COF‐300, an imine‐linked, crystalline, and microporous covalent organic framework, modified by coordination of Pd(OAc)2 to its walls, afforded a hybrid material, Pd(OAc)2@COF‐300, which was used as an efficient heterogeneous catalyst for cross‐coupling reactions. This material showed excellent catalytic activity for the phosphine‐free Suzuki–Miyaura, Heck, and Sonogashira cross‐coupling reactions with low palladium loadings (0.1 mol % Pd). X‐ray photoelectron spectroscopy analysis of the catalyst after the reaction showed that PdII is converted to Pd0, which is trapped within the COFs nanopores. This was confirmed by high‐resolution transmission electron microscopy. Moreover, promising results were obtained using Pd(OAc)2@COF‐300 under continuous‐flow conditions for a Suzuki–Miyaura cross‐coupling reaction.

Pterocarpanquinones (1a-e) and the aza-pterocarpanquinone (2) were synthesized through palladium catalyzed oxyarylation and azaarylation of conjugate olefins, and showed antineoplasic effect on leukemic cell lines (K562 and HL-60) as well as colon cancer (HCT-8), gliobastoma (SF-295) and melanoma (MDA-MB435) cell lines. Some derivatives were prepared (3-8) and evaluated, allowing establishing the structural requirements for the antineoplasic activity in each series. Compound 1a showed the best selectivity index in special for leukemic cells while 2 showed to be more bioselective for HCT-8, SF-295 and MDA-MB435 cells. Pterocarpanquinones 1a and 1c-e, as well as 8 were the most active on amastigote form of Leishmania amazonensis in culture. Compounds 1a, 1c and 8 showed the best selectivity index.

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The pentacyclic 1,4-naphthoquinones 1a-d were cytotoxic (IC(50) approximately 2-7 microM) to human leukemic cell lines K562 (oxidative stress-resistant), Lucena-1 (MDR phenotype) and Daudi. Fresh leukemic cells obtained from patients, some with the MDR phenotype, were also sensitive to these compounds. The pentacyclic 1,4-naphthoquinones 1a and 1c induced apoptotic cell death in cells from leukemic patients as determined by flow cytometry. Conversely, the cell lines were highly insensitive to lapachol (2) and alpha-lapachone (3). Mitomycin-C inhibited cell proliferation at concentrations as low as 0.5 microM. The low toxicity against lymphocytes activated by phytohemagglutinin shows that these compounds are selective for the cancer cells studied. Previous data suggest that these compounds (1a-d) can be bioactivated in situ by reduction followed by rearrangement leading to enones, which are powerful alkylating agents. In contrast, lapachol (2) and beta-lapachone (3), which cannot be bioactivated by reduction, showed little activity against the same cell lines.