Background/Objectives: In recent years, silver complexes have shown strong antibacterial, antifungal, and antitumor activity with high selectivity toward cancer cells. Their cytotoxic effects are mainly linked to apoptosis induction, DNA damage, and enzyme inhibition, while the antitumor activity of silver(I) complexes with S-alkyl thiosalicylic acid derivatives remains unexplored. Methods: Silver(I) complexes with S-alkyl derivatives of thiosalicylic acid (C1–C5) were obtained through the direct reaction of silver(I) nitrate, the corresponding ligand of thiosalicylic acid, and a sodium hydroxide solution. The interactions between the complexes and CT-DNA/BSA were studied using UV-Vis, fluorescence spectroscopy, and molecular docking studies. The cytotoxic capacity of the newly synthesized complexes was assessed by an MTT assay. Results: Complexes C1–C5 exhibited strong cytotoxicity against murine and human breast (4T1, MDA-MB-468), colon (CT26, HCT116), and lung (LLC1, A549) cancer cell lines. The C3 complex significantly diminished tumor progression in an orthotropic mammary carcinoma model while demonstrating good systemic tolerance. Conclusions: The tested complex C3 triggered apoptosis in 4T1 cells by altering the delicate balance between pro- and anti-apoptotic Bcl-2 family members, increasing reactive oxygen species (ROS) levels, and reducing mitochondrial membrane depolarization. Moreover, the C3 arrested the 4T1 cell cycle in G0/G1 phase, decreasing the expression of cyclin D3 and increasing the expression of p16, p21, and p27.

The treatment of diabetes in the modern era, with its growing patient population, represents a significant challenge due to the wide range of adverse effects associated with medications that target complex biochemical processes. Consequently, researchers are investigating the hypoglycemic potential of existing drugs. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat pain, fever, and various inflammatory conditions. Recent studies have shown that NSAIDs, particularly salicylates, can influence glycemia through multiple mechanisms, including inhibition of gastrointestinal enzymes, blockade of K_ATP channels, activation of AMP-activated protein kinase (AMPK), and inhibition of NF-κB signaling, among others. Accordingly, this review explores the hypoglycemic potential of NSAIDs as well as their derivatives, and the diverse mechanisms through which these molecules may influence glucose homeostasis.

Background/Objectives: Inflammation plays a role at multiple levels, contributing to tumorigenesis, cellular proliferation, cell survival, and metastasis. The established link between chronic inflammation and tumor development has shifted the therapeutic focus toward nonsteroidal anti-inflammatory drugs, which exert their effects primarily through cyclooxygenase inhibition. Methods: In the present study, the antitumor potential of novel synthesized oxaprozin derivatives was evaluated using the MTT assay. The immunomodulatory effects of the selected derivative were determined in vitro by measuring cytokine concentrations and performing flow cytometry. To investigate the inhibitory capacity of these derivatives against cyclooxygenase enzymes, an in vitro inhibition assay was conducted using fluorometric screening kits, followed by in silico validation. Results: All tested tumor cell lines exhibited sensitivity to compound 1, which demonstrated the lowest cytotoxic effect against non-cancerous mMSCs and MRC-5 cells. This compound can effectively target tumor cells, inducing potent apoptosis in 4T1 breast cancer cells through a strategic shift in the Bax/Bcl-2 balance and the downregulation of the oncogenic driver Bcl-6. Although the synthesized oxaprozin derivatives showed moderate affinity for COX-1, none of the newly synthesized compounds achieved more than 50% inhibition against COX-2 at a concentration of 100 μM. Consistently, in silico procedures validated the results of the in vitro COX inhibition assay. Conclusions: The findings of this study indicate that compound 1 has the ability to modulate immune responses under stimulated conditions, and its potent antitumor activity may not be directly related to cyclooxygenase inhibition, suggesting the involvement of COX-independent pathways.