B7-33
Also known as: B7-33 relaxin, Single-chain relaxin-2 analog, H2 relaxin B-chain 7-33, Relaxin B-chain peptide
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B7-33
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Key Facts: B7-33
- Category
- Healing
- FDA Status
- Not FDA Approved
- Clinical Status
- Preclinical - No FDA approval and no registered human trials. The parent hormone's drug version (serelaxin) failed phase 3 in acute heart failure and was not approved. WADA: not named on the 2026 Prohibited List; as a substance with no regulatory approval for human use it falls under S0 (Non-Approved Substances), prohibited at all times.
- Banned in Sport (WADA)
- Not named on the WADA list, but WADA's S0 catch-all bans any substance without human therapeutic approval, which covers it. Prohibited at all times.
- Administration
- Intraperitoneal or subcutaneous injection (including osmotic minipumps) in rodents
- Typical Dose
- No established human dose
- Frequency
- Once to twice daily in mouse studies
- Duration
- 1-2 weeks in most rodent studies
How does B7-33 work?
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.
What does the research show?
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.
What doses have been studied?
Note: Animal study doses may not translate directly to humans.
Typical Dosingⓘ
Community experience
No established human dose
Not established (mouse studies used 0.25 mg/kg per dose)
Once to twice daily in mouse studies
There is no published human dosing, pharmacokinetic, or safety data for B7-33. The very short serum half-life seen in lab testing means once-daily dosing may not keep levels up, which is why the mouse studies used twice-daily injections or continuous pumps. Any human dose discussed online is a guess.
Research Dosingⓘ
Scientific studies
Doses observed in rodent research. No human dose has been studied.
Doses from Studies
0.25 mg/kg IP twice daily for 7 days
Preclinical Research - Devarakonda et al., J Am Heart Assoc 2020 (mouse myocardial infarction) ↗
Rodent fibrosis models (heart and lung)
Preclinical Research - Hossain et al., Chem Sci 2016 (original B7-33 paper) ↗
Duration
1-2 weeks in most rodent studies
Administration
Intraperitoneal or subcutaneous injection (including osmotic minipumps) in rodents
When and how is B7-33 taken?
Best Time to Take
No evidence-based timing
Twice daily or continuous in animal studies
Food Recommendation
With or without food
Why This Timing?
Mouse studies used twice-daily injections or continuous infusion because the peptide clears quickly. No human timing data exist.
What are the side effects of B7-33?
Not everyone experiences these effects. Individual responses vary based on dosage, duration, and personal factors.
- ●No human safety data of any kind
- ●Very short half-life in serum (about 6 minutes in vitro)
- ●Relaxin-family signaling relaxes connective tissue; long-term effects on joints and ligaments unknown
- ●Theoretical cancer concern from the relaxin family (B7-33 did not promote prostate tumors in mice, but this is not tested in humans)
- ●Injection site reactions possible
- ●Product purity unknown outside of research labs
References
- https://pubmed.ncbi.nlm.nih.gov/30155023/
- https://pubs.rsc.org/en/content/articlehtml/2016/sc/c5sc04754d
- https://pmc.ncbi.nlm.nih.gov/articles/PMC7428518
- https://pmc.ncbi.nlm.nih.gov/articles/PMC10454739/
- https://www.acc.org/latest-in-cardiology/clinical-trials/2017/05/07/16/09/relax-ahf-2
Research This Peptide Further
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B7-33
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Frequently Asked Questions
What does B7-33 do?
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.
How does B7-33 work?
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.
Is B7-33 FDA approved?
No, B7-33 is not currently FDA approved. Current status: Preclinical - No FDA approval and no registered human trials. The parent hormone's drug version (serelaxin) failed phase 3 in acute heart failure and was not approved. WADA: not named on the 2026 Prohibited List; as a substance with no regulatory approval for human use it falls under S0 (Non-Approved Substances), prohibited at all times.
Is B7-33 banned in sport?
Not named on the WADA list, but WADA's S0 catch-all bans any substance without human therapeutic approval, which covers it. Prohibited at all times.
What are the side effects of B7-33?
Reported side effects include: No human safety data of any kind, Very short half-life in serum (about 6 minutes in vitro), Relaxin-family signaling relaxes connective tissue; long-term effects on joints and ligaments unknown, Theoretical cancer concern from the relaxin family (B7-33 did not promote prostate tumors in mice, but this is not tested in humans), Injection site reactions possible. Individual responses vary based on dosage, duration, and personal health factors.
What is the typical dose of B7-33?
Community-reported common dose: No established human dose (Once to twice daily in mouse studies). Range: Not established (mouse studies used 0.25 mg/kg per dose). Administration: Intraperitoneal or subcutaneous injection (including osmotic minipumps) in rodents. Community-reported doses. Not medical advice. Consult healthcare provider.
Related Peptides
Peptides commonly compared with B7-33 or used in similar applications.
TB-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.)
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.
HealingPentadecapeptide
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.
HealingDermorphin
PreclinicalDermorphin 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.
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