Peptide B7-33 Reduces Coronavirus Binding Sites While Supporting Healthy Blood Pressure

by Dr. James Ross

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B7-33 and the ACE2 Coronavirus Binding Site

A central concern with some blood pressure medications is that they can inadvertently increase the expression of ACE2, the very receptor used by coronaviruses such as SARS-CoV-2 to enter cells. For example, studies have shown that blocking the angiotensin II type 2 receptor (AT2R) with compounds like PD123319 leads to a rise in ACE2 transcription.

By contrast, B7-33, a derivative of human relaxin-2, activates AT2R rather than blocking it. Research confirms this mechanism by demonstrating that B7-33’s actions are halted when AT2R antagonists like PD123319 are present, proving it works through this receptor. Importantly, activation of AT2R has been linked to reducing ACE2 transcription, thereby potentially lowering the number of viral binding sites available.

Mechanisms of B7-33 Signaling

B7-33 achieves its effects by binding to RXFP1–AT2R heterodimers, specialized receptor complexes that trigger beneficial cellular signaling. This binding stimulates pathways such as ERK1/2 activation, which boosts matrix metalloproteinases (MMPs) and promotes anti-fibrotic activity. The shared binding motif “RXXXRXXI” shows that B7-33 mimics the action of relaxin-2 while being structurally smaller and safer.

Protective Effects on Blood Vessels and Circulation

One of the most notable properties of relaxin-2 and its fragment B7-33 is vascular protection. Relaxin-2 has been well documented as a rapid vasodilator, improving circulation in the brain, kidneys, and lungs within minutes. It decreases systemic vascular resistance and enhances vessel compliance.

B7-33 mirrors these vasoprotective actions. Studies show it improves endothelium-dependent relaxation, supports bradykinin signaling, and prevents endothelial dysfunction in disease models such as preeclampsia. By doing so, B7-33 lowers pulmonary pressures and helps stabilize systemic blood flow without the drawbacks of standard therapies.

RXFP1 and the Control of Vascular Inflammation

RXFP1, the relaxin receptor, plays a vital role in preventing vascular inflammation. When RXFP1 is deficient, blood vessels exhibit greater inflammation, increased macrophage and neutrophil infiltration, and poor remodeling after vascular injury. By activating RXFP1, B7-33 reduces the upregulation of inflammatory cytokines and promotes healthier vessel walls.

B7-33 Offers Anti-Fibrotic Benefits Without Cancer Risk

H2 relaxin, while beneficial, has been shown to stimulate prostate tumor growth in certain models. B7-33 was designed to avoid this problem while preserving therapeutic benefits. Unlike H2 relaxin, B7-33 did not increase tumor size in prostate cancer studies, even when administered at higher doses.

Instead, B7-33 retains strong anti-fibrotic actions, encouraging collagen breakdown and protecting tissues from fibrosis through selective RXFP1–AT2R signaling. This makes it a safer alternative for long-term therapeutic use.