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Targeting BTK with FDA-approved anticancer drugs, such as acalabrutinib and ibrutinib, which are metabolized by the CYP3A enzyme, common to both fungi and humans, can be combined with fungal morphogenesis inhibitors to enhance the apoptotic effect [183]
Further, it is reported that fungal dysbiosis can trigger the multiplication of myeloid-derived suppressor cells to contribute to the development of colorectal cancer by promoting an immunosuppressive action that triggers pyruvate kinase M1/2-dependent glycolysis [16]
This structure stabilizes the complex and supports its role as a redox-inactive carrier of bioavailable copper (Pickart, Vasquez-Soltero, and Margolina 2012)
This article reviews mechanistic insights, potential domains of implication in research, and speculative directions for the BPC-157 / TB-500 blend
