Bronchogen

Bronchogen is a bioregulator designed to support respiratory health. Research indicates its potential to reduce pulmonary inflammation, restore epithelial structure, and enhance lung function, particularly in models of chronic obstructive pulmonary disease (COPD). Its actions are attributed to modulation of gene expression and epigenetic pathways within bronchial tissues. Bronchogen is a synthetic peptide composed of alanine, glutamic acid, aspartic acid, and leucine. It belongs to the Khavinson family of short peptides, which exhibit tissue-specific regulatory functions. Bronchogen interacts with DNA and histone proteins, influencing chromatin structure and gene expression relevant to inflammation, surfactant production, and epithelial repair. Studies in animal models have demonstrated its capacity to restore bronchial architecture, reduce inflammatory infiltration, and enhance respiratory resilience.

- Experience chronic respiratory inflammation

- Seek to restore bronchial epithelial integrity

- Aim to enhance mucosal immunity and surfactant production

- Wish to mitigate age-related pulmonary decline

- Exploring non-hormonal interventions for lung tissue regeneration

Mechanism of Action

How this peptide works in the body

DNA Binding and Epigenetic Regulation

Bronchogen (AEDL) exhibits selective affinity for CTG-rich DNA sequences and interacts with core histones H1, H2B, H3, and H4, suggesting a role in chromatin remodeling. This peptide facilitates nucleosome repositioning and modulates DNA accessibility, enabling transcription of key genes involved in epithelial repair and anti-inflammatory signaling. Bronchogen is postulated to function as an epigenetic bioregulator, influencing the activity of histone deacetylases (HDACs) and DNA methyltransferases (DNMTs), leading to site-specific changes in chromatin conformation. These changes selectively affect genes in bronchial epithelial cells, supporting differentiation and tissue regeneration.

Transcription Factor Activation and Gene Modulation

Bronchogen upregulates Hoxa3, a homeobox transcription factor critical for epithelial morphogenesis, mucosal barrier integrity, and tissue polarity restoration. In aged and senescent bronchial cell cultures, Hoxa3 expression is significantly increased following peptide exposure, supporting its role in geroprotective epitheliogenesis. Additionally, the peptide may influence the GATA family (notably GATA6), known for its role in alveolar epithelial cell development and surfactant gene expression, although direct evidence remains under investigation.

Inflammation Modulation via Cytokine Reprogramming

Bronchogen downregulates pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β, while potentially enhancing IL-10 and other regulatory interleukins. This cytokine shift contributes to a reduction in neutrophilic infiltration and bronchial remodeling, both hallmarks of chronic airway diseases like COPD and asthma. Evidence suggests modulation of the NF-κB pathway, attenuating the transcription of inflammation-promoting genes. Bronchogen may also inhibit TLR4-mediated signaling, reducing sensitivity to airborne irritants and microbial triggers.

Enhancement of Surfactant Biosynthesis

Bronchogen promotes transcription of SFTPB (surfactant protein B), a critical protein involved in lowering alveolar surface tension and preventing collapse. By enhancing alveolar stability, it contributes to more efficient gas exchangeand improved lung compliance, particularly in fibrotic or inflamed lungs.

Tissue Remodeling and Stem Cell Support

Bronchogen indirectly supports bronchial epithelial progenitor cells by enhancing niche integrity and promoting epithelial-to-mesenchymal transition (EMT) reversal. This may involve modulation of TGF-β/SMAD signaling, with downstream suppression of fibrotic activity and preservation of epithelial phenotype.

Antioxidant and Mitochondrial Regulation (Emerging Evidence)

Preliminary in vitro studies suggest that Bronchogen may upregulate Nrf2, a master regulator of the antioxidant response, thereby reducing reactive oxygen species (ROS) burden in bronchial epithelial cells. Concurrently, it may preserve mitochondrial membrane potential and integrity via PGC-1α-associated pathways, improving cellular resilience under hypoxic stress.