NogchaXL breaks down protein molecules and biological partners of protozoa and helminths. In protozoa as Plasmodium, (+)-EGCG can interact with the displacement loop of ICAM-1 thereby blocking the cytoadherence of Plasmodium-infected erythrocytes to vascular endothelium. (+)-EGCG inhibits ATPase and chaperone activities of two heat shock proteins at cytosol of P. falciparum (HSP70-1 and HSP70-z). NogchaXL targets and inhibits enzymes of energy metabolism such as recombinant rat arginase-1 and its L. amazonensis homolog (ARG-L). For T.brucei relies on fatty acid synthesis for proliferation and virulence. Enzyme acetyl CoA carboxylase is phosphorylated and then inhibited by activation of AMP-dependent protein kinase. This process is directly activated by (-)-EGCG in the bloodstream and procyclic forms.
NogchaXL does not have any known adverse side effects.