Tissue repair
B7-33
A synthetic single-chain peptide derived from the relaxin-2 B-chain that signals at RXFP1; evidence is cell and animal work only.
- How settled this rating is:
- low confidence in the current evidence rating
- Routes studied:
- Not established · Subcutaneous injection (marketed but never approved)
- Also known as:
- B7-33 relaxin mimetic, single-chain relaxin B-chain analogue
- Last reviewed:
- 2026-09-26
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Evidence passport
B7-33
A one-screen evidence identity for this compound. These fields describe research maturity, confidence and legal status. They are not a safety guarantee, efficacy percentage or recommendation.
- Evidence level
- L1Theory only
- Confidence
- Low confidence in rating
- Regulatory status
- Not approved for this use
- Development status
- Preclinical
Evidence strength
Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.
Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.
The 0-100 values rate the strength and maturity of evidence, not how effective or safe the compound is.
- Evidence base
- Mostly animal and laboratory research
- Furthest established stage
- Not established
- Human research maturity
- Preclinical (cell and rodent studies)
- Source curation
- Sources fully curated
Routes recorded
Most of this evidence comes from animals and cells
Overview
Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.
Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.
Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.
How to read these scores
Every number here rates the evidence, not the compound. They are editorial 0-100 strength ratings, not percentages, and not a rating out of five stars.
- Human efficacy evidence strength — Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.
- Preclinical evidence strength — Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.
- Human safety evidence strength — Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number. A score of 80 does not mean “80% safe”.
- Evidence level (L0-L5) — the strongest type of study behind the compound, from anecdote (L0) to large replicated human trials (L5). It is a description of the study evidence, not a quality, safety or recommendation rating.
- Confidence — how likely we think it is that this rating changes as new research lands. Low confidence means the picture is unsettled, not that the compound is bad.
None of these ratings is medical advice, a safety guarantee, or a recommendation to use anything. How we grade evidence.
How far human research has progressed: Preclinical (cell and rodent studies)
Routes & formulations
Marketed / research routes — never approved
Published studies used laboratory and animal administration. No human route has been studied, so marketed routes carry no evidence.
Route availability is not evidence of efficacy, and evidence from one route does not transfer to another. The Registry never provides dosing or sourcing information.
Peptide lifecycle
Discovery
Preclinical
Phase I
Phase II
Phase III
Approved
What it is
A minimised, single-chain derivative of the human relaxin-2 B-chain designed by academic groups in Melbourne. It is reported to act as a functionally selective RXFP1 agonist, preferentially activating ERK1/2 rather than the full signalling profile of native relaxin. It is not serelaxin (recombinant relaxin-2), which reached late-stage human trials.
What people claim
- Anti-fibrotic effects in heart, lung or kidney
- Tissue repair and recovery
What the evidence actually says
Credible academic preclinical literature exists, including rodent models of lung and cardiac fibrosis and post-infarction remodelling. No human trial of B7-33 was identified. Serelaxin's human trial record must not be transferred to B7-33 — they are different molecules with different signalling.
Related evidence
Useful next reads based on this compound — not recommendations.
- Related compound
KPV evidence profile
A three-amino-acid fragment of alpha-MSH marketed for gut healing and inflammation, with no human clinical studies identified by the FDA.
- Compare
Compare B7-33 vs KPV evidence
Same questions, same fields, side by side — including how much human evidence exists.
- Context
Muscle growth evidence
What the human evidence does and does not show for growth and recovery claims.
- Context
Research Desk
How to read animal, early-phase and controlled human studies without over-reading them.
Human evidence
- No human interventional study of B7-33 was identified in our curated record.
- Human trials of serelaxin (a different, full-length relaxin molecule) are not evidence for B7-33.
Preclinical evidence
- Original characterisation as a functionally selective RXFP1 agonist with anti-fibrotic activity in rodent models (Hossain et al., Chemical Science 2016).
- Mouse myocardial-infarction model: reported attenuation of adverse cardiac remodelling (Devarakonda et al., JAHA 2020).
- Experimental cardiomyopathy model: reported cardioprotective and anti-fibrotic effects compared with perindopril (PMID 36753958).
- A lipidated derivative was developed because the parent peptide has limited serum stability (Int J Mol Sci 2023) — an open pharmacokinetic limitation.
Animal and cell findings are Level 1–2 evidence.
Mechanism and pathways
- Binds RXFP1, the cognate receptor for relaxin-2, with biased (ERK1/2-preferring) signalling.
- Anti-fibrotic effects are attributed to reduced myofibroblast activity and collagen deposition in animal tissue.
Safety and unknowns
- No human safety data identified.
- Animal studies are not designed to establish human safety.
- Material sold online is unregulated: identity, purity, sterility and labelled quantity are separate questions from what the published molecule does.
Cancer relevance
This section covers questions raised by how the compound works in the body, plus anything regulators and trial teams keep an eye on. It is not a statement that this compound causes cancer — for most compounds here, no human data exist in either direction.
No established human signal
Regulatory status
Regulatory decisions apply to specific jurisdictions, products, formulations and indications. An approval elsewhere is not automatically an approval in your country.
Check the regulatory note and linked primary sources for jurisdiction-specific details.
Not an approved medicine in any major jurisdiction. Sale as a 'research chemical' is a legal and supply-chain statement, not evidence of benefit or harm.
Evidence grade
Mechanistic rationale or early development without qualifying compound-specific outcome evidence. A registered trial is not a result.
What would change our rating?
- A registered Phase 1 study with published human safety and pharmacokinetics.
- Independent replication of anti-fibrotic outcomes in additional animal models.
References and sources
Source transparency
A provenance snapshot of this profile. Counts show what kinds of sources are cited, not how much scientific weight each source deserves.
- Last editorial review
- 2026-09-26
- Recently reviewed · 20 days ago
- Linked curated sources
- 4
- Sources still pending
- 0
- External specialist reviews
- 0
- None recorded for this profile
Review provenance
Registry editorial review: Colin Jackson-White, creator and editor, who is not a doctor or clinician. External specialist review is credited only when a named reviewer has completed a review of this exact profile.
Literature-discovery and AI tools may help locate or challenge candidate evidence, but they are not counted as evidence sources here. Registry judgements are tied to the underlying papers, trial records, regulator documents and official study records.
- Peer-reviewedHossain et al. A single-chain derivative of the relaxin hormone is a functionally selective agonist of RXFP1. Chem Sci 2016
- Peer-reviewedDevarakonda et al. B7-33 attenuates myocardial infarction-related adverse cardiac remodeling in mice. JAHA 2020
- Peer-reviewedB7-33 maintains cardioprotective effects of relaxin in an experimental cardiomyopathy model (PMID 36753958)PMID: 36753958
- Peer-reviewedPraveen et al. A lipidated single-B-chain derivative of relaxin exhibits improved in vitro serum stability. Int J Mol Sci 2023
Source hierarchy: regulatory documents and trial registries first, peer-reviewed work next, sponsor material flagged as non-independent. We never use supplier or clinic marketing as evidence, and where a verified source has not yet been curated we say so rather than inventing one.
Evidence change history
These entries record changes to our assessment of the published evidence — not changes to the compound itself.
No recorded changes yet. Baseline position set on 2026-09-26.