Category · 12 entries
Immune & Anti-Inflammatory
Thymic, inflammatory, and immune-modulating peptides.
hBD-1
The constitutive epithelial β-defensin — first isolated from haemodialysate urine by Bensch, Schröder and colleagues (FEBS Letters 1995). Constitutively expressed (unlike hBD-2 and hBD-3, which are inducible), salt-sensitive in standard assays, and a major component of urogenital and airway surface antimicrobial defense.
hBD-2
The inducible β-defensin — cloned by Harder, Bartels, Christophers and Schröder (Nature 1997) from the lesional scales of psoriasis patients, with the paper framing psoriatic skin as a paradoxical "almost-never-infected" phenotype driven by massive β-defensin induction. Induced by TLR / NF-κB signalling in response to bacterial lipopolysaccharide and pro-inflammatory cytokines (IL-1, TNF-α).
hBD-3
The broad-spectrum β-defensin — active against Gram-positive, Gram-negative and fungal targets, and largely salt-insensitive (unlike hBD-1). Isolated independently in 2001 by Harder et al. and by García et al. from psoriatic skin and tonsil respectively. The β-defensin most studied for clinical translation because of its salt tolerance.
HD5
The Paneth cell α-defensin — the dominant antimicrobial peptide of the human small intestine, stored at millimolar concentrations in Paneth cell secretory granules and released into the crypt lumen upon cholinergic or bacterial stimulus. Reduced HD5 expression is a recognised feature of ileal Crohn disease.
HD6
The Paneth cell α-defensin that does not kill directly — HD6 traps enteric pathogens by self-assembling into fibrillar "nanonets" (Chu et al., Science 2012), a mechanism unique among the defensin family. Poor microbicidal activity in vitro was a decade-long puzzle until the trapping mechanism was discovered.
HNP-1
The prototype human α-defensin — isolated from neutrophil granules by Ganz, Selsted and Lehrer in 1985; the dominant antimicrobial peptide in human neutrophils and a workhorse molecule of innate immunity. Research peptide only: no defensin has ever been developed as an approved drug.
HNP-2
The N-terminally truncated HNP-1 variant — 29 residues instead of 30, same disulfide scaffold, the same biological activity profile. A direct proteolytic or post-translational derivative of the prodefensin encoded by DEFA1/DEFA3; isolated alongside HNP-1 and HNP-3 by Ganz et al. in 1985. Research peptide only — no clinical development.
HNP-3
The third of the three classical neutrophil α-defensins — identical to HNP-1 except the first residue (Asp vs. Ala). Encoded predominantly by DEFA3, a nearly-identical paralog of DEFA1 that arose from segmental duplication. Research peptide only.
Thymopentin
A synthetic pentapeptide fragment of thymopoietin — historically marketed as Timunox for immunodeficiency, now primarily used in research and limited European clinical practice.
Thymosin α1
The most clinically studied thymic peptide — approved in 35+ countries as Zadaxin for hepatitis B and C, with 30+ RCTs across more than 11,000 subjects. Not FDA-approved despite extensive global use.
Thymulin
A zinc-dependent thymic peptide — biologically active only when zinc-saturated, making serum thymulin activity a functional readout of zinc status.
VIP
An endogenous 28-amino-acid peptide with vasodilatory, bronchodilatory, and immunomodulatory effects; explored in sarcoidosis, CIRS/mold illness, and acute respiratory distress.