Dermorphin
Also known as: Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2, Frog juice, Frog opioid peptide
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Key Facts: Dermorphin
- Category
- Healing
- FDA Status
- Not FDA Approved
- Clinical Status
- Not approved by the FDA, EMA, or any regulator for human or veterinary use. Classified as a Class 1 prohibited substance in US horse racing (Association of Racing Commissioners International). Not on the 2026 WADA Prohibited List; WADA tracks dermorphin and its analogues in its 2026 Monitoring Program (in-competition). We could not confirm a US federal controlled-substance scheduling decision; check local law before assuming it is legal to possess.
- Banned in Sport (WADA)
- Not named on the WADA Prohibited List. WADA tracked it in its 2026 Monitoring Program. As a substance with no human therapeutic approval it may still fall under the S0 catch-all, so check with your anti-doping agency.
- Administration
- Intravenous infusion (human study); intravenous or intramuscular (horse study)
- Typical Dose
- No safe human dose established
- Frequency
- Not established
- Duration
- Single administrations in research settings
How does Dermorphin work?
Dermorphin binds the mu-opioid receptor with very high affinity and selectivity. In rat brain binding work it had a Ki of 0.7 nM at mu receptors versus 62 nM at delta and over 5,000 nM at kappa receptors, a selectivity on par with the reference lab mu-agonist DAMGO. It is unusual for a natural peptide because its second amino acid is a D-alanine, which protects it from the enzymes that normally chew up opioid peptides within seconds. Mu activation blocks pain signaling in the spinal cord and brain, and it also drives the classic opioid problems: euphoria, sedation, slowed breathing, constipation, tolerance and dependence. There is no special 'safe' mechanism here. Claims that it is less addictive than morphine are mostly marketing and horse-racing talk, not proven in people.
What does the research show?
Most of the science is animal pharmacology and drug-testing chemistry. A 1990 rat-brain study confirmed dermorphin as a near-specific mu 'super-agonist' and found that, injected into the brains of mice, it was up to 670 times more potent than morphine as a painkiller, with higher doses causing catalepsy. The human data are tiny: a 1986 Brain Research study gave an intravenous infusion of 0.16 mg/kg to healthy volunteers and found a marked, long-lasting rise in the threshold of a spinal pain reflex; naloxone only reversed about half the effect. No modern clinical trials exist. In horses, a 2015 pharmacokinetic study (about 9 mcg/kg IV or IM) found an elimination half-life under an hour, excitation with a raised heart rate after IV dosing, and detection in urine for 48 to 72 hours. The doping story is the reason most people have heard of it: around 30 positive tests turned up in Southern US racing in 2012, including 11 horses tied to nine trainers in Louisiana, which led to suspensions of up to 10 years, and racing labs in Australia, the US and Hong Kong have since built sensitive tests for dermorphin and its synthetic analogs. A 2017 federal indictment charged a Louisiana veterinarian with supplying it to trainers.
What doses have been studied?
Note: Animal study doses may not translate directly to humans.
Typical Dosingⓘ
Community experience
No safe human dose established
Not established (one 1986 lab study used 0.16 mg/kg IV under supervision)
Not established
Dermorphin is a potent mu-opioid. The only human exposure in the literature was a single supervised IV infusion in a research lab. Self-dosing an unregulated opioid of uncertain purity carries real overdose risk, and naloxone may not fully reverse it.
Research Dosingⓘ
Scientific studies
Doses from research studies only. There is no safe or recommended human dose.
Doses from Studies
Duration
Single administrations in research settings
Administration
Intravenous infusion (human study); intravenous or intramuscular (horse study)
When and how is Dermorphin taken?
Best Time to Take
Not applicable
No established frequency; repeated use would be expected to cause tolerance and dependence
Food Recommendation
With or without food
Why This Timing?
There is no therapeutic use or validated human regimen. Its only human data come from a single supervised laboratory infusion.
What are the side effects of Dermorphin?
Not everyone experiences these effects. Individual responses vary based on dosage, duration, and personal factors.
- ●Respiratory depression (the main way opioids kill people)
- ●Sedation, catalepsy at higher doses in animals
- ●Tolerance and physical dependence expected with repeated use
- ●Withdrawal symptoms after stopping
- ●Nausea, vomiting and constipation (typical mu-opioid effects)
- ●Excitation and raised heart rate after IV dosing in horses
- ●Dangerous with alcohol, benzodiazepines or other opioids
- ●Naloxone only partly reversed its effect in the one human study
- ●Unknown purity and dose accuracy in research-grade product
- ●No long-term human safety data
References
- https://pubmed.ncbi.nlm.nih.gov/2161761/
- https://pubmed.ncbi.nlm.nih.gov/3697765/
- https://pubmed.ncbi.nlm.nih.gov/25376170/
- https://pubmed.ncbi.nlm.nih.gov/24320126/
- https://pubmed.ncbi.nlm.nih.gov/32805775/
- https://pmc.ncbi.nlm.nih.gov/articles/PMC9582840/
- https://thehorse.com/?p=17627
- https://www.dvm360.com/view/veterinarian-charged-with-plot-drug-horses-races
- https://www.tennisireland.ie/wp-content/uploads/2025/11/2026-Monitoring-Programme.pdf
Research This Peptide Further
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Frequently Asked Questions
What does Dermorphin do?
Dermorphin is a seven-amino-acid opioid peptide (Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2) first found in the skin of South American Phyllomedusa frogs. It is a strong, highly selective mu-opioid agonist, the same receptor morphine and fentanyl hit, and in mouse brain-injection studies it was hundreds of times more potent than morphine. It is not approved anywhere for human use. Its main claim to fame is doping: it was caught in dozens of American racehorses in 2012, where it was nicknamed 'frog juice'. This is an opioid, and it should be treated like one.
How does Dermorphin work?
Dermorphin binds the mu-opioid receptor with very high affinity and selectivity. In rat brain binding work it had a Ki of 0.7 nM at mu receptors versus 62 nM at delta and over 5,000 nM at kappa receptors, a selectivity on par with the reference lab mu-agonist DAMGO. It is unusual for a natural peptide because its second amino acid is a D-alanine, which protects it from the enzymes that normally chew up opioid peptides within seconds. Mu activation blocks pain signaling in the spinal cord and brain, and it also drives the classic opioid problems: euphoria, sedation, slowed breathing, constipation, tolerance and dependence. There is no special 'safe' mechanism here. Claims that it is less addictive than morphine are mostly marketing and horse-racing talk, not proven in people.
Is Dermorphin FDA approved?
No, Dermorphin is not currently FDA approved. Current status: Not approved by the FDA, EMA, or any regulator for human or veterinary use. Classified as a Class 1 prohibited substance in US horse racing (Association of Racing Commissioners International). Not on the 2026 WADA Prohibited List; WADA tracks dermorphin and its analogues in its 2026 Monitoring Program (in-competition). We could not confirm a US federal controlled-substance scheduling decision; check local law before assuming it is legal to possess.
Is Dermorphin banned in sport?
Not named on the WADA Prohibited List. WADA tracked it in its 2026 Monitoring Program. As a substance with no human therapeutic approval it may still fall under the S0 catch-all, so check with your anti-doping agency.
What are the side effects of Dermorphin?
Reported side effects include: Respiratory depression (the main way opioids kill people), Sedation, catalepsy at higher doses in animals, Tolerance and physical dependence expected with repeated use, Withdrawal symptoms after stopping, Nausea, vomiting and constipation (typical mu-opioid effects). Individual responses vary based on dosage, duration, and personal health factors.
What is the typical dose of Dermorphin?
Community-reported common dose: No safe human dose established (Not established). Range: Not established (one 1986 lab study used 0.16 mg/kg IV under supervision). Administration: Intravenous infusion (human study); intravenous or intramuscular (horse study). Community-reported doses. Not medical advice. Consult healthcare provider.
Related Peptides
Peptides commonly compared with Dermorphin or used in similar applications.
Pentadecapeptide
PreclinicalPentadecapeptide almost always means BPC-157, a synthetic 15-amino-acid chain (Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val) derived from a protein found in human gastric juice. It is one of the most hyped 'healing' peptides online, marketed for tendon, gut, and muscle repair, but here is the catch: essentially all of the supporting evidence is from rats and mice. There is no FDA approval and no completed human clinical trial proving it does any of this.
HealingZiconotide
FDAZiconotide is a real, FDA-approved painkiller pulled from the venom of a marine cone snail. It is not an opioid, and unlike morphine, people do not build tolerance to it over time. The catch: it only works delivered directly into the spinal fluid through an implanted pump, and its side effect profile is rough enough that it carries a black box warning.
HealingBPC-157
PreclinicalBPC-157 is a synthetic 15-amino-acid peptide (sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val) based on a fragment of a protective protein found in human gastric juice. It is studied almost entirely in animals for tendon, ligament, gut, and tissue healing, and it has racked up hundreds of preclinical papers. The catch: it is not approved by any regulator for any use, and the human evidence is a handful of small pilot studies, not real clinical proof.
HealingTB-500
PreclinicalTB-500 is a synthetic peptide that copies the active region of thymosin beta-4, a natural protein that controls how cells build and move their internal skeleton. Most TB-500 products reproduce the short LKKTETQ sequence (residues 17 to 23) responsible for binding actin and driving cell migration, which is why it gets marketed for tendon, muscle, and wound repair. Here is the honest part: there are essentially no completed human trials of the TB-500 fragment itself, and almost all the human clinical data is for the full-length thymosin beta-4 molecule, which is related but not the same thing.
HealingThymosin Beta-4
Clinical TrialsThymosin beta-4 (Tbeta4) is a small 43 amino acid peptide found in nearly every cell in the body, originally isolated from the thymus. Its main job is binding and sequestering G-actin, the building block of the cell's internal scaffolding, which lets it influence cell movement, wound repair, and tissue regeneration. It is researched heavily for healing of skin, cornea, and heart tissue, but it is not an FDA-approved drug. (The injectable sold as TB-500 is a synthetic fragment marketed as related to Tbeta4, not the full natural peptide.)
HealingB7-33
PreclinicalB7-33 is a 27-amino-acid, single-chain peptide cut down from the B-chain of human relaxin-2, the hormone that loosens tissue during pregnancy. Relaxin itself has strong anti-scarring effects but is a complex two-chain molecule that is hard and expensive to make, so an Australian group (Hossain and colleagues, 2016) designed B7-33 as a simpler version. In rodent models it reduced heart and lung fibrosis about as well as full relaxin. It has never been tested in humans.
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