EZH2 inhibition impacts both tumor cells and TME Gaining a deeper understanding of the multiple effects of EZH2i in these patients could potentially aid in predicting clinical responses.
The first immune checkpoint inhibitor for clinical use: CTLA-4 inhibitor. However, it enhances immune function, specifically by boosting the cytotoxicity of immune cells, which often results in more adverse effects.
COX-2 inhibitors aid in the release of prostaglandins, which are synthesized from arachidonic acid. Prostaglandins play a key role in inflammatory responses.
Several selective CDK7 inhibitors, which have entered clinical trials, have demonstrated effective anti-cancer results in numerous pre-clinical models.
CDK4 inhibitors can inhibit the formation of complexes between CDK4 and cyclin D, block ATP binding, thereby severing upstream growth signals, and prevent the transition from G1 to S phase.
The overexpression of the anti-apoptotic factor Myeloid Cell Leukemia 1 (MCL-1), caused by the activation of CDK9, will lead to the transformation of malignant tumor cells. Therefore, inhibiting CDK9 will downregulate MCL-1, thereby suppressing tumor growth.
Small-molecule CDK2 selective inhibitors would be significant chemical probes for dissecting cellular processes or understanding the basics of diseases.
Calcineurin inhibitors, acting as immunosuppressive agents, are employed in the treatment of autoimmune disorders like lupus nephritis, atopic dermatitis, interstitial lung disease, and idiopathic inflammatory myositis, among others.