B7-33 peptide 10 mg vial product photo with freeze-dried powder on neutral beige background

B7-33 10mg vial

€50,00 EUR
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B7-33 peptide 10 mg vial product photo with freeze-dried powder on neutral beige background
B7-33 10mg vial

B7-33 10mg vial

€50,00 EUR
Taxes included.

                                          NOT FOR HUMAN CONSUMPTION 

B7-33 is an investigational peptide derived from the B-chain of human H2 relaxin. It was designed as a simplified, single-chain relaxin mimetic that retains anti-fibrotic and tissue-protective actions while showing biased signaling at the relaxin family peptide receptor 1 (RXFP1). Compared with native relaxin, B7-33 appears to favor ERK1/2-linked anti-fibrotic signaling over strong cAMP activation, which is one reason it has drawn interest as a potentially safer and cheaper relaxin-like scaffold. Evidence so far is preclinical only; I did not find any registered human efficacy trials for B7-33, and it is not FDA- or EMA-approved.

Additional Benefits of B7-33 Now Under Investigation

BENEFIT KEY TAKE-AWAYS
1 Anti-fibrotic activity In rodent heart, lung, and fibroblast models, B7-33 reduced fibrosis and improved function with activity comparable to H2 relaxin in some native-cell systems.
2 Biased RXFP1 signaling B7-33 preferentially activates ERK1/2 in native fibroblasts while showing relatively weak cAMP signaling in overexpression systems, supporting a “biased agonist” profile.
3 Cardioprotection after ischemic injury In mouse myocardial infarction work, B7-33 reduced cardiomyocyte death, attenuated ER-stress signaling, limited adverse remodeling, and preserved cardiac function.
4 Cardiomyopathy remodeling benefits In an isoprenaline cardiomyopathy model, B7-33 maintained relaxin-like cardioprotective effects and reduced left-ventricular fibrosis more rapidly than perindopril over the studied interval.
5 Vasoprotective actions Preclinical vascular studies suggest B7-33 can replicate key vasoprotective effects of serelaxin, including prevention of endothelial dysfunction.
6 Lower tumor-promotion concern vs H2 relaxin One preclinical paper reported that, unlike H2 relaxin, B7-33 did not exacerbate prostate tumor growth in mice; this is hypothesis-generating, not proof of human safety.
7 Simpler and cheaper scaffold Because it is a single-chain peptide rather than a two-chain, three-disulfide hormone, B7-33 is easier to synthesize and modify than native H2 relaxin.
8 Biomaterial/device applications B7-33 has also been explored in polymer coatings to reduce fibrotic encapsulation around implanted devices.
9 Platform for long-acting analogues Native B7-33 is short-lived, but lipidated derivatives have improved in-vitro serum stability, supporting ongoing medicinal-chemistry work.

2. Molecular Mechanism of Action

2.1 Receptor Pharmacodynamics

RXFP1:
B7-33 is a relaxin-receptor agonist derived from the relaxin B-chain sequence and acts at RXFP1. It was designed to preserve beneficial relaxin biology while reducing some signaling liabilities associated with native H2 relaxin.

Biased signaling:
In engineered HEK-RXFP1 systems, B7-33 shows relatively weak affinity/potency, especially for cAMP, but in fibroblasts endogenously expressing RXFP1 it produced ERK1/2 activation with similar potency and efficacy to H2 relaxin. That native-cell behavior is central to why B7-33 is described as a functionally selective / biased agonist.

2.2 Down-stream Biology

PATHWAY FUNCTIONAL OUTCOME CONTEXT
ERK1/2 Anti-fibrotic signaling Native fibroblasts; core biased-signaling observation
MMP-2 upregulation Matrix remodeling / collagen turnover Linked to anti-fibrotic effects in vitro and in vivo
TGF-β / Smad antagonism Reduced pro-fibrotic signaling Proposed relaxin-pathway mechanism behind fibrosis reduction
Cardiomyocyte stress signaling Less ER stress and cell death Myocardial infarction model
Vascular/endothelial actions Vasoprotection, endothelial support Short-term vascular studies vs serelaxin

3. Pharmacokinetics

Route:
Published animal studies used parenteral administration, commonly subcutaneous delivery in rodent experiments.

Absorption / half-life:
A major limitation of B7-33 is its very short serum stability. One 2023 study reports an in-vitro serum half-life of about 6 minutes for the parent peptide.

Distribution / clearance:
As a small peptide, B7-33 is expected to undergo proteolytic degradation; detailed human PK is unavailable because there are no clinical studies yet. The available medicinal-chemistry literature is aimed at overcoming this short-lived exposure.

Stability engineering:
Fatty-acid conjugation with a suitable spacer increased the reported in-vitro half-life from ~6 minutes to ~60 minutes, showing a plausible route toward longer-acting analogues, though this is still preclinical.

4. Pre-clinical and Clinical Evidence

4.1 Fibrosis

The 2016 discovery paper reported that B7-33 reduced fibrosis across three in-vivo disease models and showed functional equivalence to H2 relaxin in several anti-fibrotic assays. Later reviews and medicinal-chemistry follow-up papers describe efficacy across multiple rodent cardiovascular and lung fibrosis models.

4.2 Cardiac injury and remodeling

A 2020 myocardial infarction paper found that B7-33 attenuated MI-related adverse remodeling, reduced cardiomyocyte death and ER stress, and preserved cardiac function in mice.

A 2023 study in experimental cardiomyopathy found B7-33 retained cardioprotective effects of relaxin and reduced LV fibrosis more rapidly than perindopril in that model and time frame.

4.3 Vascular biology

A vascular pharmacology study reported that B7-33 replicated important vasoprotective functions of human relaxin-2/serelaxin and prevented endothelial dysfunction in preclinical testing.

4.4 Human evidence

At present, the evidence base is preclinical. I did not find published phase 1/2 human B7-33 trials or an approved product. That is a major difference from drugs like retatrutide.

Evidence quality note:
The mechanistic story is interesting, but all efficacy claims should be viewed as animal/cell-data only until human pharmacokinetics, dose-ranging, and safety studies exist.

5. Emerging Clinical Interests

FIELD RATIONALE STATUS
Cardiac fibrosis / remodeling Strong relaxin-like anti-fibrotic activity in preclinical heart models Preclinical
Pulmonary fibrosis Anti-fibrotic signals seen in rodent lung disease models Preclinical
Vascular dysfunction Vasoprotective and endothelial-support effects Preclinical
Implant/device fibrosis Drug-eluting coatings to reduce fibrotic encapsulation Preclinical / materials research
Long-acting relaxin mimetics Need to solve very short half-life of parent peptide Lead-optimization stage

6. Safety and Tolerability

Known human safety profile:
There is no established human safety profile for B7-33 because it has not progressed through standard clinical development.

Theoretical / preclinical considerations:
Because B7-33 targets RXFP1 and modulates relaxin biology, the main concerns needing future study would include:

  • off-target or receptor-context effects across tissues,

  • blood-pressure / vascular effects,

  • reproductive or endocrine effects,

  • immunogenicity,

  • and long-term proliferative signaling risks.

These remain open questions, not established toxicities. The most concrete published limitation today is poor stability / short exposure, not a mature catalog of adverse events.

Potential comparative upside:
Authors have proposed that weaker cAMP activation could reduce some unwanted effects associated with native H2 relaxin, and one mouse study noted lack of prostate-tumor exacerbation compared with H2 relaxin. That is interesting, but it is far too early to claim a proven safety advantage in humans.

Comparative safety/translation matrix

FEATURE B7-33 H2 RELAXIN / SERELAXIN
Development stage Preclinical Clinical history exists for relaxin-class molecules, though not approved broadly for chronic fibrosis uses
Core receptor RXFP1 RXFP1
Signaling profile Biased toward ERK1/2 in native cells; weak cAMP in some systems Broader signaling including stronger cAMP
Half-life Very short parent peptide Native relaxin also short-lived, though clinically formulated differently
Synthesis complexity Simpler single-chain scaffold More complex two-chain peptide with three disulfides
Human efficacy data None Some human data exist for relaxin-class agents, not B7-33 specifically

7. Regulatory Landscape

Approval status:
B7-33 is investigational only and has no marketing authorization.

Programs:
The published literature is centered on academic and preclinical translational work, plus medicinal-chemistry efforts to create more stable analogues.

Use outside research:
There is no validated, regulated clinical-use framework for B7-33 at present. Any non-research use would be outside the evidence base.

8. Future Directions

  • First-in-human PK/safety studies are the biggest missing step.

  • Long-acting analogues are a major priority because parent B7-33 is too short-lived for practical therapeutic use.

  • Fibrosis-focused programs in heart, lung, and device encapsulation appear to be the most evidence-aligned translational directions.

  • Mechanistic work is still needed to clarify when B7-33 behaves like a weak agonist versus an effective native-cell biased agonist.

  • Comparative studies against relaxin, ACE inhibitors, and anti-fibrotic standards will matter more than receptor pharmacology alone.

Selected References

  • Hossain MA, et al. A single-chain derivative of the relaxin hormone is a functionally selective agonist of the GPCR RXFP1. Chem Sci. 2016. Core discovery paper for B7-33; biased signaling and anti-fibrotic activity.

  • Devarakonda T, et al. B7-33, a Functionally Selective Relaxin Receptor 1 Agonist, Attenuates Myocardial Infarction–Related Adverse Cardiac Remodeling in Mice. J Am Heart Assoc. 2020.

  • Alam F, et al. The single-chain relaxin mimetic, B7-33, maintains the cardioprotective effects of relaxin and more rapidly reduces left ventricular fibrosis compared to perindopril in an experimental model of cardiomyopathy. Biochem Pharmacol. 2023.

  • Marshall SA, et al. B7-33 replicates the vasoprotective functions of human relaxin-2 (serelaxin). Life Sci. 2017.

  • Praveen P, et al. A Lipidated Single-B-Chain Derivative of Relaxin Exhibits Improved In Vitro Serum Stability without Altering Activity. 2023.

  • Handley TNG, et al. Further Developments towards a Minimal Potent Derivative of Human Relaxin-2. Int J Mol Sci. 2023. Useful review/update on scaffold optimization and B7-33’s preclinical profile.