Nexagon (Gap Junction Peptide)
Overview
Nexagon is a synthetic peptide designed to transiently modulate gap junction intercellular communication by mimicking a segment of the connexin protein family. The mechanism involves temporary inhibition of connexin43-mediated channels during the early inflammatory phase of wound healing, which may reduce inflammatory cell infiltration and subsequent scar formation. This approach aims to shift the healing process toward regeneration rather than fibrosis.
Key Research Findings
Early clinical studies in venous leg ulcers demonstrated improved healing rates and reduced scar tissue formation. A phase II trial showed statistically significant reduction in scar size when applied topically to acute wounds, though larger confirmatory trials have not been widely published.
Topical
In Clinical Trials
Interested in Nexagon (Gap Junction Peptide)?
Find a verified provider experienced with Nexagon (Gap Junction Peptide) protocols in your area. All providers are credentialed and use compliant sourcing.
Find a Nexagon (Gap Junction Peptide) ProviderRelated Peptides
BPC-157
Research PhaseA synthetic gastric pentadecapeptide derived from a protein found in human gastric juice. BPC-157 promotes angiogenesis and the expression of growth factors including VEGF, EGF, and NO-mediated pathways. It has demonstrated cytoprotective and wound-healing properties across multiple tissue types in preclinical models, including tendon, muscle, ligament, and gastrointestinal mucosa.
TB-500 (Thymosin Beta-4)
In Clinical TrialsThymosin Beta-4 is a 43-amino acid actin-sequestering protein involved in cell migration, differentiation, and tissue repair. It promotes wound healing by upregulating cell-building proteins such as actin and laminin, facilitating cell migration to sites of injury. TB-500 also has anti-inflammatory properties mediated through NF-kB pathway modulation.
GHK-Cu
Research PhaseA naturally occurring copper-binding tripeptide (glycyl-L-histidyl-L-lysine) found in human plasma, saliva, and urine. GHK-Cu activates tissue remodeling by stimulating collagen synthesis, glycosaminoglycan production, and angiogenesis while suppressing fibrinogen synthesis. It modulates the activity of matrix metalloproteinases and influences over 4,000 genes related to tissue repair.
DSIP (Delta Sleep-Inducing Peptide)
Research PhaseA naturally occurring nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) originally isolated from cerebral venous blood of rabbits during induced sleep. DSIP modulates sleep architecture by promoting delta wave (slow-wave) sleep through interactions with the GABAergic system and hypothalamic sleep centers. It also exhibits stress-protective, analgesic, and neuromodulatory properties.