The synthetic peptide B7-33 is intended to simulate the effects of the peptide hormone relaxin in research studies. Relaxin hormone, along with its g protein-coupled receptor RXFP1, is present in the aorta, small renal arteries, and mesenteric arteries, among other blood vessels. The potential variability in RXFP1 localization between arteries and veins and human umbilical vein and artery endothelial and vascular smooth muscle cells contributes to the variation in relaxin-RXFP1 signaling pathways. Treatment with recombinant human relaxin 2 (H2 relaxin or serelaxin) has been shown in prior research to have vasoprotective effects, including the reduction of myogenic reactivity and the enhancement of endothelium-dependent relaxation in various arteries.
However, its complex structure hinders the clinical application of serelaxin by restricting production and affordability. A single-B-chain relaxin mimetic, denoted as B7-33, was synthesized to address this challenge. Although B7-33 functions as a weak agonist of RXFP1, its potency is comparable to that of serelaxin. Furthermore, it has been shown that chronic administration of B7-33 may reduce organ fibrosis and dysfunction in rodent models of cardiovascular or pulmonary disease. [R]
Despite its longstanding clinical use and efficacy in correcting subclinical states, there is a lack of comprehensive understanding regarding the full spectrum of effects exerted by B7-33. This product was made by BehemothLabz to help researchers learn more about the effects of these compounds, not for human use.
What is B7-33?
B7-33, an innovative derivative of the relaxin family peptides, stands out for its unique structural composition. In its design, the focus zeroed in on the B-chain, known for its involvement in high-affinity binding. The initial challenge of creating a single-chain peptide was overcome by strategically truncating the N-terminal and elongating the C-terminal of the B-chain, resulting in the soluble and active peptide known as B7-33.[R]
This structurally refined peptide demonstrated distinct behavior in various cellular contexts. While proving to be a weak agonist in cells with RXFP1 overexpression, B7-33 showcased robust efficacy in rat renal myofibroblasts and human cardiac fibroblasts—both native RXFP1-expressing cells. Particularly noteworthy was its ability to match the potency of H2 relaxin in promoting matrix metalloproteinase 2, a pivotal collagen-degrading enzyme. In vivo experiments in rat and mouse models further underscored B7-33’s capabilities, revealing its potential to reverse lung and heart fibrosis and establishing it as a potent functionally selective agonist in rodent systems. Beyond its therapeutic promise for fibrosis and related disorders, B7-33’s specific activation of ERK phosphorylation in fibroblasts points to a nuanced understanding of its actions, marking it as a lead molecule with profound implications for unraveling relaxin’s mechanisms in specific cell types.[R]
How Does B7-33 Work?
B7-33, a synthetic variant of the B-chain of relaxin, functions by interacting with the relaxin family peptide receptor 1 (RXFP1), a receptor involved in cellular signaling. In simpler terms, it’s like B7-33 has a key that fits into a specific lock on the surface of cells. Unlike traditional relaxin, B7-33 activates a signaling pathway called Erk 1/2 without triggering another pathway known as cAMP in fibroblasts, which are a type of cell. To put it simply, it influences certain cell activities without setting off potentially harmful responses observed in heart failure.
This unique mechanism is important because it avoids the negative effects associated with cAMP signaling, commonly seen in heart issues. By activating Erk 1/2, B7-33 follows a strategy known to reduce the size of damaged heart tissue and prevent cell death during the reperfusion phase, which is when blood flow is restored after a heart attack.[R]
B7-33 Peptides Benefits
Below are other research-based additional potential benefits B7-33 brings:
B7-33 and Vasoprotective Properties
B7-33 peptide emerges as a potential cost-effective breakthrough in cardiovascular research, holding immense promise for addressing vascular challenges. In a comparative study with serelaxin, B7-33 showcased its potential therapeutic effects in heart failure and fibrosis. The study, conducted on male Wistar rats, revealed that an acute bolus injection of B7-33 selectively enhanced bradykinin-mediated endothelium-dependent relaxation in the rat mesenteric artery, highlighting its vasoprotective properties.[R]
Further research in this area of the cardiovascular system could explore the binding affinity of this endogenous relaxin protein to anti-fibrotic effects, and acute and chronic diseases.
B7-33 and Preeclampsia
In a study similar to the one previously referenced, substantial advancements were observed in the battle against preeclampsia, a disorder characterized by high blood pressure during pregnancy. through the administration of B7-33 peptide. Utilizing experiments carried out on the mesenteric arteries of virgin female mice, B7-33 successfully inhibited endothelial dysfunction brought about by placental trophoblast-conditioned media—a distinctive attribute associated with preeclampsia. By emulating the immediate vascular benefits observed with serelaxin, equimolar doses of B7-33 also demonstrated a preventive effect against endothelial dysfunction. The findings of this study indicate that B7-33 may have the potential to be a viable and significant therapeutic option, with a specific focus on addressing the complexities of preeclampsia. This creates opportunities for additional investigation and potential interventions in the critical field of cardiovascular health.[R]
In another study, researchers looked into how B7-33 peptide might help treat preeclampsia. The research was mostly about marinobufagenin (MBG) and how it affects cytotrophoblast (CTB) cells. It showed that MBG makes CTB cells work less well. The study used B7-33 as a cheaper alternative to H2 relaxin and found that it helped CTBs recover from malfunction caused by MBG. This suggests that B7-33 could be used to prevent preeclampsia. The results make it clear that more research needs to be done on B7–33 to see how it can help with the complicated problem of preeclampsia.[R]
B7-33 and Post-Myocardial Infarction
The effects of B7-33 administration following ischemia-reperfusion injury in adult male CD1 mice were found to be remarkable. Compared to the control group, the peptide reduced infarct size by nearly half, demonstrating its acute cardioprotective properties. The results of the echocardiography demonstrated that B7-33 not only maintained fractional shortening but also significantly enhanced cardiac function, a benefit that endured even seven days after the myocardial infarction.
Additional knowledge was acquired via in vitro investigations involving primary cardiomyocytes, in which B7-33 demonstrated a protective effect against a simulated ischemia-reperfusion injury. In addition to improving cellular viability, the peptide reduced endoplasmic reticulum stress, an essential element for cardiac well-being. Significantly, it was discovered that the effects of B7-33 are reliant on the extracellular signal-regulated kinase 1/2 pathway, underscoring the targeted and advantageous mechanisms by which it operates. In summary, B7-33 demonstrates great potential to provide acute cardioprotection, and restrict detrimental remodeling after myocardial infarction by targeting cardiomyocyte demise and endoplasmic reticulum stress, all while maintaining optimal cardiac functionality.[R]
B7-33 and Reduction of Foreign Body Response
In the realm of medical research, the potential benefits of B7-33 peptide shine in addressing the challenges posed by the foreign body response (FBR). This natural relaxin peptide analogue has shown promising results in reducing organ fibrosis in animal models. Utilizing a biodegradable polymer, poly(lactic-co-glycolic) acid (PLGA), as a coating allows for the sustained release of B7-33. Through careful in vitro studies, the controlled release of this antifibrotic peptide from PLGA coatings has been confirmed. Notably, when subcutaneously implanted in mice, PLGA-coated polypropylene samples, with and without B7-33, demonstrated a substantial 49.2% reduction in capsule thickness over 6 weeks. This underscores the potential of B7-33 to pave the way for advanced implantable medical devices, marking a noteworthy advancement in medical research. [R]
B7-33 and Pulmonary Fibrosis
The study looks into the potential of inhaled B7, a B-chain derived from recombinant human relaxin, as a possible treatment for pulmonary fibrosis (PF), a condition that makes it impossible for the lungs to breathe. Traditional treatments, like recombinant H2 relaxin, have had trouble because they are hard to make and cost a lot of money.
The study is mostly about how breathing in B7 can stop bleomycin from making the lungs swell up in mice. Interestingly, B7 was able to lower the number of inflammatory leukocytes and neutrophils in bronchoalveolar lavage fluid, improve the structure of damaged alveoli, and lower the amount of collagen buildup. Notably, B7 looked at some of the most important pathological features of idiopathic pulmonary fibrosis, such as the levels of α-smooth muscle actin, vimentin, and mRNAs that are linked to inflammation and collagen deposition. The results show that inhaled B7 is a potentially strong anti-inflammatory agent. This opens the door to a simple and highly effective way to potentially treat pulmonary fibrosis.[R]
B7-33 and Tumor Concerns
The intricate structure and potent cAMP signaling of H2 relaxin, a hormone evaluated for acute heart failure treatment, pose challenges, including reported tumor-promoting actions. In response, the creation of B7-33 emerges as a transformative breakthrough. This pioneering peptide serves as the first functionally selective agonist for the complex GPCR, RXFP1. Notably, B7-33 displays potent anti-fibrotic effects, successfully preventing or reversing organ fibrosis and dysfunction in rodent models of heart or lung disease. The molecular mechanism involves the activation of RXFP1-angiotensin II type 2 receptor heterodimers, prompting selective downstream signaling of the perk pathway and MMP-2, a collagen-degrading enzyme. Most significantly, in contrast to H2 relaxin, B7-33 does not promote prostate tumor growth in vivo. This advancement represents a pivotal step in streamlining a two-chain cyclic insulin-like peptide to a single-chain linear peptide, maintaining potent beneficial effects while addressing concerns related to tumor promotion.[R] Further study is still needed to understand its impact on prostate cancer progression and if does not promote cancer progression.
B7-33 and Liver Metastasis
Liver metastasis is a big problem for people with pancreatic cancer (PC), and it often ends in death. Metastases grow faster when activated hepatic stellate cells (HSCs) create an environment that is good for them to do their job. This causes liver fibrosis. B7-33 is a potentially therapeutic peptide and an analog of relaxin. It targets relaxin family peptide receptors on activated HSCs, stopping the pSMAD2/3 signaling pathway and breaking down the fibrogenic properties. But B7-33 has some problems because its half-life is short and its sequence stays the same. Because of this, adding the cRGD sequence to B7-33 keeps it working well and makes it easier for it to fit into vesicles made from vascular endothelial cell membranes, specifically interacting with integrin αv²3. These cleverly created vesicles, called B7-33-HNPs, get around the problem of B7-33’s limited use in living things by making its half-life longer and building up in the liver to stop HSC activation. It’s worth mentioning that B7-33-HNPs are very good at stopping the growth and formation of liver metastases in a mouse model of PC that has spread. This study shows a good way to build a potentially therapeutic peptide delivery system by using certain interactions.[R]
Frequently Asked Questions
Is B7-33 legal?
Currently, there is insufficient information available to provide clear guidance on the legality of B7-33. Limited studies have been conducted on the safety of B7-33, with the majority of research confined to animal studies. It is crucial to emphasize that further research is necessary, particularly in the context of human safety and clinical trials. As a result, the legality of this solid-phase synthesis product remains undetermined at this point.
Can B7-33 cause prostate tumors in studies?
No, B7-33 does not promote tumor growth. Unlike its predecessor, H2 relaxin, which has been reported to have tumor-promoting actions due to its intricate structure and potent cAMP signaling, B7-33 serves as a transformative breakthrough in this regard. The pioneering peptide, functioning as the first functionally selective agonist for the complex GPCR, RXFP1, demonstrates potent anti-fibrotic effects without promoting prostate tumor growth in vivo.
What’s the main difference between relaxin and B7-33?
The key difference between relaxin and B7-33 lies in their structures and clinical applications. Relaxin, a peptide hormone, and its protein-coupled receptor RXFP1 are present in various blood vessels, contributing to diverse signaling pathways. Despite its vasoprotective effects, the complex structure of recombinant human relaxin 2 (H2 relaxin or serelaxin) poses challenges in clinical use due to production constraints.
In response, B7-33, a single-chain derivative, was developed to overcome these challenges. While functioning as a weak agonist of RXFP1, B7-33’s potency matches that of serelaxin. Notably, chronic administration of B7-33 shows promise in reducing organ fibrosis and dysfunction in rodent models of cardiovascular or pulmonary disease. This innovative peptide, synthesized to address limitations in relaxin’s clinical application, represents a step forward in research and is not intended for human use, serving as a tool for researchers to explore the compound’s effects.
In conclusion, B7-33 emerges as a pivotal player in peptide research, exhibiting significant potential across various health domains and diseases. Its role in cardiovascular health, pulmonary fibrosis, and post-myocardial infarction showcases its versatility and promise. The structurally refined B7-33, acting as a single-B-chain relaxin mimetic, circumvents the complexities of its predecessor, H2 relaxin, offering a unique pathway for therapeutic interventions.
Moreover, the peptide’s intriguing anti-inflammatory effects, particularly in preventing tumor growth without the reported actions of H2 relaxin, mark a substantial advancement in safety. The modification of B7-33 into B7-33-HNPs to counter liver metastasis further exemplifies its adaptability and potential impact. Despite these promising attributes, it’s crucial to acknowledge the current gaps in understanding, particularly regarding legality and comprehensive safety data.
Further research and clinical trials are imperative to unlock the full spectrum of B7-33’s effects and ascertain its potential as a therapeutic agent. As the field progresses, B7-33 stands poised as a beacon of hope for future advancements in medical research.
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