Ruthenium tetrazene complexes with general formula [Cp*RuCl(1,4-R 2 N 4)] (Cp* = η 5-C 5 Me 5), where R = benzyl (1), 2-fluorobenzyl (2), β-D-glucopyr anosyl-unprotected (3a) and acyl-protected (3b-d), 2-acetamido-β-Dglucopyranosyl-unprotected (4a) and acyl-protected (4b-d), propyl-β-D-glucopyranoside-unprotected (5a), and O-acetylated (5b), were synthesized and characterized using nuclear magnetic resonance and electrospray ionizationmass spectrometry. In addition, the molecular structure of 3b was determined using X-ray crystallography. The cytotoxicity of complexes against ovarian (A2780, SK-OV-3) and breast (MDA-MB-231) cancer cell lines and noncancerous cell line HEK-293 was evaluated and compared to cisplatin activity. The carbohydrate-modified complexes bearing acyl-protecting groups exhibited higher efficacy (in low micromolar range) than unprotected ones, where the most active 4d was superior to cisplatin up to five times against all investigated cancer cell lines; however, no significant selectivity was achieved. The complex induced apoptotic cell death at low micromolar concentrations (0.5 μM for A2780 and HEK293; 2 μM for SK-OV-3 and MDA-MB-231). K E Y W O R D S anticancer activity, glucose derivatives, ruthenium complexes, tetrazene ligands V. Hamala and A. Martišová contributed equally to this study.

A chlorination of tertiary (5 examples), secondary (3 examples) and primary (PhSiH3) hydrosilanes by Ph3CCl with a catalytic amount of B(C6F5)3 is presented. The reaction was substantially faster than its non‐catalyzed version. The chlorination of secondary hydrosilanes and PhSiH3 proceeded in a stepwise manner, which allowed selective isolation of chlorohydrosilanes. The mechanism of catalytic hydrosilane chlorination seems to be distinct to mainstream B(C6F5)3 catalyzed reactions involving hydrosilanes (i.e. activation of Si‐H bond by the R3Si‐‐H‐‐B (C6F5)3 adduct formation). Contrary, the present process is based on an instant formation of [Ph3C]+[ClB(C6F5)3]− from B(C6F5)3 and Ph3CCl, followed by a hydride transfer from particular hydrosilane to tritylium cation with a concomitant generation of unstable silylium cation compensated by borate anion [ClB(C6F5)3]−. Subsequent decomposition of this ionic species leads to the corresponding chlorosilane and recuperation of B(C6F5)3.