Background: The significant study was made to investigate the interaction of an antidiabetic drug, glimepiride with bovine serum albumin (BSA) by fluorescence quenching method in two different temperatures (298K and 308K). Methods: The study was carried out through fluorescence spectroscopic analysis. Stern-Volmer equation determined the fluorescence quenching constant. The various thermodynamic parameters such as free energy (ΔG), enthalpy (ΔH), and entropy (ΔS) was found out by Van’t Hoff equation. Results: The data revealed that glimepiride interact with BSA and both tryptophan and tyrosine residues of BSA are responsible for interactions with glimepiride. BSA undergo static quenching in presence of glimepiride, a quencher. The hydrophobic forces participated in chief roles for BSA-glimepiride complexation and this was indicated by the values of thermodynamic parameters. The binding number (n) obtained was ≈1 pointed out that glimepiride and BSA has bound with 1:1 ratio. Conclusions: Through fluorescence spectroscopic technique we revealed the nature of interaction of glimepiride with BSA, quenching mechanism for the interaction and associated thermodynamic parameters.

The study aims to investigate the protein binding kinetics of nicotine and a PPI (pantoprazole) with Bovine Serum Albumin (BSA) through UV spectroscopy and computational modeling. Data was obtained by using nicotine and pantoprazole and warfarin and diazepam as the two site specific probes on Bovine serum albumin (BSA). In-vitro and in-silico modeling was carried out in creating an environment that simulates the body environment. Cellulose membrane tubes were cut into 9 cm and tied tightly not to let any mixtures leak out. To determine number of binding sites, association constants by using Scatchard plot, predominant binding site of each drug and rise in % of free fraction of one by the other were analyzed using equilibrium dialysis method. Molecular docking further verifies the observations. In Scatchard plot analysis, for nicotine, n 1 , n 2 , k 1 and k 2 = 2.2, 7.6, 0.18 µM −1 and 0.02 µM −1 and for pantoprazole, n 1 , n 2 , k 1 and k 2 = 0.42, 1.2, 0.40 µM −1 and 0.03 µM −1. Nicotine binds more to diazepam site (site-II) and pantoprazole mainly to warfarin site (site-I). In molecular docking, the binding affinity of nicotine being −5.7 kcal/mole demonstrates higher affinity for site-II than that of pantoprazole whose binding affinity is −8.0 kcal/mole. In absence and presence of warfarin, the free fraction of pantoprazole bound to BSA (1:1) was increased from 37.79% to 82.44% and 51.78% to 98.80% respectively by nicotine. On the other hand, free fraction of nicotine was raised by pantoprazole from 12.89% to 75.70% and 50.08% to 99.66% in the absence and presence of diazepam. Both the results of spectroscopic and computational molecular docking suggest that administering pantoprazole with nicotine might increase the % free fraction of pantoprazole more. Thus, nicotine consumption can be beneficial for smoker people taking PPI like pantoprazole.