Glucocorticoids (GCs) are defined by their role in maintaining glucose homeostasis and natural GCs are a class of corticosteroids secreted by the adrenal cortex. Cortisol is the most important natural GC in humans. Cellular cortisol levels are regulated by the tissue-specific metabolic enzymes 11β-hydroxysteroid dehydrogenase 1 and 2 (11β-HSD 1 and 2); 11β-HSD 1 converts inactive cortisone to active cortisol, while 11β-HSD 2 has the opposite function.

Since the discovery of escaping mechanism of tumor from negative immune regulation, the paradigm of drug discovery for anti-cancer agents has been dramatically shifted to cancer immunotherapy (e.g., dendritic cell therapy, CAR-T cell therapy, or antibody therapy) by stimulating patient’s immune system to treat cancer. 

Molecular docking approaches explore the receptor-ligand conformations within the binding sites of macromolecular targets [1]. Structure-based drug discovery is widely used by the scientific community in Medicinal Chemistry to estimate the ligand-receptor binding free energy by evaluating critical phenomena involved in the intermolecular recognition process [2,3].

TTK is a dual-specific protein kinase that phosphorylates serine and threonine. The spindle assembly checkpoint (SAC) acts as a molecular monitoring mechanism that regulates mitosis and ensures accurate separation of chromosomes. TTK is a key regulator of the SAC. Activated TTK localizes to kinetochores and activates SAC function. Simultaneously, TTK promotes error correction by phosphorylating several substrates. 

The advent of immune checkpoint inhibition revolutionized cancer care, yet many people will fail to respond due to innate or acquired resistance. Combination therapies with immune checkpoint inhibitors are being explored to enhance their efficacy and improve patient outcomes. Focal adhesion kinase (FAK), known for its roles in cell adhesion and migration, has emerged as a potential therapeutic target due to the identification of its additional functions in cancer progression, including its ability to establish a pro-tumorigenic, immunosuppressive microenvironment.