B7-33 vs Dermorphin
Comprehensive side-by-side comparison of mechanisms, dosing, side effects, and research
Also: B7-33 relaxin, Single-chain relaxin-2 analog
B7-33 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.
Also: Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2, Frog juice
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.
Key Comparison Insights
- Both peptides belong to the Healing category, suggesting similar primary applications.
Detailed Comparison
| Attribute | B7-33 | Dermorphin |
|---|---|---|
| Category | Healing | Healing |
| FDA Status | Not FDA Approved | Not FDA Approved |
| Clinical Status | Pre I II III IV FDA | Pre I II III IV FDA |
| Mechanism of Action | B7-33 activates RXFP1, the relaxin receptor, but in an unusual way. In cells that naturally carry RXFP1 (like fibroblasts), it preferentially switches on the pERK1/2 pathway rather than the cAMP pathway, which made it the first described functionally selective (biased) RXFP1 agonist. Its anti-fibrotic action runs through RXFP1 paired with the angiotensin II type 2 receptor, increasing MMP-2, an enzyme that breaks down collagen. In other words, it pushes scar tissue to be broken down rather than built up. Two practical caveats: it binds RXFP1 poorly in standard engineered cell lines, so its potency depends heavily on the cell type, and it is short-lived in serum (roughly 6 minutes in lab tests), which is why researchers have tried fatty-acid versions to stretch its half-life. | 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. |
| Common Dosing | No established human dose Once to twice daily in mouse studies | No safe human dose established Not established |
| Administration | Intraperitoneal or subcutaneous injection (including osmotic minipumps) in rodents | Intravenous infusion (human study); intravenous or intramuscular (horse study) |
| Typical Duration | 1-2 weeks in most rodent studies | Single administrations in research settings |
| Best Time to Take | No evidence-based timing | Not applicable |
Possible Side Effects May vary by individual |
|
|
| Research Summary | The founding paper (Hossain et al., Chemical Science, 2016) reported that B7-33 prevented or reversed organ fibrosis and dysfunction in three rodent models of heart or lung disease with potency similar to full relaxin-2, and, unlike native relaxin, it did not promote prostate tumor growth in mice. That last point matters because relaxin has been linked to tumor growth. Later mouse work extended the findings: Devarakonda et al. (Journal of the American Heart Association, 2020) gave 0.25 mg/kg twice daily by injection after a heart attack and found smaller infarcts, better heart function, and less fibrosis at 7 days. A 2023 follow-up from the original group confirmed that B7-33 cannot be shortened further without losing receptor binding. Important context: the full hormone (serelaxin) went all the way to a large phase 3 trial in acute heart failure (RELAX-AHF-2) and failed both primary endpoints, a reminder that strong animal anti-fibrotic data in this family have not translated easily to people. For B7-33 itself there are no human studies, no human pharmacokinetics, and no human safety data. | 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. |
Frequently Asked Questions: B7-33 vs Dermorphin
What is the difference between B7-33 and Dermorphin?
B7-33 is a healing peptide that b7-33 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. Dermorphin is a healing peptide that 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. The main differences lie in their mechanisms of action and clinical applications.
Which is better, B7-33 or Dermorphin?
Neither is universally "better" - the choice depends on your specific goals. B7-33 is typically used for healing purposes, while Dermorphin is used for healing. Always consult with a healthcare provider to determine which may be appropriate for your situation.
Can B7-33 and Dermorphin be used together?
Some peptide protocols combine multiple compounds for synergistic effects. However, using B7-33 and Dermorphin together should only be considered under medical supervision, as both compounds have their own side effect profiles and potential interactions. Research on their combined use may be limited.