/DISCLAIMER · RESEARCH_COMPOUND

This page is reference information only. Most compounds described here are research chemicals, not FDA-approved medications. MyTRT does not sell, recommend, or endorse the use of these substances. Always consult a qualified physician.

/DERMORPHIN

Peptide

Dermorphin

Heptapeptide μ-Opioid Receptor Agonist

/HALF_LIFE

Short and context-dependent; rapid plasma degradation typical of peptides (minutes to low hours in preclinical models). Central effects may outlast plasma exposure.

/DELIVERY

Primarily central routes in animal research (e.g., intrathecal, intracerebroventricular). Peripheral or intranasal routes have limited CNS penetration due to peptide nature; carrier systems or analogs are often explored in preclinical work.

/WHAT_IT_IS

Dermorphin is a natural heptapeptide (H-Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2) originally isolated from Phyllomedusa frog skin secretions. It is a highly potent and μ-opioid–selective agonist, used in research to probe nociception, analgesia, and opioid receptor signaling bias.

/USAGE

Employed in pain and neuropharmacology research to study μ-receptor activation, G-protein/β-arrestin signaling, antinociception, tolerance development, and receptor selectivity versus δ/κ pathways.

/MECHANISM_OF_ACTION

Binds μ-opioid receptors (MOR) with high affinity; activates Gi/o proteins to inhibit adenylyl cyclase, reduce cAMP, open GIRK channels, and inhibit voltage-gated Ca2+ channels—dampening neurotransmitter release in pain pathways.

Reported Benefits

+Robust antinociceptive effects in animal models
+High μ-receptor selectivity versus other opioid receptors
+Tool compound for biased-agonism and tolerance studies

Reported Side Effects

−Respiratory depression
−Sedation, dizziness, nausea
−Pruritus and constipation
−Bradycardia or hypotension (dose/context-dependent)
−Tolerance, dependence, and withdrawal with repeated exposure
−Risk of misuse/abuse; clinical use is generally not approved

/STACKED_WITH

Naloxone/naltrexone (antagonist controls in receptor-specific studies)Peripherally restricted antagonists (to parse central vs peripheral effects)Biased-agonist comparators (e.g., TRV130/oliceridine) for MOR signaling studies

/RESEARCH_NOTES

Extremely potent MOR agonist—use conservative dosing paradigms in controlled laboratory settings with respiratory monitoring. Not approved for human therapeutic use. Consider protease stability, blood–brain barrier limitations, and include antagonist controls to confirm on-target effects.

/TRACK_THIS

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