NGAL inhibitors, short for Neutrophil Gelatinase-Associated Lipocalin inhibitors, constitute a class of chemical compounds designed to target and modulate the activity of Neutrophil Gelatinase-Associated Lipocalin (NGAL). NGAL is a small protein that plays a crucial role in various physiological processes, particularly in the innate immune response and cellular stress. It is involved in the regulation of iron homeostasis, antimicrobial defense, and the transport of small hydrophobic molecules within cells. NGAL has garnered significant attention in the field of biomedical research due to its associations with various diseases and conditions, including kidney injury, cancer, and inflammatory disorders. Consequently, NGAL inhibitors have emerged as a promising avenue for investigating the underlying mechanisms of these conditions and exploring interventions.
Structurally, NGAL inhibitors can vary widely but generally possess functional groups or molecular motifs that allow them to interact with specific binding sites on the NGAL protein, modulating its activity. By inhibiting NGAL, these compounds may influence the pathways and cellular processes in which NGAL is involved, offering insights into disease mechanisms and targets for future drug development. Researchers are actively exploring NGAL inhibitors to unravel the intricate roles of NGAL in health and disease, shedding light on the molecular pathways that could be harnessed for a range of biomedical applications. Understanding the biochemistry and pharmacology of NGAL inhibitors has the ability to yield valuable insights into the development of novel diagnostic tools
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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α-Lipoic Acid | 1077-28-7 | sc-202032 sc-202032A sc-202032B sc-202032C sc-202032D | 5 g 10 g 250 g 500 g 1 kg | $68.00 $120.00 $208.00 $373.00 $702.00 | 3 | |
Modulates NGAL via Nrf2 pathway activation. | ||||||
Ursolic Acid | 77-52-1 | sc-200383 sc-200383A | 50 mg 250 mg | $55.00 $176.00 | 8 | |
Downregulates NGAL expression via NF-κB inhibition. |