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Journal of Chemistry
Volume 2015 (2015), Article ID 136285, 12 pages
Research Article

Spectral Investigation and In Vitro Antibacterial Evaluation of NiII and CuII Complexes of Schiff Base Derived from Amoxicillin and α-Formylthiophene (αft)

Bio-Inorganic and Materials Chemistry Research Laboratory, Tribhuvan University, M.M.A.M. Campus, Biratnagar 56613, Nepal

Received 3 October 2015; Accepted 8 November 2015

Academic Editor: Liviu Mitu

Copyright © 2015 Narendra Kumar Chaudhary and Parashuram Mishra. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Two new metal complexes of general formula M(Haαft)2 [M = and ] of asymmetrical Schiff base ligand (HL = Haαft) derived from amoxicillin and α-formylthiophene have been prepared and characterized by various physicochemical and spectral techniques. Molar conductance measurement indicates nonelectrolytic nature of the metal complexes. FT-IR spectral study reveals the ligation of metal ions at two different nitrogen [NN] donor sites of Haαft. FT-IR and electronic absorption spectral evidences suggest distorted tetrahedral and square planar geometry for and complexes, respectively. The structure optimization by molecular mechanics (MM) force field calculation through ArgusLab 4.0.1 version software also supports the concerned geometry of the complexes. The cell dimensions as suggested by XRPD study, (6.753 Å), (13.904 Å), (20.122 Å), α (142.76°), β (106.580°), and γ (72.4343°) for and (24.2547 Å), (6.6371 Å), (5.5047 Å) (α = β = γ = 90°) for complexes, are in good agreement with their triclinic and orthorhombic crystal systems. Particle size calculation by Scherrer’s formula indicates nanocrystalline nature of the complexes. The antibacterial sensitivity study suggests promising activities of Haαft (Ligand) and M(Haαft)2 complexes against four clinical pathogenic bacteria, namely, E. coli, P. vulgaris, P. aeruginosa, and S. aureus, though being less active than the standard drug amikacin.