The rapid emergence of carbapenem-resistant Acinetobacter baumannii has become a major health concern, primarily driven by the dissemination of class D β-lactamases, particularly OXA-23, which compromise the efficacy of last-line β-lactam antibiotics. Drug repurposing combined with structure-based computational approaches provides a promising strategy for accelerating the discovery of novel therapeutic candidates against multidrug-resistant pathogens. This study aimed to identify FDA-approved non-steroidal anti-inflammatory drugs (NSAIDS) with potential inhibitory activity against OXA-23 β-lactamase by using a comprehensive computational drug discovery workflow. Twenty-six FDA-approved NSAIDs were evaluated using an integrated computational pipeline comprising network pharmacology, KEGG pathway analysis, molecular docking, molecular dynamics simulations and ADMET profiling. KEGG pathway analysis confirmed the central role of OXA-23 in β-lactam resistance, while network pharmacology prioritized nine candidates NSAIDS for subsequent structure-based investigation. Molecular docking was performed using the crystal structure of OXA-23 β-lactamase (PDB ID: 4K0X), followed by molecular dynamics simulations to assess the stability of the protein–ligand complexes. Among the prioritized compounds, sulfasalazine demonstrated the most favorable predicted binding affinity (−8.3 kcal/mol), forming stable interactions with key catalytic residues, including SER126, VAL128, and LEU166 and exhibiting a more favorable docking profile than the reference drug imipenem (−5.7 kcal/mol). Molecular dynamics simulations supported the structural stability of the sulfasalazine OXA-23 complex throughout the simulation period. Furthermore, ADMET analysis indicated favorable pharmacokinetic characteristics including good oral bioavailability, high gastrointestinal absorption, low central nervous system penetration, and an acceptable predicted safety profile. This integrated computational study identifies sulfasalazine as a promising repurposing candidate for targeting OXA-23 β-lactamase in carbapenem-resistant A. baumannii. The findings demonstrate the utility of combining network pharmacology with molecular modeling to prioritize candidate therapeutics and provide a computational framework for accelerating antimicrobial drug discovery. Experimental validation is warranted to confirm the inhibitory activity and therapeutic potential of sulfasalazine against multidrug-resistant A. baumannii.

Colon cancer (CC) is a common malignancy characterized by poor prognostic outcomes and considerable mortality. Oxaliplatin (OXP) is commonly used in the treatment of CC; however, its efficacy may be limited by side effects and the development of resistance. β-sitosterol (β-Sit), a phytosterol derived from plants, has been documented to be effective in the treatment of tumors. This study aimed to investigate the potential of β-Sit to enhance the antitumor efficacy of OXP in COLO-205 cells, focusing on apoptosis induction and suppression of the vascular endothelial growth factor A (VEGF-A)/survival pathway. Molecular docking studies were performed to assess the binding affinity of β-Sit with the target proteins B-cell lymphoma 2 (Bcl-2), phosphoinositide 3-kinase (PI3K), and VEGF receptor-2 (VEGFR-2). COLO-205 cells were treated with OXP, β-Sit, or a combination of OXP + β-Sit for 48 h. The combination treatment substantially lowered the IC₅₀ achieved with 3.24 µM of OXP and 36.01 µM of β-Sit, compared to 25.64 µM for OXP alone and 275.9 µM for β-Sit alone, demonstrating a pronounced synergistic impact. The combined therapy altered the cell cycle distribution by decreasing the number of cells in the G0/G, S, and G2/M phases, coupled with an increase in the Sub-G1 population. Furthermore, apoptosis was augmented by a shift in cell death from necrosis to late apoptosis, as indicated by an increased BAX/BCL2 ratio relative to each treatment alone. Moreover, the inhibitory effect on angiogenesis was enhanced via the reduction of VEGF-A, and β-catenin and nuclear factor κB (NF-κB-p65) were suppressed, thereby preventing the growth and survival of resistant cancer cells. Additionally, molecular docking supported high binding affinities of β-Sit to Bcl-2, PI3K, and VEGFR-2. This study highlights the potential of β-Sit to enhance the anti-cancer efficacy of OXP in CC.

The extensive use of Alachlor, a chloroacetanilide herbicide, poses significant environmental concerns due to its persistence and toxicological implications. In this study, an in-silico framework was employed to evaluate the potential of cytochrome P450 monooxygenase from Claviceps purpurea as a biocatalyst for the biodegradation of Alachlor and its derivatives. Structural analysis was conducted using an AlphaFold-predicted heme-bound model, and active site regions were identified through PrankWeb pocket prediction. Molecular docking revealed favourable binding affinities between the enzyme and multiple Alachlor metabolites, with Alachlor-2-acetoxy and Sec-Alachlor oxanilic acid exhibiting the highest affinities (−6.5 kcal/mol). /Ligplot+ interaction analysis demonstrated that ligand stabilization within the catalytic pocket is predominantly governed by hydrophobic interactions, with limited polar contributions, notably involving His128. All top-ranked ligands were positioned in proximity to the heme cofactor, indicating catalytically relevant binding orientations. Toxicity assessment using Toxtree classified Alachlor and its metabolites as Cramer Class III, with no specific prediction of carcinogenic or genotoxic alerts, supporting the environmental feasibility of enzymatic transformation. Collectively, these findings establish a structure-function basis for the interaction of C. purpurea cytochrome P450 monooxygenase with Alachlor derivatives and provide a computational foundation for future experimental validation and bioremediation-oriented enzyme studies.

This study aims to develop an environmentally sustainable microfluidic carbon sequestration system using HR-ZnO nanoconjugates. The nanoparticles are evaluated for their efficiency, stability, and eco-compatibility for enhanced carbon capture applications. The extract (0.1 %) of mushroom was used for preparation of HR-ZnO NCs. Higher propensity of HR-ZnO NCs was obtained by optimizing multiple parameters i.e., amount of salt (0.02 M), level of optimal extract (1.5 mL) and procurement period (120 min). The UV–Vis spectrum showed peak at approx. 315 nm for extract and sharp peaks for HR-ZnO NCs were observed at approx. 325 and 340 nm. FTIR revealed hydroxyl, carbonyl, and amine groups in nanoparticles at 3,264.24, 2,165.41, 2,022.57, 1,973.09, 1,635.54, 1,532.60, 1,397.74, 1,030.66 and 929.32 cm ⁻¹ . XRD confirmed the hexagonal wurtzite crystalline nature of myco-synthesized ZnO NCs. SEM images of ZnO NPs confirmed the irregular structure of ZnO NCs. At 6 % salinity, HR-ZnO NCs exhibited a significantly greater reduction in CO ₂ bubble size than free ZnO nanoparticles, indicating superior CO ₂ dissolution and sequestration. Salinity-dependent studies (3–15 % NaCl) revealed enhanced sequestration efficiency with increasing ionic strength up to an optimum of 12 % NaCl. This study presents the first eco-engineered microfluidic carbon sequestration system establishing a sustainable and biologically integrated approach to carbon capture.