The chemical class labeled MDA-7 Inhibitors comprises a variety of compounds, each characterized by their potential to indirectly suppress the activity of MDA-7, also known as Interleukin-24. These inhibitors primarily exert their effects by modulating different signaling pathways and cellular processes that are crucial for the regulation and expression of MDA-7. This class includes corticosteroids like Dexamethasone and Hydrocortisone, which are known for their potent anti-inflammatory properties. These compounds can inhibit MDA-7 by suppressing cytokine production within immune response pathways.
Nonsteroidal anti-inflammatory drugs (NSAIDs) such as Aspirin and Ibuprofen also belong to this class. They function by altering the COX pathway, leading to reduced inflammatory mediator levels, which can in turn inhibit MDA-7 production. The class is further diversified with the inclusion of kinase inhibitors like Sorafenib and Imatinib. These compounds target multiple receptors and signaling pathways, potentially leading to the inhibition of MDA-7 by modulating cytokine production and associated cellular signaling. Moreover, compounds like Rapamycin, Wortmannin, and SP600125 add complexity to this class by targeting mTOR, PI3K, and JNK pathways respectively. Their inhibition of these pathways can lead to reduced MDA-7 activity by affecting cell growth, proliferation, stress responses, and inflammatory signaling. MEK inhibitors such as U0126 and PD98059 further contribute to this class by potentially inhibiting MDA-7 through their modulation of the MAPK/ERK pathway, affecting cell signaling and cytokine production. Lastly, compounds like BAY 11-7082, which inhibit the NF-κB pathway, are also significant members of this class.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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BAY 11-7082 | 19542-67-7 | sc-200615B sc-200615 sc-200615A | 5 mg 10 mg 50 mg | $61.00 $83.00 $349.00 | 155 | |
An NF-κB pathway inhibitor that can potentially inhibit MDA-7 by affecting transcriptional regulation of cytokines and inflammatory mediators. |