BIO 300 - Mechanism of Action
Cellular division is a critical determinant of how radiation effects human cells, as this is the fundamental concept underlying the utility of radiation therapy to kill rapidly dividing cancer cells. BIO 300's unique, selective mechanism slows down the cell cycle of healthy cells, rendering them radioresistant, while not conferring such benefits to the rapidly dividing tumor cells. BIO 300 further works to protect healthy tissues from radiation damage by repressing the radiation-induced inflammatory pathways which cause tissue-remodeling events such as pulmonary fibrosis.
BIO 300 primarily acts as an agonist for estrogen receptor-beta (ERbeta), which is a transcription factor that represses classic estrogen signaling controlled by estrogen receptor-alpha. ERbeta-mediated signal transduction pathways are additionally involved in the regulation of cellular proliferation and tumor suppressor genes such as p53, both of which are integral to the radiation response. The majority of these activities are through its interaction with general (non-estrogenic) transcription factors (GTFs). Thus, BIO 300 treatment can alter expression of numerous genes, which together confer a radioresistant state to healthy cells. As ERbeta, or its target genes, are commonly mutated in cancer, these protections do not extend to cancer cells.