B7-33
single-chain relaxin analog, H2 relaxin B-chain derivative
REC PPT-B7-33 // REV 2026-10-04 // assessment changes are logged, never silent
A single-chain derivative of human relaxin-2 with anti-fibrotic effects reported in rodent organs; the entire literature is about a dozen papers and none of them involves a human subject.
What it is
A linear peptide built from the B-chain of human gene-2 relaxin, reported by Hossain and colleagues in Chemical Science in 2016. It is a functionally selective agonist at the relaxin receptor RXFP1, preferentially driving the pERK pathway over cAMP.
What it does
Studied in rodents for organ fibrosis in heart, kidney and lung, for endothelium-dependent vascular responses in isolated rat arteries, for adverse cardiac remodelling after experimental myocardial infarction in mice, and as an implant coating intended to reduce fibrotic encapsulation.
Does it work?
This is one of the thinnest evidence bases on the site: Europe PMC returns 10 records for the search term used here and 12 that name B7-33 in a title or abstract, and ClinicalTrials.gov holds no registered study. The originating 2016 paper reported reversal of fibrosis in three rodent models and, relevantly for a growth-factor-adjacent peptide, no promotion of prostate tumour growth in the animals tested. Later rodent work extended the observations to post-infarction remodelling in mice and to device coatings. The cautionary context is that serelaxin, the recombinant full-length relaxin that B7-33 was designed to imitate, was tested in 6545 patients with acute heart failure in the RELAX-AHF-2 trial and missed both of its primary endpoints, so the human translation of relaxin biology has already been attempted at scale and did not succeed.
Claims vs data
Each marketing claim, tagged by what the evidence actually supports.
| Activates the relaxin receptor RXFP1 with bias toward the pERK pathway | preclinical only |
| Reduces fibrosis in rodent heart, kidney and lung models | animal data only |
| Reproduces vascular effects of serelaxin in isolated rat vessels | animal data only |
| An anti-fibrotic treatment for human heart, kidney or lung disease | overreach |
Reference figures
Quoted from published reference material. These are not Peptuity recommendations.
The evidence, counted
Live counts from Europe PMC and ClinicalTrials.gov.
85 publications indexed, 0 registered interventional studies, no randomised controlled trials indexed. Evidence is minimal.
SRC // EUROPE PMC + CTGOV // "B7-33" // FETCHED 2026-10-04 // 85 RECORDS
Most-cited literature
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[01]
THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein-coupled receptors
Alexander SPH, Christopoulos A, Davenport AP, Kelly E, Mathie A, Peter · Br J Pharmacol 2019 · 525 citations · DOI 10.1111/bph.14748
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[02]
T-cell antigen CD28 mediates adhesion with B cells by interacting with activation antigen B7/BB-1
Linsley PS, Clark EA, Ledbetter JA. · Proc Natl Acad Sci U S A 1990 · 519 citations · DOI 10.1073/pnas.87.13.5031
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[03]
The Concise Guide to PHARMACOLOGY 2023/24: G protein-coupled receptors
Alexander SPH, Christopoulos A, Davenport AP, Kelly E, Mathie AA, Pete · Br J Pharmacol 2023 · 332 citations · DOI 10.1111/bph.16177
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[04]
G-Protein-Coupled Receptors in Heart Disease
Wang J, Gareri C, Rockman HA. · Circ Res 2018 · 236 citations · DOI 10.1161/circresaha.118.311403
Regulatory status
Formal, dated regulatory actions.
WADA — Prohibited List 2026
Prohibited in sport — WADA S0 (substance without any health-authority approval)
Common questions
How much research exists on B7-33?
Very little. Europe PMC returns 10 records for the term as measured for this entry, and only 12 papers name it in a title or abstract at all. For comparison, that is a literature small enough to read in a single afternoon, and every item in it is a cell or animal experiment.
Why does relaxin biology matter here?
Relaxin is a natural human hormone with vasodilatory and anti-fibrotic activity, and B7-33 was designed as a smaller, more synthesisable stand-in for it. That inheritance cuts both ways: the biology is real, and the full-length version already failed a large human outcome trial in acute heart failure.
Does the fibrosis result in animals mean it would work in people?
That inference is not available from this evidence. Rodent fibrosis models are short, induced and reversible in ways human chronic organ disease is not, and no bridging human pharmacology, dose-finding or safety study has been published for B7-33.
Is B7-33 approved or regulated?
It is not approved by the FDA, the Saudi FDA or any other regulator for any indication, and it is not a licensed medicine anywhere. Having no human therapeutic approval anywhere, it falls inside the WADA S0 category of non-approved substances.
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