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Finally, the orally bioavailable class III c-MET allosteric inhibitor tivantinib (ARQ197, Daiichi-Sankyo, Tokyo, Japan), which binds to an inactive dephosphorylated c-MET conformation, stabilizing it and hence blocking its downstream signaling [20, 125], has been extensively investigated in several cancer types, including HCC, CRC, NSCLC, breast, and GI cancers [126], although results have been disappointing so far