(E)-2-((4-hydroxybenzylidene)amino)phenol (iminophenol a) reacted with Pd(OAc)2 giving place to compound 1a, in which the iminophenol was bonded to palladium(II) in a κ3-Cortho,N,Oortho tridentate chelating mode. Thus, 1a was formed by neutral mononuclear units of schematic formula Pd(C,N,O), consisting of two fused five-membered metallacycles. Self-assembly of the Pd(C,N,O) units gave place to the polynuclear structure of 1a. Treatment of 1a with PPh3 or PPh2CH2CH2PPh2 in molar ratio Pd(II)/PPh3 = 1/1 or Pd(II)/PPh2CH2CH2PPh2 = 2/1 produced the mononuclear or dinuclear compound of schematic formula [Pd(C,N,O)(PPh3)] (2a) or {[Pd(C,N,O)]2(µ2-PPh2CH2CH2PPh2)} (3a), respectively. Compounds a were characterized by elemental analysis, high resolution ESI-(+) mass spectrometry, IR, and NMR. In addition, the crystal structure of the adducts 2a·2(CH2Cl-CH2Cl) and 3a·5(dmso) was determined by single crystal X-ray diffraction analysis. Most compounds a were noncytotoxic or poorly cytotoxic. Nonetheless, 2a was moderately cytotoxic against the MCF-7 breast and HCT-116 colon human cancer cell lines, and presented very low cytotoxicity towards normal skin human BJ cells. Compounds a showed moderate antibacterial activity against some Gram-positive (B. subtilis and S. aureus) and Gram-negative (E. coli) bacterial strains, and displayed also moderate antioxidant activity, producing 3a the best antioxidant activity. 1a changed the electrophoretic mobility of the pBluescript SK+ plasmid DNA. This change followed the pattern of cisplatin, but it started at a concentration twenty times higher than with cisplatin. Moreover, compounds 1a - 3a inhibited topoisomerase IIα at concentrations of 10, 50 and 25 µM, respectively.