Research Article Utilization of Boron Compounds for the Modification of Suberoyl Anilide Hydroxamic Acid as Inhibitor of Histone Deacetylase Class II Homo sapiens Ridla Bakri, 1 Arli Aditya Parikesit, 1 Cipta Prio Satriyanto, 1 Djati Kerami, 2 and Usman Sumo Friend Tambunan 1 1 Bioinformatics Group, Department of Chemistry, Faculty of Mathematics and Science, University of Indonesia, Depok 16424, Indonesia 2 Mathematics Computation Group, Department of Mathematics, Faculty of Mathematics and Science, University of Indonesia, Depok 16424, Indonesia Correspondence should be addressed to Usman Sumo Friend Tambunan; usman@ui.ac.id Received 3 June 2014; Revised 12 August 2014; Accepted 12 August 2014; Published 24 August 2014 Academic Editor: Antoine van Kampen Copyright © 2014 Ridla Bakri et al. his 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. Histone deacetylase (HDAC) has a critical function in regulating gene expression. he inhibition of HDAC has developed as an interesting anticancer research area that targets biological processes such as cell cycle, apoptosis, and cell diferentiation. In this study, an HDAC inhibitor that is available commercially, suberoyl anilide hydroxamic acid (SAHA), has been modiied to improve its eicacy and reduce the side efects of the compound. Hydrophobic cap and zinc-binding group of these compounds were substituted with boron-based compounds, whereas the linker region was substituted with p-aminobenzoic acid. he molecular docking analysis resulted in 8 ligands with Δ binding value more negative than the standards, SAHA and trichostatin A (TSA). hat ligands were analyzed based on the nature of QSAR, pharmacological properties, and ADME-Tox. It is conducted to obtain a potent inhibitor of HDAC class II Homo sapiens. he screening process result gave one best ligand, Nova2 (513246-99-6), which was then further studied by molecular dynamics simulations. 1. Introduction Cervical cancer is cause by human papillomavirus (HPV) and in the second rank as a cause of cancer death in women worldwide [1]. Cervical cancer occurs in the cervical region, which is located in the hollow area between the vagina and the uterus or commonly called cervix Cervical cancer can be contagious among all women; a ratio of 1 out of every 4 women is likely to sufer from it [2]. Based on data from the World Health Organization, in 2008, it is estimated 530,232 cases of cervical cancer in the world, with 275,008 mortality cases [3]. hrough these data, the estimated global mortality rate from cervical cancer is 50% [2]. HPV is a virus of the family Papillomaviridae and has a nonenveloped, icosahedral-shaped capsid and the double stranded circular DNA as its genetic material [4–6]. It is 7,800–7,900 base pairs long with a 55 nm diameter [7, 8]. HPV has more than 100 diferent genotypes, and over 40 types of it can infect any part of the epithelial and mucosal lining of the anogenital tissue [9]. he HPV virus is divided into two classes, namely, low-risk HPV (e.g., HPV-6 and HPV- 11) and high-risk HPV (e.g., HPV 16 and HPV 18) [10]. Low- risk HPV usually causes a bulge impact on disease areas such as anogenital condylomata (wart) that usually grows on the cervix and vulva [11]. HPV genome is divided into 3 regions, namely, upstream regulatory (URR, noncoding), early gene, and late gene regions [12]. Proteins E6 and E7 oncogenes can make HPV- infected cells to become immortal [13]. E6 protein is associ- ated with ubiquitin (protein ligase), which in turn interacts Hindawi Publishing Corporation Advances in Bioinformatics Volume 2014, Article ID 104823, 10 pages http://dx.doi.org/10.1155/2014/104823