What is B7-33?
B7-33 is a synthetic peptide designed to mimic part of a natural hormone called relaxin-2. Relaxin is a hormone your body makes — it's best known for loosening ligaments during pregnancy, but it also plays a big role in reducing scar tissue (fibrosis) and protecting blood vessels. The problem? Natural relaxin has a complicated two-chain structure with three internal bonds, making it expensive and tricky to produce in the lab.[5]
Scientists solved that problem by stripping the molecule down to just the essential working piece — the B-chain — and engineering it into a single, simpler strand called B7-33.[5] Think of it like taking a complicated two-part tool and redesigning it as a single, sleeker instrument that does the same key job. The result is a molecule that's far easier and cheaper to synthesize while still activating the same receptor — called RXFP1 (relaxin family peptide receptor 1).[3]
Important note: B7-33 is a research compound studied in preclinical (animal and cell) models. It is not approved for human use, and nothing here constitutes medical advice.
How B7-33 Works
Your cells have locks called receptors. B7-33 fits into the RXFP1 lock — the same one relaxin uses — and turns on a specific signaling pathway inside the cell involving proteins called ERK 1/2 (extracellular signal-regulated kinases).[2] This is called functionally selective activation: B7-33 doesn't trigger every signal relaxin does, just a targeted subset.
Here's the plain-language version: imagine the receptor as a smart thermostat with many programs. Full relaxin runs all the programs. B7-33 runs just the anti-scarring and vessel-protecting programs — potentially with fewer unwanted side effects.
That targeted ERK 1/2 signal tells cells to calm down the production of excess collagen (the protein that forms scar tissue) and to protect the lining of blood vessels.[2][3]
What the Research Shows
Heart protection and anti-fibrosis after cardiac injury
In a mouse model of heart attack (ischemia-reperfusion injury), B7-33 treatment significantly reduced infarct size — the dead heart tissue area — from roughly 45% of the heart wall down to about 22%.[2] It also preserved how well the heart squeezed (fractional shortening), an important measure of heart function.[2] In cell studies, B7-33 reduced a stress marker called GRP78, suggesting it protects heart muscle cells from a type of cellular stress that occurs during and after a heart attack.[2]
Cardiomyopathy model: faster than a standard drug
In a mouse model of cardiomyopathy (drug-induced heart muscle disease), B7-33 reduced left ventricular fibrosis, calmed inflammation, reversed heart muscle cell enlargement (hypertrophy), and restored blood vessel density — matching the effects of the full relaxin hormone.[3] Compared to perindopril, a widely used ACE inhibitor heart drug, B7-33 reduced fibrosis more rapidly and also tackled hypertrophy — something perindopril failed to do in this model.[3]
Protecting blood vessels
In rat experiments, a single injection of B7-33 enhanced the ability of the mesenteric artery (a gut-supplying blood vessel) to relax in response to bradykinin — a natural vessel-dilating signal.[1] It did this by boosting a mechanism called endothelium-derived hyperpolarization.[1] In a preeclampsia model (a dangerous pregnancy complication involving blood vessel problems), B7-33 prevented the development of endothelial dysfunction when blood vessels were exposed to harmful placental signals.[1]
Reducing scar tissue around implanted devices
When B7-33 was loaded into a biodegradable PLGA polymer coating on implanted devices and placed under mouse skin, the thickness of the fibrotic capsule that formed around the implant was reduced by nearly 50% over six weeks.[4] This matters for medical devices like biosensors and implants, which often get walled off by scar tissue.
Cancer-related fibrosis (emerging research)
A 2025 study engineered nanovesicles carrying B7-33 (alongside anti-angiogenic components) to tackle the dense fibrous tissue that shields bile duct tumors (cholangiocarcinoma) from treatment. The B7-33-carrying nanovesicles disrupted the feedback loop between cancer-associated fibroblasts and tumor blood vessel growth.[6] This is early-stage work, but it shows how B7-33's anti-fibrotic action is being explored beyond heart disease.
What B7-33 Is Being Studied For
- Cardiac fibrosis and adverse remodeling after heart attack or cardiomyopathy[2][3]
- Vascular protection and endothelial function[1]
- Preeclampsia-related endothelial dysfunction[1]
- Foreign body fibrosis around medical implants[4]
- Tumor-associated fibrosis in cancer models[6]
How B7-33 Is Dosed in Research
Doses used in preclinical research vary considerably depending on the model and delivery method — from microgram single boluses for acute vascular studies to daily subcutaneous injections over one to two weeks for cardiac fibrosis models, and even ultra-low doses delivered via nanoparticle systems on a multi-day schedule. Because the right reference point depends entirely on the study design being replicated, researchers should consult the dosage chart on this page for a full breakdown of the specific amounts and schedules used across published studies, and use the calculator to work out weight-adjusted amounts where applicable.
Mixing and Storing B7-33
B7-33 is a peptide, which means it comes as a delicate powder that must be handled carefully. For reconstitution, researchers typically dissolve the lyophilized (freeze-dried) powder in a mild buffer — sterile water or a dilute acetic acid solution (such as 20 mM sodium acetate, as used in published studies[1]) is common. Add the solvent slowly down the side of the vial and gently swirl — never shake vigorously, as peptides can break down. Once dissolved, aliquot into smaller portions to avoid repeated freeze-thaw cycles, which degrade the peptide over time. Store unused powder at −20 °C or colder, away from light and moisture. Reconstituted solution should be kept at 4 °C and used promptly, typically within a few days. Always check the supplier's certificate of analysis for purity and specific storage recommendations before beginning any experiment.
Sources
- B7-33 replicates the vasoprotective functions of human relaxin-2 (serelaxin). — European journal of pharmacology, 2017. PMID 28478069.
- B7-33, a Functionally Selective Relaxin Receptor 1 Agonist, Attenuates Myocardial Infarction-Related Adverse Cardiac Remodeling in Mice. — Journal of the American Heart Association, 2020. PMID 32295457.
- 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. — Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023. PMID 36753958.
- Coatings Releasing the Relaxin Peptide Analogue B7-33 Reduce Fibrotic Encapsulation. — ACS applied materials & interfaces, 2019. PMID 31713411.
- Single chain peptide agonists of relaxin receptors. — Molecular and cellular endocrinology, 2019. PMID 30641102.
- Dual-functional nanovesicles simultaneously inhibit stromal fibrosis and angiogenesis to suppress cholangiocarcinoma progression. — Journal of nanobiotechnology, 2025. PMID 41430305.