SLC22A29 Inhibitors

The Slc22a29 Inhibitors represent a diverse class of chemicals designed to modulate the function of Slc22a29, a protein predicted to be involved in anion antiporter, short-chain fatty acid transmembrane transporter, and sodium-independent organic anion transmembrane transporter activities. This protein plays a crucial role in cellular processes, particularly in the transport of various ions and organic anions across the basolateral plasma membrane. Probucol, an antioxidant, directly inhibits Slc22a29 by influencing the composition of the basolateral plasma membrane, disrupting anion antiporter activity. Cimetidine, an H2 receptor antagonist, indirectly inhibits Slc22a29 by modulating intracellular pH, affecting sodium-independent organic anion transport, and disrupting its transmembrane transporter activity. Indomethacin, a nonsteroidal anti-inflammatory drug, interferes with organic anion transport, indirectly inhibiting Slc22a29 and disrupting its predicted role in cellular processes. Furosemide, a loop diuretic, impacts Slc22a29 by altering sodium homeostasis, indirectly inhibiting anion antiporter activity and influencing basolateral plasma membrane composition. Nateglinide, an anti-diabetic agent, indirectly inhibits Slc22a29 by influencing short-chain fatty acid transport, disrupting its transmembrane transporter activity, and modulating cellular processes.

Gemfibrozil, a lipid-lowering agent, inhibits Slc22a29 by affecting basolateral plasma membrane composition, disrupting anion antiporter activity, and interfering with organic anion transport. Losartan, an angiotensin II receptor antagonist, indirectly inhibits Slc22a29 by modulating intracellular signaling pathways, disrupting sodium-independent organic anion transport, and impacting transmembrane activity. Sulfinpyrazone, a uricosuric agent, indirectly inhibits Slc22a29 by interfering with organic anion transport, disrupting predicted functions in cellular processes. Methotrexate, an antimetabolite and antifolate, inhibits Slc22a29 by influencing short-chain fatty acid transport, disrupting its transmembrane transporter activity, and modulating cellular processes. Irbesartan, an angiotensin II receptor antagonist, indirectly inhibits Slc22a29 by modulating intracellular signaling pathways, disrupting sodium-independent organic anion transport, and impacting transmembrane activity. Collectively, these inhibitors showcase the intricate ways in which specific chemical compounds can modulate the function of Slc22a29, offering potential avenues for further exploration and understanding of cellular transport mechanisms.