●Exceptional Potency: Dermorphin is significantly more potent than morphine. Studies estimate it to be 30-50 times more potent than morphine when administered intracerebroventricularly (directly into the brain ventricles) in rodent models. Even peripherally, it demonstrates high potency.
●D-Amino Acid Key: The D-Ala residue is non-negotiable for activity. Synthetic analogs with L-Ala are virtually inactive. This D-amino acid makes dermorphin highly resistant to degradation by common peptidases (enzymes that break down peptides) like aminopeptidases and chymotrypsin, contributing to its long duration of action compared to similar endogenous peptides.
●High Mu-Opioid Receptor Selectivity: While it can interact with delta and kappa receptors at higher concentrations, dermorphin exhibits a strong preference and high affinity for the mu-opioid receptor. This selectivity drives its potent analgesic and euphoric effects.
●Metabolic Stability: The D-Ala and the C-terminal amidation enhance its stability against enzymatic breakdown in the bloodstream and tissues compared to endogenous opioid peptides like enkephalins. This contributes to a longer half-life than many natural peptides.
●Blood-Brain Barrier (BBB) Penetration: Despite being a peptide, dermorphin demonstrates surprisingly effective penetration of the BBB, a rarity for peptides. This is partly attributed to its lipophilic (fat-soluble) characteristics and possibly active transport mechanisms, allowing it to reach its central nervous system targets effectively after systemic administration.
●Species-Specific Effects: Its profound effects are primarily observed in mammals. In its natural frog hosts, its function is speculated to involve defense (deterring predators) or skin protection, but its exact physiological role in amphibians isn't fully defined.
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