B7-33

updated

B7-33 is a single-chain peptide analogue of human relaxin-2 that reduced organ fibrosis in rodent models of heart, kidney and lung injury. No controlled human study exists: a PubMed search on 9 October 2026 returned no clinical trial, and the records reviewed hold no human dose, pharmacokinetics or safety data. The one experiment that measured blood pressure found no change with B7-33.

Single-chain relaxin-2 analogue acting on the relaxin receptor RXFP1

  • B7-33 is built from the B chain only of human gene-2 relaxin and binds RXFP1; PubChem returned no compound record for it on 9 October 2026.
  • In a mouse model of cardiac ischemia-reperfusion, B7-33 reduced infarct size to 21.99% versus 45.32% with vehicle (P=0.02).
  • In mice with isoprenaline-induced cardiomyopathy, B7-33 reduced left ventricular fibrosis but did not change systolic blood pressure, while the ACE inhibitor perindopril lowered it.
  • In vitro serum half-life is about 6 minutes; no animal or human pharmacokinetic profile for plain B7-33 had been published as of the design group's stability paper.
  • RELAX-AHF-2 (6545 adults with acute heart failure) found no benefit from serelaxin, the two-chain parent hormone, on cardiovascular death at 180 days (8.7% versus 8.9%, hazard ratio 0.98, P=0.77).
  • A PubMed search on 9 October 2026 for B7-33 with relaxin returned 11 records, and a search limited to clinical trial or randomized controlled trial publication types returned 0.

What is B7-33, and is it approved for anything?

B7-33 is a single-chain peptide analogue of human relaxin-2. No approval for any use appears in the records reviewed, and PubChem returned no compound record for it on 9 October 2026, so a vial labeled B7-33 cannot be matched to a public chemical record by name alone.

B7-33 is built from the B chain only of human gene-2 relaxin, the same hormone tested in trials as serelaxin. It binds the relaxin receptor RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors of the design paper describe as the first functionally selective agonist of that receptor.

PubChem returned no compound record on 9 October 2026 for B7-33, B7-33 peptide, relaxin B7-33, H2 relaxin B7-33 or B7-33 TFA. There is therefore no public chemical record to anchor a formula, molecular weight or CAS number to, and none is printed here.

ClinicalTrials.gov queries on 9 October 2026 for B7-33, B7-33 relaxin and B7-33 peptide returned no studies, and a PubMed search for B7-33 limited to clinical trial or randomized controlled trial publication types returned 0 records. No approval for any use appears in the records reviewed.

Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
Searches, 9 October 2026: no clinical trial and no human data for B7-33

PubMed search record

PubMed search run on 9 October 2026: B7-33 AND relaxin, 11 records. A PubMed search for B7-33 restricted to clinical trial or randomized controlled trial publication types returned 0 records. ClinicalTrials.gov queries for B7-33, B7-33 relaxin and B7-33 peptide run the same day.

The search for B7-33 with relaxin returned 11 records: the design paper, the rodent cardiac, renal and vascular studies, two chemistry papers, a nanoparticle delivery study, a nanovesicle cholangiocarcinoma study, an implant coating study, a mouse pain study and a review. The search restricted to clinical trial or randomized controlled trial publication types returned 0 records, and the ClinicalTrials.gov queries returned no studies. The records reviewed contain no human dose, no human pharmacokinetics, no human safety data and no clinical trial for B7-33.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 9 October 2026
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source

What did rodent studies find for heart, kidney and lung injury?

In rodent models of heart, lung and kidney injury, B7-33 reduced fibrosis, and in a mouse model of heart attack it lowered infarct size to 21.99% versus 45.32% on vehicle. All of this is animal and cell work, and no study gave B7-33 to a person.

The design paper reported that B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease, with similar potency to human gene-2 relaxin. The paper is rodent and cell work and reports no human exposure.

In adult male CD1 mice that underwent 30 minutes of left anterior descending artery ligation, B7-33 reduced infarct size to 21.99% versus 45.32% with vehicle (P=0.02) and preserved fractional shortening at 29% versus 23% (P=0.02) after 24 hours of reperfusion. At 7 days the fractional shortening figures were 29% versus 20%. In isolated adult mouse cardiomyocytes, B7-33 at 50 and 100 nmol/L improved cell survival and reduced expression of the stress marker GRP78.

In adult male 129sv mice given isoprenaline subcutaneously to induce cardiomyopathy, subcutaneous B7-33 at 0.25 mg/kg/day from days 7 to 14 reduced left ventricular fibrosis equivalently to relaxin, normalised inflammation and cardiomyocyte hypertrophy, and restored blood vessel density and aortic contractility.

In mice with surgical obstruction of one ureter, treated for 7 days with B7-33 at 0.25 mg/kg/day, prevention of kidney fibrosis correlated with thinner collagen fibers and higher fiber counts. B7-33 or relaxin also raised renal matrix metalloproteinase-2 and lowered tissue inhibitor of metalloproteinase-1 (all P less than .01 versus obstruction alone). That paper's stated purpose was validating a collagen imaging platform, with the peptides used as reference anti-fibrotic agents.

These are mouse and rat results from a small set of papers, and none is a human result.

Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
Infarct model: CD1 mice, infarct size 21.99% versus 45.32% on vehicle

Animal study

Devarakonda T et al. J Am Heart Assoc. 2020;9(8):e015748. PMID 32295457.

After 30 minutes of left anterior descending artery ligation followed by 24 hours of reperfusion, B7-33 reduced infarct size to 21.99% versus 45.32% with vehicle (P=0.02) and preserved fractional shortening at 29% versus 23% (P=0.02). At 7 days the fractional shortening figures were 29% versus 20%. In isolated adult cardiomyocytes, B7-33 at 50 and 100 nmol/L improved cell survival and reduced expression of the endoplasmic reticulum stress marker GRP78.

Participants / model
Adult male CD1 mice; primary adult mouse cardiomyocytes
Treatment
B7-33 as dosed in the report, after ischemia-reperfusion
Follow-up
24 hours or 7 days of reperfusion
Study design
Original preclinical study
Funding
not stated in the source

Mouse and cell results. No route or dose for the mouse experiment is stated in the information reviewed.

Read the original source
Isoprenaline cardiomyopathy: 129sv mice, fibrosis reduced, blood pressure unchanged

Animal study

Alam F et al. Biomed Pharmacother. 2023;160:114370. PMID 36753958.

Adult male 129sv mice were given isoprenaline at 25 mg/kg/day subcutaneously to induce cardiomyopathy, then treated subcutaneously from days 7 to 14 with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or the ACE inhibitor perindopril 1 mg/kg/day. B7-33 and relaxin equivalently reduced left ventricular fibrosis and normalised inflammation and cardiomyocyte hypertrophy, and restored blood vessel density and aortic contractility. Perindopril lowered systolic blood pressure but did not reduce fibrosis or hypertrophy. The injured mice showed no change in body weight or systolic blood pressure at day 14, so in this experiment B7-33 did not lower blood pressure; the comparator drug did.

Participants / model
Adult male 129sv mice with isoprenaline-induced cardiomyopathy
Treatment
Subcutaneous B7-33, 0.25 mg/kg/day, days 7 to 14
Follow-up
Days 7 to 14 after the start of isoprenaline
Study design
Original preclinical study with an active comparator
Funding
not stated in the source

This is the one study found that measured systolic blood pressure. It tested the blood pressure part of the supplier claim directly and did not support it.

Read the original source
Kidney fibrosis: mice with ureteric obstruction, 7 days, collagen imaging

Animal study

Bhuiyan S et al. FASEB J. 2021;35(5):e21595. PMID 33908676.

In mice with unilateral ureteric obstruction treated for 7 days with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or perindopril 1 mg/kg/day, a second-harmonic generation imaging platform found that the drug-induced prevention of renal fibrosis correlated with significantly reduced collagen fiber thickness and collagen-to-tissue cross reticulation ratio and increased collagen fiber counts. Relaxin or B7-33 treatment also increased renal matrix metalloproteinase-2 and reduced tissue inhibitor of metalloproteinase-1 (all P less than .01 versus obstruction alone).

Participants / model
Mice with surgical unilateral ureteric obstruction
Treatment
B7-33 0.25 mg/kg/day for 7 days; route not stated in the information reviewed
Follow-up
7 days
Study design
Original preclinical imaging-platform study
Funding
not stated in the source

The paper's stated purpose was validating the imaging platform, with the peptides used as reference anti-fibrotic agents.

Read the original source

Did B7-33 change blood vessels or blood pressure in animals?

In rats it enhanced one kind of vessel relaxation in the mesenteric artery 3 hours after a single injection, with no overall effect in the small renal artery or the aorta. In the one study that measured systolic blood pressure, B7-33 did not change it.

In male Wistar rats given a single tail vein injection of B7-33 at 13.3 micrograms/kg, bradykinin-mediated endothelium-dependent relaxation in the mesenteric artery was selectively enhanced 3 hours later by an increase in endothelium-derived hyperpolarization. There was no overall effect on relaxation in the small renal artery or the aorta. In mouse mesenteric arteries pre-incubated in placental trophoblast conditioned media ex vivo, B7-33 at 15 and 30 nM prevented endothelial dysfunction.

This is an acute vessel-reactivity result in two arteries of one rodent bed. It is not a blood pressure outcome and not a human result.

The blood pressure question was tested directly in the isoprenaline cardiomyopathy study. The injured mice showed no change in body weight or systolic blood pressure at day 14, so in that experiment B7-33 did not lower blood pressure. The ACE inhibitor perindopril, given as a comparator, lowered systolic blood pressure but did not reduce fibrosis or hypertrophy.

Vessel reactivity: Wistar rats 3 hours after one injection, mouse arteries ex vivo

Animal study

Marshall SA et al. Eur J Pharmacol. 2017;807:190-197. PMID 28478069.

Three hours after a tail vein injection in male Wistar rats, B7-33 at 13.3 micrograms/kg and serelaxin at 26.6 micrograms/kg both selectively enhanced bradykinin-mediated endothelium-dependent relaxation in the mesenteric artery by increasing endothelium-derived hyperpolarization, with no overall effect on relaxation in the small renal artery or the aorta. In mouse mesenteric arteries pre-incubated in placental trophoblast conditioned media ex vivo, B7-33 or serelaxin at 15 and 30 nM prevented endothelial dysfunction.

Participants / model
Male Wistar rats; virgin female mouse mesenteric arteries ex vivo
Treatment
Placebo, B7-33 or serelaxin as a single intravenous bolus in rats; bath incubation ex vivo
Follow-up
Vessels assessed 3 hours after the rat injection
Study design
Original preclinical study
Funding
not stated in the source

This is an acute vessel-reactivity result in two arteries of one rodent bed. It is not a blood pressure outcome and not a human result.

Read the original source
Isoprenaline cardiomyopathy: 129sv mice, fibrosis reduced, blood pressure unchanged

Animal study

Alam F et al. Biomed Pharmacother. 2023;160:114370. PMID 36753958.

Adult male 129sv mice were given isoprenaline at 25 mg/kg/day subcutaneously to induce cardiomyopathy, then treated subcutaneously from days 7 to 14 with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or the ACE inhibitor perindopril 1 mg/kg/day. B7-33 and relaxin equivalently reduced left ventricular fibrosis and normalised inflammation and cardiomyocyte hypertrophy, and restored blood vessel density and aortic contractility. Perindopril lowered systolic blood pressure but did not reduce fibrosis or hypertrophy. The injured mice showed no change in body weight or systolic blood pressure at day 14, so in this experiment B7-33 did not lower blood pressure; the comparator drug did.

Participants / model
Adult male 129sv mice with isoprenaline-induced cardiomyopathy
Treatment
Subcutaneous B7-33, 0.25 mg/kg/day, days 7 to 14
Follow-up
Days 7 to 14 after the start of isoprenaline
Study design
Original preclinical study with an active comparator
Funding
not stated in the source

This is the one study found that measured systolic blood pressure. It tested the blood pressure part of the supplier claim directly and did not support it.

Read the original source

What happened when the full relaxin-2 hormone was tested in heart failure?

Serelaxin, the two-chain recombinant hormone, did not improve either primary endpoint in RELAX-AHF-2, a trial of 6545 adults hospitalized for acute heart failure. It is a different molecule from B7-33, so the result does not transfer.

RELAX-AHF-2 randomized 6545 adults hospitalized for acute heart failure to a 48-hour intravenous infusion of serelaxin, recombinant human relaxin-2, at 30 micrograms per kilogram per day, or to placebo. Death from cardiovascular causes at 180 days occurred in 285 of 3274 (8.7%) on serelaxin and 290 of 3271 (8.9%) on placebo (hazard ratio 0.98, 95% CI 0.83 to 1.15, P=0.77). Worsening heart failure at day 5 occurred in 227 (6.9%) versus 252 (7.7%) (hazard ratio 0.89, 95% CI 0.75 to 1.07, P=0.19).

There were no significant differences in all-cause death at 180 days, in the composite of cardiovascular death or rehospitalization, or in length of stay, and adverse event incidence was similar. The trial is registered as NCT01870778.

Serelaxin has two chains and B7-33 has one, and no result from one transfers to the other. The trial matters as context: it is the best human test of the relaxin pathway that sellers market as a cardiovascular benefit, and both primary endpoints were negative.

RELAX-AHF-2: 6545 patients, serelaxin, no benefit on either primary endpoint

Randomized controlled trial

Metra M et al. N Engl J Med. 2019;381(8):716-726. PMID 31433919.

Death from cardiovascular causes at 180 days occurred in 285 of 3274 (8.7%) on serelaxin and 290 of 3271 (8.9%) on placebo (hazard ratio 0.98, 95% CI 0.83 to 1.15, P=0.77). Worsening heart failure at day 5 occurred in 227 (6.9%) versus 252 (7.7%) (hazard ratio 0.89, 95% CI 0.75 to 1.07, P=0.19). There were no significant differences in all-cause death at 180 days, the composite of cardiovascular death or rehospitalization, or length of stay, and adverse event incidence was similar.

Participants / model
6545 adults hospitalized for acute heart failure
Treatment
48-hour intravenous infusion of serelaxin (recombinant human relaxin-2) at 30 micrograms per kilogram per day, or placebo
Follow-up
180 days of follow-up for cardiovascular death
Study design
Randomized placebo-controlled phase 3 trial
Funding
not stated in the source

Serelaxin is a different molecule from B7-33, with two chains versus one, and this result does not transfer to B7-33. It is context for the relaxin pathway being sold as a cardiovascular benefit. Registered as NCT01870778.

Read the original source

Does B7-33 support the heart, kidney, lung and blood pressure claims?

Only in rodents. The heart, kidney and lung anti-fibrotic claims rest on mouse and rat work, vascular compliance is supported only as an acute effect in rat and mouse arteries, and the blood pressure claim is contradicted by the one study that measured it.

Sellers describe B7-33 as anti-fibrotic support for the heart, kidney and lung, plus vascular compliance and blood pressure support, from a single-chain relaxin-2 analogue.

The anti-fibrotic claims for heart, kidney and lung rest entirely on rodent work and should be read that way. The vascular compliance claim is supported only as acute endothelium-dependent relaxation in rat mesenteric arteries and in mouse arteries ex vivo, with no effect in the renal artery or aorta. The blood pressure claim is contradicted by the one study that measured systolic blood pressure: B7-33 did not change it, and the comparator drug did.

A PubMed search on 9 October 2026 for B7-33 with relaxin returned 11 records. They were the design paper, the rodent cardiac, renal and vascular studies, two chemistry papers, a nanoparticle delivery study, a nanovesicle cholangiocarcinoma study, an implant coating study, a mouse pain study and a review. A search restricted to clinical trial or randomized controlled trial publication types returned 0 records, and ClinicalTrials.gov queries returned no studies. The records reviewed contain no human dose, no human pharmacokinetics, no human safety data and no clinical trial.

Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
Isoprenaline cardiomyopathy: 129sv mice, fibrosis reduced, blood pressure unchanged

Animal study

Alam F et al. Biomed Pharmacother. 2023;160:114370. PMID 36753958.

Adult male 129sv mice were given isoprenaline at 25 mg/kg/day subcutaneously to induce cardiomyopathy, then treated subcutaneously from days 7 to 14 with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or the ACE inhibitor perindopril 1 mg/kg/day. B7-33 and relaxin equivalently reduced left ventricular fibrosis and normalised inflammation and cardiomyocyte hypertrophy, and restored blood vessel density and aortic contractility. Perindopril lowered systolic blood pressure but did not reduce fibrosis or hypertrophy. The injured mice showed no change in body weight or systolic blood pressure at day 14, so in this experiment B7-33 did not lower blood pressure; the comparator drug did.

Participants / model
Adult male 129sv mice with isoprenaline-induced cardiomyopathy
Treatment
Subcutaneous B7-33, 0.25 mg/kg/day, days 7 to 14
Follow-up
Days 7 to 14 after the start of isoprenaline
Study design
Original preclinical study with an active comparator
Funding
not stated in the source

This is the one study found that measured systolic blood pressure. It tested the blood pressure part of the supplier claim directly and did not support it.

Read the original source
Vessel reactivity: Wistar rats 3 hours after one injection, mouse arteries ex vivo

Animal study

Marshall SA et al. Eur J Pharmacol. 2017;807:190-197. PMID 28478069.

Three hours after a tail vein injection in male Wistar rats, B7-33 at 13.3 micrograms/kg and serelaxin at 26.6 micrograms/kg both selectively enhanced bradykinin-mediated endothelium-dependent relaxation in the mesenteric artery by increasing endothelium-derived hyperpolarization, with no overall effect on relaxation in the small renal artery or the aorta. In mouse mesenteric arteries pre-incubated in placental trophoblast conditioned media ex vivo, B7-33 or serelaxin at 15 and 30 nM prevented endothelial dysfunction.

Participants / model
Male Wistar rats; virgin female mouse mesenteric arteries ex vivo
Treatment
Placebo, B7-33 or serelaxin as a single intravenous bolus in rats; bath incubation ex vivo
Follow-up
Vessels assessed 3 hours after the rat injection
Study design
Original preclinical study
Funding
not stated in the source

This is an acute vessel-reactivity result in two arteries of one rodent bed. It is not a blood pressure outcome and not a human result.

Read the original source
Searches, 9 October 2026: no clinical trial and no human data for B7-33

PubMed search record

PubMed search run on 9 October 2026: B7-33 AND relaxin, 11 records. A PubMed search for B7-33 restricted to clinical trial or randomized controlled trial publication types returned 0 records. ClinicalTrials.gov queries for B7-33, B7-33 relaxin and B7-33 peptide run the same day.

The search for B7-33 with relaxin returned 11 records: the design paper, the rodent cardiac, renal and vascular studies, two chemistry papers, a nanoparticle delivery study, a nanovesicle cholangiocarcinoma study, an implant coating study, a mouse pain study and a review. The search restricted to clinical trial or randomized controlled trial publication types returned 0 records, and the ClinicalTrials.gov queries returned no studies. The records reviewed contain no human dose, no human pharmacokinetics, no human safety data and no clinical trial for B7-33.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 9 October 2026
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source

How does B7-33 work, and how stable is it?

B7-33 binds the relaxin receptor RXFP1 and favors the pERK pathway over cAMP. Its in vitro serum half-life is about 6 minutes, and no animal or human half-life or exposure profile for the plain peptide had been published.

B7-33 binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express that receptor. In rodent heart and lung models its effects involved RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2, and in mice with kidney obstruction it raised renal matrix metalloproteinase-2 and lowered tissue inhibitor of metalloproteinase-1.

In vitro in serum, B7-33 has a half-life of about 6 minutes. Fatty-acid conjugation with an appropriate spacer length raised the in vitro half-life from 6 minutes to 60 minutes. The group that designed the peptide stated that the lead lipidated molecule would be studied in animal models to measure its pharmacokinetic and pharmacodynamic properties, which means no animal or human pharmacokinetic profile for plain B7-33 had been published as of that paper.

The 6-minute figure is a serum value from a test tube, not a half-life in an animal or a person, and no half-life is given for either.

Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
Kidney fibrosis: mice with ureteric obstruction, 7 days, collagen imaging

Animal study

Bhuiyan S et al. FASEB J. 2021;35(5):e21595. PMID 33908676.

In mice with unilateral ureteric obstruction treated for 7 days with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or perindopril 1 mg/kg/day, a second-harmonic generation imaging platform found that the drug-induced prevention of renal fibrosis correlated with significantly reduced collagen fiber thickness and collagen-to-tissue cross reticulation ratio and increased collagen fiber counts. Relaxin or B7-33 treatment also increased renal matrix metalloproteinase-2 and reduced tissue inhibitor of metalloproteinase-1 (all P less than .01 versus obstruction alone).

Participants / model
Mice with surgical unilateral ureteric obstruction
Treatment
B7-33 0.25 mg/kg/day for 7 days; route not stated in the information reviewed
Follow-up
7 days
Study design
Original preclinical imaging-platform study
Funding
not stated in the source

The paper's stated purpose was validating the imaging platform, with the peptides used as reference anti-fibrotic agents.

Read the original source
In vitro serum half-life about 6 minutes; lipidation raised it to 60 minutes

Cell study

Praveen P et al. Int J Mol Sci. 2023;24(7). PMID 37047588.

B7-33 has a short circulation time in vitro in serum, with a half-life of about 6 minutes. Fatty-acid conjugation with an appropriate spacer length raised the in vitro half-life from 6 minutes to 60 minutes. The authors stated that the lead lipidated molecule would be studied in animal models in the future to measure its pharmacokinetic and pharmacodynamic properties, so no animal or human pharmacokinetic profile for plain B7-33 had been published as of that paper.

Participants / model
In vitro serum; no treated organism
Treatment
Synthetic B7-33 and lipidated analogues in serum
Follow-up
not stated in the source
Study design
Original chemistry study from the group that designed the peptide
Funding
not stated in the source

This is a serum value, not an animal or human half-life.

Read the original source

What is known about the risks of B7-33?

Nothing is established. No human dose, pharmacokinetics or safety data exist for B7-33, PubChem returned no compound record for it, and exposure from a plain vial is uncharacterized.

The records reviewed contain no human dose, no human pharmacokinetics, no human safety data and no clinical trial for B7-33. Benefit and harm in people are unmeasured.

The design paper reported that B7-33, unlike H2 relaxin, did not promote prostate tumor growth in vivo. That is a single preclinical observation and is not a safety clearance.

Exposure from a plain peptide is uncharacterized. The only published figure is the in vitro serum half-life of about 6 minutes, and the designing group was still working on lipidated versions to address it. Because PubChem returned no compound record for B7-33, a vial sold under that name cannot be matched to a public chemical record by name alone.

In RELAX-AHF-2, adverse event incidence with serelaxin was similar to placebo. Serelaxin is a different molecule, and that result is not safety data for B7-33.

Searches, 9 October 2026: no clinical trial and no human data for B7-33

PubMed search record

PubMed search run on 9 October 2026: B7-33 AND relaxin, 11 records. A PubMed search for B7-33 restricted to clinical trial or randomized controlled trial publication types returned 0 records. ClinicalTrials.gov queries for B7-33, B7-33 relaxin and B7-33 peptide run the same day.

The search for B7-33 with relaxin returned 11 records: the design paper, the rodent cardiac, renal and vascular studies, two chemistry papers, a nanoparticle delivery study, a nanovesicle cholangiocarcinoma study, an implant coating study, a mouse pain study and a review. The search restricted to clinical trial or randomized controlled trial publication types returned 0 records, and the ClinicalTrials.gov queries returned no studies. The records reviewed contain no human dose, no human pharmacokinetics, no human safety data and no clinical trial for B7-33.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 9 October 2026
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source
Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
In vitro serum half-life about 6 minutes; lipidation raised it to 60 minutes

Cell study

Praveen P et al. Int J Mol Sci. 2023;24(7). PMID 37047588.

B7-33 has a short circulation time in vitro in serum, with a half-life of about 6 minutes. Fatty-acid conjugation with an appropriate spacer length raised the in vitro half-life from 6 minutes to 60 minutes. The authors stated that the lead lipidated molecule would be studied in animal models in the future to measure its pharmacokinetic and pharmacodynamic properties, so no animal or human pharmacokinetic profile for plain B7-33 had been published as of that paper.

Participants / model
In vitro serum; no treated organism
Treatment
Synthetic B7-33 and lipidated analogues in serum
Follow-up
not stated in the source
Study design
Original chemistry study from the group that designed the peptide
Funding
not stated in the source

This is a serum value, not an animal or human half-life.

Read the original source
RELAX-AHF-2: 6545 patients, serelaxin, no benefit on either primary endpoint

Randomized controlled trial

Metra M et al. N Engl J Med. 2019;381(8):716-726. PMID 31433919.

Death from cardiovascular causes at 180 days occurred in 285 of 3274 (8.7%) on serelaxin and 290 of 3271 (8.9%) on placebo (hazard ratio 0.98, 95% CI 0.83 to 1.15, P=0.77). Worsening heart failure at day 5 occurred in 227 (6.9%) versus 252 (7.7%) (hazard ratio 0.89, 95% CI 0.75 to 1.07, P=0.19). There were no significant differences in all-cause death at 180 days, the composite of cardiovascular death or rehospitalization, or length of stay, and adverse event incidence was similar.

Participants / model
6545 adults hospitalized for acute heart failure
Treatment
48-hour intravenous infusion of serelaxin (recombinant human relaxin-2) at 30 micrograms per kilogram per day, or placebo
Follow-up
180 days of follow-up for cardiovascular death
Study design
Randomized placebo-controlled phase 3 trial
Funding
not stated in the source

Serelaxin is a different molecule from B7-33, with two chains versus one, and this result does not transfer to B7-33. It is context for the relaxin pathway being sold as a cardiovascular benefit. Registered as NCT01870778.

Read the original source

Why does B7-33 sit in C tier?

The rodent record is detailed, with four models of heart, kidney, lung and vascular injury and a receptor mechanism that was worked out, but no human has a recorded dose or outcome, and the one measurement of blood pressure showed no change.

B7-33 has more behind it than most research peptides: consistent anti-fibrotic results across several rodent models of heart, kidney and lung injury, and a receptor mechanism that was worked out rather than assumed. That is where it stops. There is no human dose, no human pharmacokinetics, no clinical trial and no public chemical record for the molecule.

The designing group reported an in vitro serum half-life of about 6 minutes and was still working on lipidated versions to fix it. The full relaxin-2 hormone, which is the reason this pathway is marketed, missed both primary endpoints in a 6545-patient phase 3 trial. The blood pressure claim was tested in one study and not supported.

Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
Isoprenaline cardiomyopathy: 129sv mice, fibrosis reduced, blood pressure unchanged

Animal study

Alam F et al. Biomed Pharmacother. 2023;160:114370. PMID 36753958.

Adult male 129sv mice were given isoprenaline at 25 mg/kg/day subcutaneously to induce cardiomyopathy, then treated subcutaneously from days 7 to 14 with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or the ACE inhibitor perindopril 1 mg/kg/day. B7-33 and relaxin equivalently reduced left ventricular fibrosis and normalised inflammation and cardiomyocyte hypertrophy, and restored blood vessel density and aortic contractility. Perindopril lowered systolic blood pressure but did not reduce fibrosis or hypertrophy. The injured mice showed no change in body weight or systolic blood pressure at day 14, so in this experiment B7-33 did not lower blood pressure; the comparator drug did.

Participants / model
Adult male 129sv mice with isoprenaline-induced cardiomyopathy
Treatment
Subcutaneous B7-33, 0.25 mg/kg/day, days 7 to 14
Follow-up
Days 7 to 14 after the start of isoprenaline
Study design
Original preclinical study with an active comparator
Funding
not stated in the source

This is the one study found that measured systolic blood pressure. It tested the blood pressure part of the supplier claim directly and did not support it.

Read the original source
In vitro serum half-life about 6 minutes; lipidation raised it to 60 minutes

Cell study

Praveen P et al. Int J Mol Sci. 2023;24(7). PMID 37047588.

B7-33 has a short circulation time in vitro in serum, with a half-life of about 6 minutes. Fatty-acid conjugation with an appropriate spacer length raised the in vitro half-life from 6 minutes to 60 minutes. The authors stated that the lead lipidated molecule would be studied in animal models in the future to measure its pharmacokinetic and pharmacodynamic properties, so no animal or human pharmacokinetic profile for plain B7-33 had been published as of that paper.

Participants / model
In vitro serum; no treated organism
Treatment
Synthetic B7-33 and lipidated analogues in serum
Follow-up
not stated in the source
Study design
Original chemistry study from the group that designed the peptide
Funding
not stated in the source

This is a serum value, not an animal or human half-life.

Read the original source
RELAX-AHF-2: 6545 patients, serelaxin, no benefit on either primary endpoint

Randomized controlled trial

Metra M et al. N Engl J Med. 2019;381(8):716-726. PMID 31433919.

Death from cardiovascular causes at 180 days occurred in 285 of 3274 (8.7%) on serelaxin and 290 of 3271 (8.9%) on placebo (hazard ratio 0.98, 95% CI 0.83 to 1.15, P=0.77). Worsening heart failure at day 5 occurred in 227 (6.9%) versus 252 (7.7%) (hazard ratio 0.89, 95% CI 0.75 to 1.07, P=0.19). There were no significant differences in all-cause death at 180 days, the composite of cardiovascular death or rehospitalization, or length of stay, and adverse event incidence was similar.

Participants / model
6545 adults hospitalized for acute heart failure
Treatment
48-hour intravenous infusion of serelaxin (recombinant human relaxin-2) at 30 micrograms per kilogram per day, or placebo
Follow-up
180 days of follow-up for cardiovascular death
Study design
Randomized placebo-controlled phase 3 trial
Funding
not stated in the source

Serelaxin is a different molecule from B7-33, with two chains versus one, and this result does not transfer to B7-33. It is context for the relaxin pathway being sold as a cardiovascular benefit. Registered as NCT01870778.

Read the original source
Searches, 9 October 2026: no clinical trial and no human data for B7-33

PubMed search record

PubMed search run on 9 October 2026: B7-33 AND relaxin, 11 records. A PubMed search for B7-33 restricted to clinical trial or randomized controlled trial publication types returned 0 records. ClinicalTrials.gov queries for B7-33, B7-33 relaxin and B7-33 peptide run the same day.

The search for B7-33 with relaxin returned 11 records: the design paper, the rodent cardiac, renal and vascular studies, two chemistry papers, a nanoparticle delivery study, a nanovesicle cholangiocarcinoma study, an implant coating study, a mouse pain study and a review. The search restricted to clinical trial or randomized controlled trial publication types returned 0 records, and the ClinicalTrials.gov queries returned no studies. The records reviewed contain no human dose, no human pharmacokinetics, no human safety data and no clinical trial for B7-33.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 9 October 2026
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source

Studies and sources

Design paper: single-chain analogue, three rodent models, receptor selectivity

Animal study

Hossain MA et al. Chem Sci. 2016;7(6):3805-3819. PMID 30155023.

B7-33 is a single-chain analogue built from the B chain only of human gene-2 relaxin (H2 relaxin, the hormone marketed in trials as serelaxin). It binds RXFP1 and preferentially activates the pERK pathway over cAMP in cells that endogenously express RXFP1, which the authors describe as the first functionally selective agonist of that receptor. B7-33 prevented or reversed organ fibrosis and dysfunction in three preclinical rodent models of heart or lung disease with similar potency to H2 relaxin. The mechanism involved activation of RXFP1 and angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 and matrix metalloproteinase-2. Unlike H2 relaxin, B7-33 did not promote prostate tumor growth in vivo. PubChem returned no compound record for B7-33 or related names on 9 October 2026.

Participants / model
Rodent models of heart or lung disease; cells expressing RXFP1
Treatment
Synthetic B7-33 as dosed in the report
Follow-up
not stated in the source
Study design
Original preclinical study with in vitro receptor work
Funding
not stated in the source

The paper is rodent and cell work and reports no human exposure. The prostate tumor observation is a single preclinical result and is not a safety clearance.

Read the original source
Vessel reactivity: Wistar rats 3 hours after one injection, mouse arteries ex vivo

Animal study

Marshall SA et al. Eur J Pharmacol. 2017;807:190-197. PMID 28478069.

Three hours after a tail vein injection in male Wistar rats, B7-33 at 13.3 micrograms/kg and serelaxin at 26.6 micrograms/kg both selectively enhanced bradykinin-mediated endothelium-dependent relaxation in the mesenteric artery by increasing endothelium-derived hyperpolarization, with no overall effect on relaxation in the small renal artery or the aorta. In mouse mesenteric arteries pre-incubated in placental trophoblast conditioned media ex vivo, B7-33 or serelaxin at 15 and 30 nM prevented endothelial dysfunction.

Participants / model
Male Wistar rats; virgin female mouse mesenteric arteries ex vivo
Treatment
Placebo, B7-33 or serelaxin as a single intravenous bolus in rats; bath incubation ex vivo
Follow-up
Vessels assessed 3 hours after the rat injection
Study design
Original preclinical study
Funding
not stated in the source

This is an acute vessel-reactivity result in two arteries of one rodent bed. It is not a blood pressure outcome and not a human result.

Read the original source
Infarct model: CD1 mice, infarct size 21.99% versus 45.32% on vehicle

Animal study

Devarakonda T et al. J Am Heart Assoc. 2020;9(8):e015748. PMID 32295457.

After 30 minutes of left anterior descending artery ligation followed by 24 hours of reperfusion, B7-33 reduced infarct size to 21.99% versus 45.32% with vehicle (P=0.02) and preserved fractional shortening at 29% versus 23% (P=0.02). At 7 days the fractional shortening figures were 29% versus 20%. In isolated adult cardiomyocytes, B7-33 at 50 and 100 nmol/L improved cell survival and reduced expression of the endoplasmic reticulum stress marker GRP78.

Participants / model
Adult male CD1 mice; primary adult mouse cardiomyocytes
Treatment
B7-33 as dosed in the report, after ischemia-reperfusion
Follow-up
24 hours or 7 days of reperfusion
Study design
Original preclinical study
Funding
not stated in the source

Mouse and cell results. No route or dose for the mouse experiment is stated in the information reviewed.

Read the original source
Isoprenaline cardiomyopathy: 129sv mice, fibrosis reduced, blood pressure unchanged

Animal study

Alam F et al. Biomed Pharmacother. 2023;160:114370. PMID 36753958.

Adult male 129sv mice were given isoprenaline at 25 mg/kg/day subcutaneously to induce cardiomyopathy, then treated subcutaneously from days 7 to 14 with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or the ACE inhibitor perindopril 1 mg/kg/day. B7-33 and relaxin equivalently reduced left ventricular fibrosis and normalised inflammation and cardiomyocyte hypertrophy, and restored blood vessel density and aortic contractility. Perindopril lowered systolic blood pressure but did not reduce fibrosis or hypertrophy. The injured mice showed no change in body weight or systolic blood pressure at day 14, so in this experiment B7-33 did not lower blood pressure; the comparator drug did.

Participants / model
Adult male 129sv mice with isoprenaline-induced cardiomyopathy
Treatment
Subcutaneous B7-33, 0.25 mg/kg/day, days 7 to 14
Follow-up
Days 7 to 14 after the start of isoprenaline
Study design
Original preclinical study with an active comparator
Funding
not stated in the source

This is the one study found that measured systolic blood pressure. It tested the blood pressure part of the supplier claim directly and did not support it.

Read the original source
Kidney fibrosis: mice with ureteric obstruction, 7 days, collagen imaging

Animal study

Bhuiyan S et al. FASEB J. 2021;35(5):e21595. PMID 33908676.

In mice with unilateral ureteric obstruction treated for 7 days with relaxin 0.5 mg/kg/day, B7-33 0.25 mg/kg/day, or perindopril 1 mg/kg/day, a second-harmonic generation imaging platform found that the drug-induced prevention of renal fibrosis correlated with significantly reduced collagen fiber thickness and collagen-to-tissue cross reticulation ratio and increased collagen fiber counts. Relaxin or B7-33 treatment also increased renal matrix metalloproteinase-2 and reduced tissue inhibitor of metalloproteinase-1 (all P less than .01 versus obstruction alone).

Participants / model
Mice with surgical unilateral ureteric obstruction
Treatment
B7-33 0.25 mg/kg/day for 7 days; route not stated in the information reviewed
Follow-up
7 days
Study design
Original preclinical imaging-platform study
Funding
not stated in the source

The paper's stated purpose was validating the imaging platform, with the peptides used as reference anti-fibrotic agents.

Read the original source
In vitro serum half-life about 6 minutes; lipidation raised it to 60 minutes

Cell study

Praveen P et al. Int J Mol Sci. 2023;24(7). PMID 37047588.

B7-33 has a short circulation time in vitro in serum, with a half-life of about 6 minutes. Fatty-acid conjugation with an appropriate spacer length raised the in vitro half-life from 6 minutes to 60 minutes. The authors stated that the lead lipidated molecule would be studied in animal models in the future to measure its pharmacokinetic and pharmacodynamic properties, so no animal or human pharmacokinetic profile for plain B7-33 had been published as of that paper.

Participants / model
In vitro serum; no treated organism
Treatment
Synthetic B7-33 and lipidated analogues in serum
Follow-up
not stated in the source
Study design
Original chemistry study from the group that designed the peptide
Funding
not stated in the source

This is a serum value, not an animal or human half-life.

Read the original source
RELAX-AHF-2: 6545 patients, serelaxin, no benefit on either primary endpoint

Randomized controlled trial

Metra M et al. N Engl J Med. 2019;381(8):716-726. PMID 31433919.

Death from cardiovascular causes at 180 days occurred in 285 of 3274 (8.7%) on serelaxin and 290 of 3271 (8.9%) on placebo (hazard ratio 0.98, 95% CI 0.83 to 1.15, P=0.77). Worsening heart failure at day 5 occurred in 227 (6.9%) versus 252 (7.7%) (hazard ratio 0.89, 95% CI 0.75 to 1.07, P=0.19). There were no significant differences in all-cause death at 180 days, the composite of cardiovascular death or rehospitalization, or length of stay, and adverse event incidence was similar.

Participants / model
6545 adults hospitalized for acute heart failure
Treatment
48-hour intravenous infusion of serelaxin (recombinant human relaxin-2) at 30 micrograms per kilogram per day, or placebo
Follow-up
180 days of follow-up for cardiovascular death
Study design
Randomized placebo-controlled phase 3 trial
Funding
not stated in the source

Serelaxin is a different molecule from B7-33, with two chains versus one, and this result does not transfer to B7-33. It is context for the relaxin pathway being sold as a cardiovascular benefit. Registered as NCT01870778.

Read the original source

Why is B7-33 in C tier?

C fits a detailed rodent record with no human data. B7-33 reduced fibrosis in rodent models of heart, kidney and lung injury through a receptor mechanism that was worked out, but no person has a recorded dose, pharmacokinetic profile or outcome. Its parent hormone, serelaxin, missed both primary endpoints in a 6545-patient phase 3 trial, and the blood pressure claim sellers make was not supported in the one experiment that tested it.