Fibrosis is an illness characterized by the thickening or deterioration of tissues. Fibrosis commonly arises when one goes through the “end-stage” of severe, chronic diseases. In a clinical study, a protein called H2-relaxin was found in 2012 to prevent the severe, long-term scarring of the cardiac tissues as a result of heart injury. The treatment for fibrosis is diverse – ranging from therapy to surgery. B7-33 peptide for sale is a synthetic counterpart of the naturally occurring protein H2-relaxin. Similar to H2-relaxin, B7-33 also offers anti-fibrotic characteristics above other established benefits detailed further down.
What is B7-33 Peptide?
B7-33 is a unique chain peptide, a smaller homologous derivative of the native relaxin protein. The signal peptide, B chain, C chain, and COOH terminal make up most of the relaxin peptide. Initial attempts to reproduce these peptide structures failed because they were both insoluble and inactive. In 2016, after years of effort, scientists created the first-ever soluble analog – B7-33 peptide – by altering the structure, creating a B chain, and lengthening the COOH terminus.
Mechanism of Action
In addition to the structural differences, the peptide contains specific endogenous protein changes that are more helpful than H2-relaxin. The B7-33 peptide uses the pERK pathway instead of the cAMP pathway. Tumor development in the body may be stimulated by H2-relaxin’s anti-fibrotic effects, which are usually produced through the cAMP pathway. This is a prominent adverse effect of relaxin therapy. The peptide in this study also shows a significant affinity for RXFP-1 receptors. To boost MMP-2 matrix metalloproteinase peptide production, this RXFP-1 receptor-binding peptide activates the ERK pathway. These substances then hinder the scarring of the tissues and hence prevent fibrosis.
Anti Fibrotic Properties Research
As discussed before, H2 relaxin is a naturally occurring protein that helps prevent scarring of the tissues. They generally work through the cAMP pathway. Studies have demonstrated that when treated with a total extended strain of H2 relaxin protein, it generates an accelerated heart rate and accelerates the spread of cancerous cells in the body. Mostly, this can be traced back to its mechanism, which involves activating the cAMP pathway. As a result, scientists searched for a derivative that may have anti-fibrosis effects identical to cAMP activation. The upshot of their research was the B7-33 peptide.
When the peptide was provided in mice afflicted with myocardial infarction, it led to a 50 percent decrease in heart tissue fibrosis. As a consequence of this, the heart function strengthened, leading to fewer issues in the long term. Upon additional examination, it was determined that the effect was mainly because the peptide raised the level of matrix metalloproteinase protein, which counterbalanced the damaging collagen cells and avoided fibrosis.
Furthermore, research was also done on mice suffering from prostate cancer. These animals were either supplied with an optimum dosage of B7-33 (the ideal dose is usually provided to exhibit anti-fibrosis) or with a more significant dose of B7-33 (higher dose than those exhibiting anti-fibrosis effects). To researchers’ surprise, both dosages had similar effects: they stopped the progression of prostate tumors and prevented the formation of fibrosis. This process revealed that the peptide functions purely through the pERK pathway and not via cAMP activation, limiting cancer spread.
Effects of B7-33 Peptide on the Body
There is continuing work being done on the relatively new peptide B7-33. Because further research is needed, there are no known significant side effects. However, some of the predicted adverse effects are comparable to other peptides. Among them are:
- Temporary soreness and itching at the location of peptide injection
- Dryness of mouth
- Dizziness
- Cough, fever, and flu-like symptoms
- A throbbing in the joints
