| Acceptance rate | 46% |
|---|---|
| Time to first decision | 6 months* |
| Time to decision with review | 50 days* |
*Approximate number of days
**The days mentioned above are averages and do not indicate exact durations. The process may vary for each article.
ACTA Pharmaceutica Sciencia
2018 , Vol 56 , Num 1
Potential Mechanistic Profiling of an OTC Analgesic as a Cytotoxic Agent in the Treatment of Hepatocellular Carcinoma
1 National Cancer Institute, Egypt, Central Pharmacy, Cairo, Egypt2 Agricultural Research Center, Central Laboratory for Agricultural Expert Systems, Cairo, Egypt
3 Faculty of Pharmacy, Cairo University, Department of Pharmacology & Toxicology, Cairo, Egypt
4 Faculty of Computers and Information, Department of Computer Science, Cairo, Egypt
5 College of Pharmacy, University of Sharjah, Department of Pharmacy Practice and Pharmacotherapeutics, Sharjah, United Arab Emirates.
DOI : 10.23893/1307-2080.APS.05607 Viewed : 15732 - Downloaded : 5874 While being a safe over the counter drug, paracetamol has also proved to be a cytotoxic agent for cultured hepatocellular carcinoma cells (HepG2). In order to understand the biochemical mechanisms underlying its cytotoxic ability, molecular docking of paracetamol with cyclin dependent kinase 2 protein (CDK2) and breast cancer type 2 susceptibility protein (BRCA2) plus cyclooxygenase 1 (COX1) enzyme protein was undergone. Computational simulation was performed using Schrödinger software to describe the details of binding between atoms of the active sites and paracetamol. All COX1, CDK2 and BRCA2 proteins showed binding scores with paracetamol. Their G-scores were -5.32, -5.61 and -6.08 respectively leading to selective inhibition of these proteins and loss of their cell cycle related activity. The binding strength of COX1 and CDK2 with paracetamol was mainly dependent on the hydrophobic residues, while that of BRCA2 was contributed to charged residues. Binding is responsible for the subsequent loss of activity of these cell cycle related proteins and eventual cancer cell death via apoptosis. Keywords : Paracetamol; Cyclooxygenase 1; Cyclin Dependent kinase 2; Breast Cancer Type 2 Susceptibility Protein; Molecular Docking