β-defensin 5 Inhibitors
β-Defensin 5 inhibitors are a class of chemical compounds designed to interact with and inhibit the activity of β-defensin 5, a member of the defensin family of antimicrobial peptides. β-Defensin 5 is a small, cationic peptide that is part of the innate immune system, playing a crucial role in the first line of defense against microbial pathogens. This peptide exhibits antimicrobial activity by disrupting the membrane integrity of bacteria, fungi, and viruses, ultimately leading to cell lysis. The structure of β-defensin 5 consists of a characteristic beta-sheet fold stabilized by disulfide bonds, which contributes to its stability and functional conformation. Inhibitors of β-defensin 5 are typically small molecules or peptides that can bind to β-defensin 5, altering its conformation or blocking its active sites, thereby reducing its interaction with microbial membranes.
Research into β-defensin 5 inhibitors often focuses on their molecular interactions, structure-activity relationships, and their ability to modulate the activity of β-defensin 5 in various experimental settings. Structural studies using techniques like X-ray crystallography, NMR spectroscopy, and molecular dynamics simulations provide insights into how these inhibitors bind to β-defensin 5, revealing key residues and motifs critical for binding affinity and specificity. The development of β-defensin 5 inhibitors involves a comprehensive understanding of the biochemical pathways and molecular mechanisms governing β-defensin 5's role in antimicrobial defense. This includes exploring the dynamics of peptide-inhibitor interactions and assessing the impact of these inhibitors on the structural and functional properties of β-defensin 5. The study of β-defensin 5 inhibitors not only contributes to the broader understanding of defensin biology but also provides a valuable framework for designing novel molecules capable of modulating host-pathogen interactions at a molecular level.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Hydrocortisone | 50-23-7 | sc-300810 | 5 g | $100.00 | 6 | |
Hydrocortisone may downregulate β-defensin 5 by activating its receptor, which can lead to the suppression of pro-inflammatory transcription factors like NF-κB, a known inducer of β-defensin 5 gene expression during inflammatory responses. | ||||||
(−)-Epigallocatechin Gallate | 989-51-5 | sc-200802 sc-200802A sc-200802B sc-200802C sc-200802D sc-200802E | 10 mg 50 mg 100 mg 500 mg 1 g 10 g | $42.00 $72.00 $124.00 $238.00 $520.00 $1234.00 | 11 | |
Epigallocatechin Gallate could decrease β-defensin 5 expression through its inhibition of the NF-κB pathway. By hindering this pathway, EGCG might reduce the transcriptional activation of defensin genes normally upregulated in response to microbial threat or inflammation. | ||||||
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $65.00 $319.00 $575.00 $998.00 | 28 | |
As an active metabolite of vitamin A, retinoic acid may repress β-defensin 5 expression by binding to its specific nuclear receptors, which can alter the transcription of genes involved in mucosal immunity, potentially leading to decreased production of antimicrobial peptides, including β-defensin 5. | ||||||
Cholecalciferol | 67-97-0 | sc-205630 sc-205630A sc-205630B | 1 g 5 g 10 g | $70.00 $160.00 $290.00 | 2 | |
Cholecalciferol can inhibit β-defensin 5 expression by engaging the vitamin D receptor, which may lead to the negative regulation of gene expression associated with innate immune responses. This could result in a reduced presence of β-defensin 5 in epithelial cells. | ||||||
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
Lithium chloride may suppress β-defensin 5 expression by inhibiting glycogen synthase kinase-3 (GSK-3). GSK-3 inhibition has been associated with decreased activity of transcription factors that are crucial for the expression of defensin genes. | ||||||
Tetracycline | 60-54-8 | sc-205858 sc-205858A sc-205858B sc-205858C sc-205858D | 10 g 25 g 100 g 500 g 1 kg | $62.00 $92.00 $265.00 $409.00 $622.00 | 6 | |
Tetracycline could inhibit β-defensin 5 expression by directly interacting with ribosomal subunits, leading to a general inhibition of protein synthesis, which would include proteins involved in the immune response. Additionally, tetracyclines can have anti-inflammatory properties that may specifically target pathways responsible for inducing β-defensin 5 expression. | ||||||
Caffeine | 58-08-2 | sc-202514 sc-202514A sc-202514B sc-202514C sc-202514D | 50 g 100 g 250 g 1 kg 5 kg | $32.00 $66.00 $95.00 $188.00 $760.00 | 13 | |
Caffeine might reduce β-defensin 5 levels by antagonizing adenosine receptors, which may play a role in the modulation of immune and inflammatory responses. Through this antagonism, caffeine could lead to a downregulation of pro-inflammatory cytokines and subsequently β-defensin 5 expression. | ||||||
Indomethacin | 53-86-1 | sc-200503 sc-200503A | 1 g 5 g | $28.00 $37.00 | 18 | |
Indomethacin may reduce β-defensin 5 expression through its action as a nonsteroidal anti-inflammatory drug (NSAID). By inhibiting cyclooxygenase enzymes (COX-1 and COX-2), indomethacin could decrease the production of prostaglandins that are involved in the inflammatory response, which in turn might lead to reduced β-defensin 5 expression. | ||||||
Metformin | 657-24-9 | sc-507370 | 10 mg | $77.00 | 2 | |
Metformin could decrease β-defensin 5 expression via activation of AMP-activated protein kinase (AMPK), which may lead to alterations in cellular metabolism and immune responses, potentially resulting in lowered expression of genes related to innate immunity, including defensin genes. | ||||||
Sodium Salicylate | 54-21-7 | sc-3520 sc-3520A sc-3520B sc-3520C | 1 g 25 g 500 g 1 kg | $10.00 $25.00 $80.00 $136.00 | 8 | |
Sodium salicylate may inhibit β-defensin 5 expression by suppressing the activity of NF-κB. This compound, related to aspirin, could decrease inflammatory signaling pathways that are involved in the upregulation of β-defensin 5 during inflammatory states. | ||||||