B7-33

Dosing from the Literature

Published for scarring (fibrosis): animal doses only — in mice 0.25 mg/kg a day from an implanted pump or into the nose, and 0.25 mg/kg twice a day into the belly; in rats 0.5 mg/kg a day from an implanted pump (Hossain et al., 2016; Devarakonda et al., 2020). Not published: any dose given to a person, and any study in tendon, ligament or gut tissue.

No person has been given B7-33 in a published study (PubMed and Europe PMC, searched October 4, 2026). The table records what each animal study gave, with its species; these are animal doses, not recommendations. The research-chemical listing read for this page gives vial sizes — 1 mg and 2 mg of powder — and the words “for qualified laboratory research only”; it states no amount for a person.

What It Is

B7-33 is a synthetic peptide of 27 amino acids cut from one half of a hormone. Human relaxin-2 — called H2 relaxin in the literature — is built like insulin: two chains, A and B, held together by three disulfide bonds. B7-33 is the B chain alone, shortened: residues 7 to 29, plus the four residues KRSL that sit at positions 30 to 33 of the hormone’s longer B1-33 isoform (Handley et al., 2023). Its designers made two further changes. They cut six residues off the front because the full B chain is insoluble in water and inactive, and they replaced the cysteines at B-chain positions 11 and 23 with serines, which stopped the single chain from pairing up with itself and left a peptide that dissolves freely at 4 mg/mL (Hossain et al., 2016). It is made with a C-terminal amide; its mass is 2,986.5 and its formula C₁₃₁H₂₂₉N₄₁O₃₆S (PubChem CID 162662592), and the first paper’s batch was 97% pure by HPLC with a measured mass of 2986.4 as the protonated ion (Hossain et al., 2016).

The point of building it was cost and side-effects. Relaxin’s recombinant form, serelaxin, needs two chains assembled separately, four reactions to place its disulfide bonds and six purification steps; B7-33 is assembled in one piece on resin and purified once (Hossain et al., 2016). The second reason was the hormone’s cAMP signalling, which has been linked to tumour growth, so the designers looked for a peptide that would drive the ERK1/2 arm instead (Hossain et al., 2016; Handley et al., 2023). The animal work in that first paper was approved by the Florey Institute’s and Monash University’s animal ethics committees in Melbourne (Hossain et al., 2016).

What happened to the parent hormone matters for reading this page. Serelaxin was given as a 48-hour infusion, 30 µg/kg a day, to 6,545 patients hospitalised with acute heart failure in the RELAX-AHF-2 trial: cardiovascular death at 180 days was 8.7% against 8.9% on placebo, and worsening heart failure at day 5 was 6.9% against 7.7% — neither endpoint was met (Metra et al., 2019). No relaxin product appears in Drugs@FDA: openFDA returns no application for serelaxin or for relaxin (read October 4, 2026). B7-33’s own first paper, written in 2016, describes relaxin as having had “clinical evaluation and provisional FDA approval” for acute heart failure (Hossain et al., 2016); Drugs@FDA holds nothing of the kind, and the trial meant to confirm the hormone’s benefit reported none three years later (Metra et al., 2019).

PubMed returns 15 records for “B7-33” (October 4, 2026); 12 are about this peptide, and the other three are about HLA-B7 antigens or a liver-cancer paper that matches the string. Europe PMC returns 42 for “B7-33” with relaxin. The field moved past it: Sanofi chemists trimmed and lipidated the relaxin B chain into longer-acting single-chain agonists with subcutaneous bioavailability (Mallart et al., 2021; Illiano et al., 2022), and AstraZeneca took a long-acting relaxin receptor agonist, AZD3427, through a Phase 1 study in 105 healthy volunteers and heart-failure patients that finished in September 2022 (ClinicalTrials.gov NCT04630067; Wołowiec et al., 2025). B7-33 itself has never been in a registered trial, and its own designers wrote in 2023 that it “remains the minimal active sequence” they could reach (Handley et al., 2023).

Mechanism of Action

Every finding below is from cells, isolated tissue or rodents, and most of it comes from the Melbourne group that designed the peptide (Hossain et al., 2016). None of it has been measured in a person.

• RXFP1, the relaxin receptor — weak binding — In HEK-293T cells engineered to overexpress human RXFP1, B7-33 competed with labelled relaxin but bound far more weakly: pKi 5.54 ± 0.13 (n = 5) against 8.96 ± 0.03 for the hormone (Hossain et al., 2016). It did not activate the related receptor RXFP2 even at micromolar concentrations (Hossain et al., 2016). In cells carrying an engineered form of the receptor — its outer domain alone, anchored to the membrane — binding was much stronger. Cutting two more residues off the tail was tolerated; cutting four dropped the binding sharply, and taking two residues off the front reduced it as well, which is why its designers write that B7-33 “remains the minimal active sequence” (Handley et al., 2023).
• cAMP versus ERK1/2 — the “biased” part — In the same overexpressing cells its cAMP potency was weak (pEC50 5.12 ± 0.06 against 10.49 ± 0.13 for relaxin), and weak again in human THP-1 cells that carry RXFP1 naturally. But in rat renal myofibroblasts, which also carry the receptor naturally, B7-33 raised ERK1/2 phosphorylation with much the same potency and efficacy as relaxin, peaking at 5–10 minutes (Hossain et al., 2016). That split — ERK1/2 without much cAMP — is what “functionally selective” means on this page.
• MMP-2, a collagen-degrading enzyme — Over 72 hours in culture, 30 nM (about 180 ng/mL) in human cardiac fibroblasts and 16.8 nM (about 100 ng/mL) in rat renal myofibroblasts raised MMP-2 as much as relaxin at matched concentrations (both P < 0.01 against untreated cells). In the rat myofibroblasts an RXFP1 antagonist blocked it, and so did the angiotensin II type 2 receptor blocker PD123319, which the authors read as the two receptors working as a pair (Hossain et al., 2016).
• TGF-β1 and scar-cell differentiation — In BJ3 human skin fibroblasts, TGF-β1 at 2 ng/mL raised α-smooth-muscle actin, the marker of a scar-forming myofibroblast, about 4 to 4.5-fold over 72 hours; B7-33 at 100 ng/mL almost entirely suppressed that rise at 72 hours, and the suppression was gone by day 5 to 14 — the peptide ran out (Praveen et al., 2023).
• Endoplasmic-reticulum stress in heart cells — In mouse primary cardiomyocytes, 100 nmol/L B7-33 lowered the stress marker GRP78 after tunicamycin, and blocking ERK1/2 with PD98059 abolished that effect, tying the protection to the same pathway (Devarakonda et al., 2020).
• How long it lasts — In human serum in a tube, B7-33 was half gone in 6 minutes; a fatty-acid-conjugated version lasted 60 minutes (Praveen et al., 2023). A 2025 cardiology review nonetheless lists B7-33 among “long-acting relaxin analogues” (Wołowiec et al., 2025); its developers’ own measurement is the 6 minutes.

What the Research Shows

The results below come from animal work. The next section covers what exists in humans.

• Rat heart failure after an infarct — Eight weeks after a coronary artery was tied off, Sprague-Dawley rats got 0.5 mg/kg a day from an osmotic pump in the belly for 28 days. Left-ventricular collagen fell against saline (P < 0.01), as it did with relaxin, and left-ventricular end-diastolic pressure fell (P < 0.05) (Hossain et al., 2016).
• Mouse cardiomyopathy — In 129SV mice given isoprenaline, 0.25 mg/kg a day for 14 days cut interstitial left-ventricular collagen by about 51% and total collagen by about 47% (both P < 0.01 against isoprenaline alone), with no change in systolic blood pressure (Hossain et al., 2016). The same group repeated the model in 2023 with an ACE inhibitor as comparator: B7-33 and relaxin equally reduced fibrosis and normalised inflammation and cardiomyocyte enlargement by day 14, while perindopril lowered blood pressure and inflammation but not fibrosis or enlargement (Alam et al., 2023).
• Mouse airway disease — In Balb/c mice with nine weeks of ovalbumin-induced allergic airways disease, 0.25 mg/kg a day into the nose for two weeks reversed airway epithelial thickening (P < 0.001 against ovalbumin alone), brought total lung collagen back to control levels, and partly reduced airway hyperresponsiveness — which still stayed above the saline controls (Hossain et al., 2016).
• Mouse kidney scarring — In mice with one ureter tied off for seven days, 0.25 mg/kg a day left thinner collagen fibres and a lower collagen-to-tissue cross-reticulation ratio on a stain-free imaging platform — though collagen fibre counts went up — with more kidney MMP-2 and less TIMP-1 (MMP-2 and TIMP-1 both P < 0.01 against injury alone); ordinary stains could not see the fibre differences (Bhuiyan et al., 2021).
• Mouse heart attack, a different laboratory — A group funded by the NIH, with two of the peptide’s designers among its authors, gave CD1 mice 0.25 mg/kg into the belly five minutes before reperfusion, then twice daily. At 24 hours the infarct was 21.99 ± 7.17% of the at-risk area (n = 7) against 45.32 ± 5.28% on saline (n = 8), and fractional shortening was 29.57 ± 1.74% against 23.34 ± 1.84% (Devarakonda et al., 2020).
• Fibrous capsules around implants — A biodegradable PLGA coating that released B7-33 was put on polypropylene and implanted under the skin of mice; after six weeks the collagen capsule around it was 49.2% thinner than around the same coating without the peptide (Welch et al., 2019).
• Pain, injected into the brain — A single injection into a brain ventricle raised mechanical and heat pain thresholds back to baseline 30 minutes later in mice with an inflamed paw; the effect was gone at one hour, and an RXFP1 blocker prevented the mechanical part but not the heat part (Abboud et al., 2021).
• Rat preeclampsia models — a conference abstract — In the first of two models, 8 rats per group got B7-33, a B7-33-Fc fusion or an albumin conjugate into a vein twice weekly on gestational days 10 to 20; mean arterial pressure, TNF-α and sFlt-1 came back to normal-pregnancy levels on B7-33 and on the Fc fusion. In the second model only the Fc fusion was given, into the belly. This is a 2026 Society for Maternal-Fetal Medicine oral abstract with no dose stated and no full paper (Terry et al., 2026).
• Swallowed, it did nothing on its own — Given by gavage to mice with established cardiomyopathy, 25 ng a day of the free peptide every 72 hours for four weeks had no effect; the same dose bound to glycine-coated iron-oxide nanoparticles normalised heart fibrosis and beat perindopril (Somanader-Livera et al., 2025).
• Tumour models, as a conjugate — A group with none of the peptide’s designers among its authors attached B7-33 to endothelial-cell nanovesicles to quiet tumour-associated fibroblasts; in mouse bile-duct cancer grafts the particles inhibited tumour growth by 67.7 ± 17.6% against saline (p < 0.001) (Zhang et al., 2025). The peptide alone was not the treatment tested.
• The prostate-tumour check — Relaxin at 0.15 mg/kg a day enlarged mouse prostate tumours by more than 150% (P < 0.001); B7-33 at an equivalent 0.075 mg/kg a day, and at the higher 0.25 mg/kg a day, did not (n = 6 per dose) (Hossain et al., 2016).

Human Data

There is none. No published study has given B7-33 to a person, and ClinicalTrials.gov returns no record for it at all — not completed, not recruiting, not withdrawn (searched October 4, 2026, together with PubMed and Europe PMC).

• No trial, ever — A search of ClinicalTrials.gov for “B7-33” returns zero studies (October 4, 2026). The registered relaxin-receptor trials are other molecules: AZD3427, a long-acting agonist, in 105 healthy volunteers and heart-failure patients, completed September 2022 (NCT04630067; Wołowiec et al., 2025).
• Human cells, not humans — The human data are in dishes: MMP-2 raised in human cardiac fibroblasts at 30 nM, weak cAMP in human THP-1 cells (Hossain et al., 2016), α-smooth-muscle actin suppressed in human skin fibroblasts at 100 ng/mL (Praveen et al., 2023), and a 6-minute half-life in human serum (Praveen et al., 2023).
• What reached patients was the hormone — Serelaxin, recombinant relaxin-2, was infused at 30 µg/kg a day for 48 hours into 6,545 patients hospitalised with acute heart failure. Cardiovascular death at 180 days: 8.7% against 8.9% on placebo (hazard ratio 0.98). Worsening heart failure at day 5: 6.9% against 7.7% (hazard ratio 0.89). Neither primary endpoint was met, and adverse events were similar in both groups (Metra et al., 2019).
• No safety record of its own — Because no person has taken it, there is no adverse-event list, no dose-finding study, no measurement of how much of an injected dose reaches the blood, and no pharmacokinetics in any species (PubMed and Europe PMC, searched October 4, 2026).

The evidence meter on the B7-33 card reads “Animal only”, the second of its five levels: it counts published human data on the compound itself, and there is none. The animal work is not thin — three disease models and a prostate-tumour check in the first paper (Hossain et al., 2016), and eight further animal studies since — but it is animal work.

Reconstitution & Storage

No label and no trial document exists for B7-33, so there is nothing official to mix or store. What the published studies describe is laboratory handling: the peptide was made by solid-phase synthesis as a C-terminal amide, purified by reverse-phase HPLC to 97%, and dissolved in water, where it is freely soluble at 4 mg/mL — the un-substituted relaxin B chain is not soluble at all (Hossain et al., 2016).

• How the studies delivered it — Implanted osmotic mini-pumps for continuous dosing over 8 to 28 days, injections into the belly or a tail vein, and nose drops at 0.4 mg/mL for the airway model (Hossain et al., 2016; Marshall et al., 2017; Devarakonda et al., 2020). The pumps deliver continuously; its developers write that B7-33’s half-life in the body is expected to be shorter than relaxin’s roughly ten minutes, and they measured 6 minutes in human serum in a tube (Praveen et al., 2023).
• Storage and stability — No peer-reviewed study gives storage conditions, a shelf life, or stability data for B7-33 powder or for a mixed solution. The only published stability figure is that serum half-life (Praveen et al., 2023).
• Identity — B7-33’s mass is 2,986.5 and its formula C₁₃₁H₂₂₉N₄₁O₃₆S (PubChem CID 162662592); relaxin-2 itself is about twice that, roughly 6 kDa (Somanader-Livera et al., 2025). COA Check is this site’s reader for lab reports.
• What is sold — Powder vials: 1 mg and 2 mg from a research-chemical seller, 1 mg and 5 mg from a reagent catalogue that states 99.31% purity (listings read October 4, 2026). No published study has tested any sold product, and the seller listing read for this page linked no lab report at all.

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Side Effects & Risks

• No human safety data — There is no adverse-event list for B7-33, because there is no human exposure on record (PubMed, Europe PMC and ClinicalTrials.gov, searched October 4, 2026).
• What the animal studies did and did not report — The rodent papers report efficacy outcomes, not formal safety assessments. Two measurements are worth naming: systolic blood pressure was unchanged in the mouse cardiomyopathy model at 0.25 mg/kg a day (Hossain et al., 2016), and in the infarct study mice were given twice-daily 0.25 mg/kg injections for up to 7 days with no adverse effect reported (Devarakonda et al., 2020). No study has looked for organ toxicity, immune reactions or antibodies against the peptide.
• The tumour question, which is why it exists — Relaxin’s strong cAMP signalling has been linked to tumour promotion, and that is the side-effect its designers were working around (Hossain et al., 2016; Handley et al., 2023). Their test was direct: relaxin at 0.15 mg/kg a day enlarged mouse prostate tumours by more than 150%, B7-33 at 0.075 or 0.25 mg/kg a day did not (Hossain et al., 2016). One mouse model is not a clearance for a person, and the later Sanofi analogues regained cAMP potency, which the Melbourne group flagged as a risk of that approach (Handley et al., 2023).
• It is a vasodilator’s fragment — Relaxin-2 is a vasodilator hormone (Metra et al., 2019); in rats a single 13.3 µg/kg dose of B7-33 into a vein changed artery responses measured three hours later (Marshall et al., 2017), and in a rat preeclampsia model it lowered mean arterial pressure (Terry et al., 2026). What it does to a person’s blood pressure at any dose has not been studied.
• Pregnancy — The only pregnancy data are the rat preeclampsia abstract, which gave it to pregnant rats from gestational day 10 (Terry et al., 2026). No reproductive toxicology study of B7-33 was found, and the abstract has not appeared as a full paper.
• Product identity — B7-33 as its designers made it carries two serine substitutions and a C-terminal amide (Hossain et al., 2016), and the reagent listing read for this page prints that same sequence (read October 4, 2026). Its mass is 2,986.5 (PubChem CID 162662592).
• WADA — B7-33 is not named on the 2026 Prohibited List, and no section of the List names relaxin or its analogues. Section S0 prohibits at all times substances not addressed elsewhere on the List “with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued…)” (World Anti-Doping Agency, 2026). No approval of B7-33 turned up for this page, so S0 applies.

Bloodwork & Monitoring

No monitoring guidance for B7-33 has been published, and no trial has measured anything in a person taking it. The animal studies measured these:

• Scar tissue in the organ itself — Picrosirius-red and Masson’s-trichrome staining of heart, lung and kidney sections, hydroxyproline for total collagen, and a stain-free second-harmonic imaging platform for collagen fibre thickness (Hossain et al., 2016; Bhuiyan et al., 2021).
• Heart function — Left-ventricular end-diastolic pressure in rats, echocardiographic fractional shortening and chamber diameter in mice, and systolic blood pressure by tail cuff (Hossain et al., 2016; Devarakonda et al., 2020).
• Collagen turnover — MMP-2 by gelatin zymography in cells and tissue, and TIMP-1 in the kidney (Hossain et al., 2016; Bhuiyan et al., 2021).
• Inflammation and pregnancy markers — TNF-α, sFlt-1, proteinuria and mean arterial pressure in the rat preeclampsia abstract (Terry et al., 2026).
• Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

Nothing: in every published study B7-33 was given alone against a vehicle, or compared with relaxin or the ACE inhibitor perindopril in separate arms, which is a comparison rather than a combination (Hossain et al., 2016; Alam et al., 2023). No study has tested B7-33 together with another compound on this site — searches of PubMed and Europe PMC on October 4, 2026 for B7-33 with BPC-157, TB-500, GHK-Cu or KPV return no study of any pair.

A 2023 review lists B7-33 among anti-fibrotic peptides alongside others (Liu et al., 2023); a review that prints compounds side by side is not evidence that anyone has combined them.

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Legal Status

Related Compounds

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References

1. Hossain MA, Kocan M, Yao ST, Royce SG, Nair VB, Siwek C, Patil NA, Harrison IP, Rosengren KJ, Selemidis S, Summers RJ, Wade JD, Bathgate RAD, Samuel CS. A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor, RXFP1. Chem Sci. 2016;7(6):3805-3819. PMID: 30155023. DOI: 10.1039/c5sc04754d. (Full text at PMC6013806, read October 4, 2026: design, serine substitutions, 97% purity, m/z 2986.4 [M + H]+, binding and signalling data, and the four animal models.)
2. Handley TNG, Praveen P, Tailhades J, Wu H, Bathgate RAD, Hossain MA. Further Developments towards a Minimal Potent Derivative of Human Relaxin-2. Int J Mol Sci. 2023;24(16):12670. PMID: 37628851. DOI: 10.3390/ijms241612670.
3. Praveen P, Wang C, Handley TNG, Wu H, Samuel CS, Bathgate RAD, Hossain MA. A Lipidated Single-B-Chain Derivative of Relaxin Exhibits Improved In Vitro Serum Stability without Altering Activity. Int J Mol Sci. 2023;24(7):6616. PMID: 37047588. DOI: 10.3390/ijms24076616.
4. Praveen P, Kocan M, Valkovic A, Bathgate R, Hossain MA. Single chain peptide agonists of relaxin receptors. Mol Cell Endocrinol. 2019;487:34-39. PMID: 30641102. DOI: 10.1016/j.mce.2019.01.008.
5. Marshall SA, O’Sullivan K, Ng HH, Bathgate RAD, Parry LJ, Hossain MA, Leo CH. B7-33 replicates the vasoprotective functions of human relaxin-2 (serelaxin). Eur J Pharmacol. 2017;807:190-197. PMID: 28478069. DOI: 10.1016/j.ejphar.2017.05.005.
6. Devarakonda T, Mauro AG, Guzman G, Hovsepian S, Cain C, Das A, Praveen P, Hossain MA, Salloum FN. B7-33, a Functionally Selective Relaxin Receptor 1 Agonist, Attenuates Myocardial Infarction-Related Adverse Cardiac Remodeling in Mice. J Am Heart Assoc. 2020;9(8):e015748. PMID: 32295457. DOI: 10.1161/JAHA.119.015748.
7. Bhuiyan S, Shen M, Chelvaretnam S, Tan AY, Ho G, Hossain MA, Widdop RE, Samuel CS. Assessment of renal fibrosis and anti-fibrotic agents using a novel diagnostic and stain-free second-harmonic generation platform. FASEB J. 2021;35(5):e21595. PMID: 33908676. DOI: 10.1096/fj.202002053RRR.
8. Alam F, Gaspari TA, Kemp-Harper BK, Low E, Aw A, Ferens D, Spizzo I, Jefferis AM, Praveen P, Widdop RE, Bathgate RAD, Hossain MA, Samuel CS. 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. Biomed Pharmacother. 2023;160:114370. PMID: 36753958. DOI: 10.1016/j.biopha.2023.114370.
9. Welch NG, Mukherjee S, Hossain MA, Praveen P, Werkmeister JA, Wade JD, Bathgate RAD, Winkler DA, Thissen H. Coatings Releasing the Relaxin Peptide Analogue B7-33 Reduce Fibrotic Encapsulation. ACS Appl Mater Interfaces. 2019;11(49):45511-45519. PMID: 31713411. DOI: 10.1021/acsami.9b17859.
10. Abboud C, Brochoire L, Drouet A, Hossain MA, Hleihel W, Gundlach AL, Landry M. Analgesic effect of central relaxin receptor activation on persistent inflammatory pain in mice: behavioral and neurochemical data. Pain Rep. 2021;6(2):e937. PMID: 34159282. DOI: 10.1097/PR9.0000000000000937.
11. Somanader-Livera DVN, Wei C, Wang C, Li Y, Ferens D, Salimova E, Selomulya C, Hossain MA, Samuel CS, Chakraborty A. Immune cell uptake of glycinated nanoparticles conjugated to anti-fibrotic peptides enables their prolonged activity and oral administration. J Biomed Sci. 2025;32(1):104. PMID: 41382190. DOI: 10.1186/s12929-025-01198-8.
12. Zhang L, Duan X, Shi Q, Yao X, Chen Q, Wan J, Wang F, Ni C, Li Y, Wang M, Sheng Y, Zheng W, Liu J, Ji T, Qin Z. Dual-functional nanovesicles simultaneously inhibit stromal fibrosis and angiogenesis to suppress cholangiocarcinoma progression. J Nanobiotechnology. 2025;23(1):781. PMID: 41430305. DOI: 10.1186/s12951-025-03833-w.
13. Mallart S, Ingenito R, Bianchi E, Bresciani A, Esposito S, Gallo M, Magotti P, Monteagudo E, Orsatti L, Roversi D, Santoprete A, Tucci F, Veneziano M, Bartsch R, Boehm C, Brasseur D, Bruneau P, Corbier A, Froissant J, Gauzy-Lazo L, Gervat V, Marguet F, Menguy I, Minoletti C, Nicolas MF, Pasquier O, Poirier B, Raux A, Riva L, Janiak P, Strobel H, Duclos O, Illiano S. Identification of Potent and Long-Acting Single-Chain Peptide Mimetics of Human Relaxin-2 for Cardiovascular Diseases. J Med Chem. 2021;64(4):2139-2150. PMID: 33555858. DOI: 10.1021/acs.jmedchem.0c01533.
14. Illiano S, Poirier B, Minoletti C, Pasquier O, Riva L, Chenede X, Menguy I, Guillotel M, Prigent P, Le Claire S, Gillot F, Thill G, Lo Presti F, Corbier A, Le Bail JC, Grailhe P, Monteagudo E, Ingenito R, Bianchi E, Philippo C, Duclos O, Mallart S, Bathgate R, Janiak P. Characterization of a new potent and long-lasting single chain peptide agonist of RXFP1 in cells and in vivo translational models. Sci Rep. 2022;12(1):20435. PMID: 36443381. DOI: 10.1038/s41598-022-24716-2.
15. Metra M, Teerlink JR, Cotter G, Davison BA, Felker GM, Filippatos G, Greenberg BH, Pang PS, Ponikowski P, Voors AA, et al. Effects of Serelaxin in Patients with Acute Heart Failure. N Engl J Med. 2019;381(8):716-726. PMID: 31433919. DOI: 10.1056/NEJMoa1801291.
16. Wołowiec Ł, Jaśniak A, Osiak-Gwiazdowska J, Czaplińska D, Szymczak A, Pęcherz JA, Grześk G. Long-acting relaxin analogues: a novel tool in cardiology. Front Pharmacol. 2025;16:1626469. PMID: 40832606. DOI: 10.3389/fphar.2025.1626469.
17. Terry RM, Pantho AF, Harris MN, Kelso KR, Vora N, Amaral LM, Villazana-Kretzer D, Kuehl T, LaMarca B, Uddin MN. Efficacy of Novel Peptide B7-33 in Attenuating Preeclampsia Symptoms: Preclinical Study in Rat Models. Oral abstract 79, Society for Maternal-Fetal Medicine 2026 Pregnancy Meeting, in “Oral Concurrent Session 7 – Basic and Translational Science: Friday, February 13, 2026, 8:00 AM – 10:00 AM.” Pregnancy (Hoboken). 2026;2(Suppl 1):e70155. PMCID: PMC13344715. Read October 4, 2026. (Conference abstract; no dose stated, no full paper.)
18. Yuan S, Guo D, Liang X, Zhang L, Zhang Q, Xie D. Relaxin in fibrotic ligament diseases: Its regulatory role and mechanism. Front Cell Dev Biol. 2023;11:1131481. PMID: 37123405. DOI: 10.3389/fcell.2023.1131481. (The hormone, not B7-33.)
19. Liu Z, Zhang X, Wang Y, Tai Y, Yao X, Midgley AC. Emergent Peptides of the Antifibrotic Arsenal: Taking Aim at Myofibroblast Promoting Pathways. Biomolecules. 2023;13(8):1179. PMID: 37627244. DOI: 10.3390/biom13081179. (Erratum: Biomolecules. 2024;14(4):407. PMID: 38672525.)
20. National Library of Medicine. PubChem: CID 162662592 (C131H229N41O36S, 2,986.5 g/mol; CAS 1818415-56-3; synonyms are supplier catalogue codes). pubchem.ncbi.nlm.nih.gov. Read October 4, 2026.
21. FDA. Drugs@FDA through openFDA (api.fda.gov/drug/drugsfda.json): searches for B7-33, serelaxin and relaxin, October 4, 2026 — no applications. National Drug Code Directory through openFDA (api.fda.gov/drug/ndc.json): searches for B7-33 and relaxin, October 4, 2026 — no listings.
22. Code of Federal Regulations. 21 CFR 216.23 (bulk drug substances that can be used under section 503A) and 21 CFR 216.24 (drug products withdrawn or removed for safety or effectiveness). ecfr.gov. Read October 4, 2026 — neither names B7-33 or relaxin.
23. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated May 14, 2026. fda.gov/media/94155/download.
24. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503B of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated March 21, 2025. fda.gov/media/94164/download.
25. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances; S2, peptide hormones, growth factors, related substances and mimetics (neither relaxin nor its analogues is named). wada-ama.org.
26. ClinicalTrials.gov. Searches for “B7-33” (no records) and “relaxin” (40 records, none of B7-33), October 4, 2026; record of AZD3427, NCT04630067 (AstraZeneca, Phase 1, 105 participants, completed September 14, 2022). clinicaltrials.gov, API v2.
27. Searches of October 4, 2026: PubMed, “B7-33” (15 records; 12 about this peptide, the others about HLA-B7 antigens or an unrelated liver-cancer paper); Europe PMC, “B7-33” with relaxin (42 records) and with BPC-157, TB-500, GHK-Cu or KPV (no study of a combination), with tendon, ligament, gut, intestine or colitis terms (no study of B7-33 in those tissues), and with toxicology, drug-interaction and pregnancy terms (no toxicology or drug-interaction study of B7-33; in pregnancy only the 2026 conference abstract); ClinicalTrials.gov, “B7-33” (no records); FDA warning letters and import alerts, web search for B7-33 (no document naming it); reagent and research-chemical listings of B7-33 powder, read as data (sellers not named).

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