MD simulation supported the structural stability of the BRAF-RBG complex, and free energy landscape analysis further suggested the presence of a relatively stable conformational state during the simulation.<h4>Conclusions</h4>This study suggests that RBG inhibits malignant phenotypes of CRPC cells and may exert its anti-tumor effects in part through interaction with BRAF and modulation of the MAPK signaling pathway. The gene discussed is BRAF; the disease is neoplasm.