From: Metabolic reprogramming: the emerging concept and associated therapeutic strategies
Name of agent | Conventional application | Mechanism of action | Clinical significance | Target |
---|---|---|---|---|
Sulfasalazine | Rheumatic arthritis, ulcerative colitis | Specific inhibition of xCT cystine transporter | Disruption of reduced glutathione (GSH) synthesis and to make cancer cells suscptible to oxidative stress | Gastric tumor and NSCLC progression, breast cancer metastasis |
Itraconazole | Fungal infections such as Aspergillus | Inhibition of Smoothened (Smo), active Shh receptor | To inhibit proliferation of secondary mutated Shh signal (e.g. Gli2 amplification) | Difficult-to-cure medulloblastoma |
Terfenadine | Auto-immune disorders such as allergic dermatitis | Histamine receptor H1 antagonist | To prevent secretion of VEGF from mast cells localized in hypoxic lesion, and to induce ROS-mediated apoptosis and autophagy of melanoma cells | Malignant melanoma |
Simvastatin | Hyperlipidemia | Specific inhibition of HMG-CoA reductase | To prevent mutant p53 from activating mevalonate pathway for cholesterol synthesis | Breast tumor, ovarian cancer |