt-insensitive, broad-spectrum activity against many pathogens, including multi-resistant Staphylococcus aureus.
Faster wound healing in mice
hBD-3-treated mouse wounds healed faster, with more neutrophils, macrophages and new vessels; in human fibroblasts it raised FGF, PDGF and VEGF secretion and migration through FGFR1/JAK2/STAT3 signalling.
Induced by platelet growth factors
Platelet-released growth factors increased hBD-3 expression in primary human keratinocytes, and a clinical platelet-rich fibrin product increased it in artificially created human skin wounds.
A circulating psoriasis marker
In serum from 40 patients with psoriasis and 40 healthy volunteers, targeted proteomics found DEFB103 (hBD-3) among the proteins that best distinguished patients from controls, a candidate biomarker.
Signalling through CCR2
hBD-2 and hBD-3 bound the chemokine receptor CCR2 and drew human monocytes and other CCR2-bearing cells in a dose-dependent way, a route of immune signalling beyond CCR6.
Side Effects & Contraindications
Reported Side Effects
Not applicable.
Contraindications & Cautions
Not a medicine, so there is no label and no formal contraindication.
Legal Status
An endogenous peptide, not a medicine.
Frequently Asked Questions
?What makes hBD-3 different from other defensins?
It kills a broad range of microbes, including resistant Staphylococcus aureus, and keeps working at salt levels that disable most defensins.
?Does hBD-3 help wounds heal?
In mice and human cells it promoted healing and new blood vessels; it has not been tested as a wound treatment in people.
?Can you buy hBD-3 as a treatment?
No approved product exists; research-grade material is untested for human use.
References
- [pubmed] Harder J, et al. "Isolation and characterization of human beta -defensin-3, a novel human inducible peptide antibiotic." J Biol Chem, 2001;276(8):5707-13. PMID: 11085990.
- [pubmed] Takahashi M, et al. "The Antimicrobial Peptide Human β-Defensin-3 Accelerates Wound Healing by Promoting Angiogenesis, Cell Migration, and Proliferation Through the FGFR/JAK2/STAT3 Signaling Pathway." Front Immunol, 2021;12:712781. PMID: 34594328.
- [pubmed] Bayer A, et al. "The Antimicrobial Peptide Human Beta-Defensin-3 Is Induced by Platelet-Released Growth Factors in Primary Keratinocytes." Mediators Inflamm, 2017;2017:6157491. PMID: 28811680.
- [pubmed] Dźwigała M, et al. "APOA1, DEFB103A_DEFB103B and DSG3 Are Novel Circulating Biomarkers of Psoriasis." Int J Mol Sci, 2026;27(13). PMID: 42450078.
- [pubmed] Röhrl J, et al. "Human beta-defensin 2 and 3 and their mouse orthologs induce chemotaxis through interaction with CCR2." J Immunol, 2010;184(12):6688-94. PMID: 20483750.
Sources & Citations
Studies from their PubMed abstracts, read October 5, 2026. An earlier citation in our dataset turned out to be the human beta-defensin 4 discovery paper, a different peptide, and has been removed.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Consult a licensed healthcare provider before making health decisions.