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Marimastat (CAS 154039-60-8) also known as BB-2516 is an orally bioavailable inhibitor of matrix metalloproteases (MMPs) Structurally it contains a collagen-mimicking hydroxamate moiety that facilitates covalent binding to the zinc atom at MMP active sites Marimastat exhibits broad-spectrum inhibitory activity against MMP-1 MMP-2 MMP-7 MMP-9 and MMP-14 with IC50 values of 5 nM 6 nM 13 nM 3 nM and 9 nM respectively In animal models of metastatic cancers Marimastat reduces tumor dissemination and progression Clinically Marimastat is investigated for potential therapeutic effects against metastatic and non-metastatic solid tumors such as pancreatic and gastric cancers
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Batimastat (BB-94 CAS 130370-60-4) is a synthetic small-molecule inhibitor targeting matrix metalloproteinases (MMPs) Structurally a polypeptide-like analogue of collagen substrates batimastat contains a peptidic backbone and a hydroxamate moiety that binds the catalytic zinc atom of MMPs It inhibits several MMP subtypes markedly including MMP-1 MMP-2 MMP-3 MMP-7 and MMP-9 with reported IC50 values of 3 4 20 6 and 4 nM respectively In preclinical studies batimastat demonstrates inhibitory effects on tumor growth and angiogenesis across various tumor models including ovarian and colon carcinoma xenografts making it relevant for cancer research and therapeutic development
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AGI-5198 (CAS 1355326-35-0) is a selective inhibitor of mutant isocitrate dehydrogenase 1 (IDH1) harboring the R132H substitution Identified via high-throughput screening AGI-5198 blocks mutant IDH1-mediated formation of the oncometabolite R-2-hydroxyglutarate (R-2-HG) in a dose-dependent manner Mechanistically inhibition of mutant IDH1 by AGI-5198 induces expression of differentiation-associated zinc finger and BTB domain-containing protein 16 (ZBTB16 also termed PLZF) decreasing histone H3 lysine 9 trimethylation (H3K9me3) and promoting glioma cell differentiation In experimental glioma models AGI-5198 reduces tumor cell proliferation underscoring its utility for investigating differentiation therapy strategies targeting IDH1-mutant cancers
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