B7-33

B7-33 is a lab-made relaxin analog that reduced fibrosis in cells and rodent heart and lung models. The b7-33 peptide has no published human trial, approved use, or established dose. Its biology is worth watching; claims that it heals human organs or safely reverses scarring have run far ahead of the evidence.

What is B7-33?

B7-33 is a 27-amino-acid, single-chain derivative of the B-chain of human relaxin-2, also called H2 relaxin. Researchers removed the first six residues from a 33-residue B-chain form, replaced two cysteines with serines to limit aggregation, and produced a water-soluble peptide that retained activity at relaxin family peptide receptor 1 (RXFP1).

That design matters because natural relaxin is a two-chain hormone held together by three disulfide bonds. B7-33 keeps the receptor-binding section in a simpler linear molecule. The original synthesis paper measured a calculated protonated mass of 2,986.59. No exact PubChem record for B7-33 was found during this review, so a CAS number or PubChem CID is deliberately omitted.

How does B7-33 work?

B7-33 works as a biased rxfp1 agonist: it favors one branch of RXFP1 signaling over another. Native relaxin strongly raises cyclic AMP (cAMP), a common cellular messenger. B7-33 produced much weaker cAMP signaling while strongly activating phosphorylated ERK1/2 in fibroblasts, the cells that build and remodel connective tissue.

Think of RXFP1 as a control panel with several switches. Native relaxin presses several; B7-33 leans harder on the ERK switch. In human cardiac fibroblasts and rat renal myofibroblasts, that signal increased matrix metalloproteinase-2 (MMP-2), an enzyme that breaks down collagen. Blocking RXFP1 or the partnering angiotensin II type 2 receptor blocked the effect in renal cells (Hossain et al., 2016).

What does the B7-33 fibrosis research show?

B7-33 fibrosis evidence is encouraging but entirely preclinical: cultured cells, rats, and mice. In the original paper, daily B7-33 reduced left-ventricular collagen and improved a measure of heart filling pressure in rats after myocardial infarction. In mice with chemically induced cardiomyopathy, 0.25 mg/kg/day reduced interstitial and total cardiac collagen.

The same paper tested intranasal B7-33 at 0.25 mg/kg/day in mice with chronic allergic airways disease. Lung collagen and airway-wall thickening fell, while airway hyperresponsiveness improved partly rather than returning fully to normal. Later mouse work also reported less adverse remodeling after myocardial infarction (PubMed PMID 32295457), and a 2023 mouse study compared B7-33 with perindopril in experimental cardiomyopathy (PubMed PMID 36753958).

Kidney claims need a correction. The foundational study used rat renal myofibroblasts in a dish; it did not show B7-33 reversing kidney fibrosis in a living animal. No B7-33 human trial appears in the ClinicalTrials.gov search. Animal-only is the honest headline tier.

What does serelaxin’s failed Phase 3 trial mean for B7-33?

Serelaxin’s failure does not prove B7-33 will fail, but it shows why receptor biology and rodent outcomes cannot substitute for human endpoints. Serelaxin is recombinant human relaxin-2, not B7-33. In the earlier RELAX-AHF trial, one dyspnea measure improved and an unexpected mortality signal drew attention. The larger confirmation trial told a colder story.

RELAX-AHF-2 randomized 6,545 people hospitalized with acute heart failure. Serelaxin missed both primary endpoints: cardiovascular death at 180 days and worsening heart failure through day five (Metra et al., 2019). B7-33’s biased signaling could produce a different result, and fibrosis is not the same endpoint as an acute 48-hour heart-failure infusion. Still, “relaxin pathway” is a research rationale, not a clinical receipt.

What are B7-33 side effects and risks?

B7-33 side effects in humans are unknown because no human safety study has reported them. That means there is no reliable frequency table for nausea, blood-pressure changes, immune reactions, organ toxicity, drug interactions, or longer-term harm. A lack of reported side effects is empty surveillance, not a clean safety record.

The original researchers tested one specific concern in mice: unlike native H2 relaxin, B7-33 did not increase prostate-tumor growth in that model. Useful clue, narrow question. It does not establish cancer safety in people or replace reproductive, immune, cardiovascular, and chronic-toxicity testing. Vials sold as research materials also add identity, purity, dosing, and sterility risks that the animal papers did not study.

Is there a B7-33 dosage for humans?

No validated b7-33 dosage exists for humans. Published animal experiments used routes and exposures chosen for disease models, including continuous systemic delivery or daily intranasal treatment. The 0.25–0.5 mg/kg/day figures in rodents are research inputs, not conversion instructions for a person.

Human pharmacokinetics are also missing: researchers have not established how long B7-33 lasts in human blood, what exposure reaches an organ, or whether repeated dosing creates antibodies. Multiplying a mouse dose by body weight does not solve those questions. There is no approved label, clinical titration schedule, or evidence-based reconstitution protocol.

Is B7-33 legal or FDA-approved in 2026?

B7-33 is not FDA-approved for any use in the United States as of July 16, 2026. The compound has no entry in Drugs@FDA and no registered human study located under its name. “Research use only” describes a laboratory-market product; it does not authorize treatment or establish pharmacy-grade quality.

B7-33 also falls under the 2026 World Anti-Doping Agency S0 catch-all for pharmacological substances without current human therapeutic approval. That makes the compound prohibited at all times for athletes under WADA rules, even though B7-33 is not named individually on the list. The site’s guide to research-use-only labeling explains what that phrase does and does not mean.

How does B7-33 compare with other healing peptides?

B7-33 belongs in the healing peptide hub, but its research question differs from injury-repair favorites. BPC-157 is studied mostly across rodent tendon, ligament, muscle, and gut injury models. TB-500 is tied to thymosin beta-4 biology and cell migration. B7-33 targets RXFP1 and the fibrotic remodeling machinery.

That makes B7-33 a plausible research candidate for pathological collagen buildup, not an established all-purpose recovery peptide. The next evidence that would change the page is straightforward: verified human pharmacokinetics and safety first, then a controlled trial measuring a defined fibrotic disease outcome. Until then, the mechanism is mapped more clearly than the medicine.