The term Vmn1r119 Inhibitors refers to a class of compounds that can interfere with the function of the Vmn1r119 receptor, a member of the G-protein-coupled receptor (GPCR) superfamily, by targeting various components of the signaling pathways associated with its activity. These compounds do not directly bind to the Vmn1r119 receptor but can affect its signaling indirectly through the modulation of cellular mechanisms.
The inhibitors operate through diverse mechanisms to interrupt the signaling pathways of GPCRs. Some compounds, like Pertussis Toxin and GDP-beta-S, act at the level of the G-protein, blocking its ability to relay signals from the receptor to downstream molecules. Others target specific enzymes involved in the signaling cascade; for example, U73122 and Genistein inhibit phospholipase C and tyrosine kinases, respectively, both of which play a role in GPCR signal transduction. Additional compounds, such as LY294002, W-7 Hydrochloride, and KT5720, inhibit downstream signaling molecules like PI3K, calmodulin, and PKA, which are involved in cellular responses to GPCR activation. Furthermore, inhibitors like Chelerythrine Chloride and Go 6983 target PKC, a kinase with multiple roles in GPCR signaling. ML7 Hydrochloride affects the actin cytoskeleton by inhibiting myosin light chain kinase, which can also be influenced by GPCR activity. Lastly, compounds like Suramin and NF449 can disrupt the signaling processes by inhibiting growth factor receptors and G-protein subunits, respectively, thereby modulating the overall signaling output of GPCR pathways such as those engaged by Vmn1r119.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Pertussis Toxin (islet-activating protein) | 70323-44-3 | sc-200837 | 50 µg | $451.00 | 3 | |
Pertussis Toxin can disrupt GPCR signaling by inhibiting the G-protein itself, preventing the transmission of signals from the receptor to downstream effectors. | ||||||
Genistein | 446-72-0 | sc-3515 sc-3515A sc-3515B sc-3515C sc-3515D sc-3515E sc-3515F | 100 mg 500 mg 1 g 5 g 10 g 25 g 100 g | $45.00 $164.00 $200.00 $402.00 $575.00 $981.00 $2031.00 | 46 | |
Genistein can inhibit tyrosine kinases, which may be involved in the phosphorylation events that follow GPCR activation. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $123.00 $400.00 | 148 | |
LY294002 can inhibit PI3K, a kinase that participates in the signaling pathways initiated by GPCRs. | ||||||
W-7 | 61714-27-0 | sc-201501 sc-201501A sc-201501B | 50 mg 100 mg 1 g | $166.00 $306.00 $1675.00 | 18 | |
W-7 Hydrochloride can disrupt calcium signaling by antagonizing calmodulin, a protein that often interacts with GPCR pathways. | ||||||
KT 5720 | 108068-98-0 | sc-3538 sc-3538A sc-3538B | 50 µg 100 µg 500 µg | $138.00 $220.00 $972.00 | 47 | |
KT5720 can inhibit PKA, a kinase that can be activated by cAMP, a second messenger in GPCR pathways. | ||||||
Chelerythrine chloride | 3895-92-9 | sc-3547 sc-3547A | 5 mg 25 mg | $90.00 $317.00 | 17 | |
Chelerythrine Chloride can inhibit PKC, which is involved in the signaling pathways that are downstream of GPCRs. | ||||||
Gö 6983 | 133053-19-7 | sc-203432 sc-203432A sc-203432B | 1 mg 5 mg 10 mg | $105.00 $299.00 $474.00 | 15 | |
Go 6983 can block PKC isoforms, affecting signaling related to GPCRs. | ||||||
ML-7 hydrochloride | 110448-33-4 | sc-200557 sc-200557A | 10 mg 50 mg | $91.00 $267.00 | 13 | |
ML7 Hydrochloride can inhibit myosin light chain kinase, which can be part of cellular responses to GPCR signaling. | ||||||
Suramin sodium | 129-46-4 | sc-507209 sc-507209F sc-507209A sc-507209B sc-507209C sc-507209D sc-507209E | 50 mg 100 mg 250 mg 1 g 10 g 25 g 50 g | $152.00 $214.00 $728.00 $2601.00 $10965.00 $21838.00 $41096.00 | 5 | |
Suramin can disrupt various signaling pathways by inhibiting growth factor receptors and enzymes that might intersect with GPCR cascades. | ||||||
NF449 | 627034-85-9 | sc-478179 sc-478179A sc-478179B | 10 mg 25 mg 100 mg | $203.00 $469.00 $1509.00 | 1 | |
NF449 can antagonize Gαs subunits, preventing GPCR-mediated activation of adenylate cyclase. | ||||||