Dermorphin (“derm” = skin, and “morphin” = morphine) is just one compound in a family of peptides secreted by the skin of South American hylid frogs, genus Phyllomedusa.

       Most commonly found as a synthesized series of amino acids.

       Dermorphin is a hepta‐peptide known to have exceptionally long‐lasting and potent opioid activity.

       Potency is about 30–40 times greater than that of morphine, and less likely to cause a drug tolerance effect and addiction in humans.

       In humans it has been shown to block pain effectively.

       First detected in post‐race testing in Quarter Horse racing in the southwestern United States in 30 horses in 2011–2012.

       Dermorphin stimulates locomotor activity and purportedly improves focus and determination in equines.

       The D‐isomer is biologically active, but the L‐isomer is not.

       Prohibited under ARCI and AQHA rules.

       Dermorphin is a mu‐opioid receptor‐binding peptide that causes central and peripheral effects after intravenous administration to rats, dogs, and humans.

       In addition to dermorphin, the family of mu‐opioid agonists include seven naturally occurring dermorphin analogs, and at least 30 known synthetic analogs. The inactive L‐isomer of dermorphin is also known as “pseudomorphin”. Another close relative is HYP6‐dermorphin, which contains hydroxyproline instead of proline in the otherwise same amino acid sequence.

       Some members of the dermorphin peptide family can cross the blood–brain barrier (BBB) and produce central antinociception after peripheral administration, but dermorphin itself is not able to cross the BBB.

       Onset of action is rapid with clinical signs appearing in minutes.

       Duration of action is short, with most clinical signs subsiding within hours.

       Hepatic and renal metabolism was observed in rats.

       Urinary excretion primarily.

       Toxicity observed in horses in doses of 5 mg.

       Compounded versions may have variable toxicity.

       Dermorphin is unstable at room temp, with some studies showing > 50% degradation after 4 hours at room temperature which may contribute to toxicity. The L‐isomer (inactive stereoisomer) is more labile than the D‐isomer (active form).

       Neurological – head shaking, sedation, sweating, increased locomotion, catalepsy.

       Gastrointestinal – colic, decreased borborygmi.

       Cardiovascular – tachypnea.

       Musculoskeletal – antinociception.

       Iatrogenic.

       Owners and trainers may be reluctant to admit possession or use.

       Likely in competitive equine sports environment (e.g., racing, barrel racing, etc.).

       Clinical signs begin less than a minute after administration.

       Common signs include head shaking, sedation, sweating, trance‐like state, colic, tachypnea, and antinociception.

       CNS depressants (benzodiazepine, opioids).

       Hallucinogenic plants and mushrooms.

       Ethanol.

       Rabies.

       Colic of other etiology.

       Routine bloodwork:Hyponatremia/hypokalemia reported in humans but may be attributable to other causes.