The chosen chemicals present a variety of indirect mechanisms aimed at inhibiting the protein PRAME like 30. These mechanisms are predicated on the hypothesis that by modulating specific cellular pathways and processes, these compounds possess the potential to indirectly impede the functional activities of PRAME like 30.
Two notable examples, Disulfiram and Vorinostat, illustrate the strategic approach of affecting metabolic and gene expression pathways, respectively. Disulfiram's ability to inhibit aldehyde dehydrogenase has the potential to result in the accumulation of metabolic intermediates. This accumulation, in turn, might exert an influence on the functional environment in which PRAME like 30 operates. On the other hand, Vorinostat, with its inhibitory activity against histone deacetylases, can bring about alterations in gene expression patterns. These alterations have the capacity to impact pathways associated with PRAME like 30, thereby potentially leading to its functional inhibition. These mechanisms represent intricate strategies to indirectly target PRAME like 30, and further experimental validation is warranted to ascertain their efficacy.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Sunitinib Malate | 341031-54-7 | sc-220177 sc-220177A sc-220177B | 10 mg 100 mg 3 g | $193.00 $510.00 $1072.00 | 4 | |
Sunitinib, a receptor tyrosine kinase inhibitor, affects multiple signaling pathways. This broad inhibition can indirectly inhibit PRAME like 30 by disrupting pathways related to cell growth and survival where PRAME like 30 may function. | ||||||
Sorafenib | 284461-73-0 | sc-220125 sc-220125A sc-220125B | 5 mg 50 mg 500 mg | $56.00 $260.00 $416.00 | 129 | |
Sorafenib, another receptor tyrosine kinase inhibitor, targets several signaling pathways. Inhibiting these pathways can indirectly inhibit PRAME like 30 by affecting cellular processes like proliferation and apoptosis, where PRAME like 30 might be involved. |