Evaluating NSAIDs in SARS-CoV-2: Immunomodulatory mechanisms and future therapeutic strategies.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely recognized for their analgesic and anti-inflammatory properties. Amidst the SARS-CoV-2 pandemic, the role of NSAIDs in modulating viral and bacterial infections has become a critical area of research, sparking debates and necessitating a thorough review. This review examines the multifaceted interactions between NSAIDs, immune responses, and infections. Focusing on the immunomodulatory mechanisms of NSAIDs in SARS-CoV-2 and their implications for other viral and bacterial infections, we aim to provide clarity and direction for future therapeutic strategies. NSAIDs demonstrate a dual role in infectious diseases. They reduce inflammation by decreasing neutrophil recruitment and cytokine release, yet potentially compromise antiviral defense mechanisms. They also modulate cytokine storms in SARS-CoV-2 and exhibit the potential to enhance anti-tumor immunity by inhibiting tumor-induced COX-2/PGE2 signaling. Specific NSAIDs have shown efficacy in inhibiting viral replication. The review highlights NSAIDs' synergy with other medications, like COX inhibitors and immunotherapy agents, in augmenting therapeutic effects. Notably, the World Health Organization's analysis found no substantial link between NSAIDs and the worsening of viral respiratory infections. The findings underscore NSAIDs' complex role in infection management. Understanding these interactions is crucial for optimizing therapeutic approaches in current and future pandemics. However, their dual nature warrants cautious application, particularly in vulnerable populations. NSAIDs present a paradoxical impact on immune responses in viral and bacterial infections. While offering potential benefits, their usage in infectious diseases, especially SARS-CoV-2, demands a nuanced understanding to balance therapeutic advantages against possible adverse effects.

Target-Based Small Molecule Drug Discovery for Colorectal Cancer: A Review of Molecular Pathways and In Silico Studies.

Colorectal cancer is one of the most prevalent cancer types. Although there have been breakthroughs in its treatments, a better understanding of the molecular mechanisms and genetic involvement in colorectal cancer will have a substantial role in producing novel and targeted treatments with better safety profiles. In this review, the main molecular pathways and driver genes that are responsible for initiating and propagating the cascade of signaling molecules reaching carcinoma and the aggressive metastatic stages of colorectal cancer were presented. Protein kinases involved in colorectal cancer, as much as other cancers, have seen much focus and committed efforts due to their crucial role in subsidizing, inhibiting, or changing the disease course. Moreover, notable improvements in colorectal cancer treatments with in silico studies and the enhanced selectivity on specific macromolecular targets were discussed. Besides, the selective multi-target agents have been made easier by employing in silico methods in molecular de novo synthesis or target identification and drug repurposing.