Date published: 2025-10-25

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R-Spondin Inhibitors

R-Spondin inhibitors constitute a unique chemical class of compounds with the primary objective of modulating the activity of R-Spondins, a group of secreted proteins that play essential roles in cell signaling and developmental processes. These inhibitors are designed to target specific interactions within the Wnt signaling pathway, where R-Spondins function as agonists to enhance Wnt signaling activity. The Wnt pathway is a crucial regulator of cellular proliferation, differentiation, and tissue homeostasis, making R-Spondin inhibitors of great interest in various research fields.

The chemical structures of R-Spondin inhibitors vary, and they can be categorized into diverse classes, such as small molecules or peptidomimetics. These inhibitors act by blocking the binding of R-Spondins to their cognate receptors, LGR4, LGR5, and LGR6, which subsequently leads to the inhibition of Wnt signaling pathway activation. By modulating the activity of R-Spondins, these inhibitors have the potential to exert profound effects on cellular processes, including stem cell self-renewal, tissue regeneration, and organogenesis. Researchers have been actively investigating R-Spondin inhibitors to better understand the intricacies of Wnt signaling and its implications in various conditions. The development of R-Spondin inhibitors is an active area of ongoing research, with scientists continuously exploring novel chemical scaffolds.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

LGK 974

1243244-14-5sc-489380
sc-489380A
5 mg
50 mg
$352.00
$1270.00
2
(0)

This is another small-molecule inhibitor that selectively targets the Wnt signaling pathway, including R-spondins.

IWP-2

686770-61-6sc-252928
sc-252928A
5 mg
25 mg
$94.00
$286.00
27
(1)

IWP-2 has inhibitory effects on R-spondin-mediated Wnt signaling.

PRI-724

1422253-38-0sc-507535
25 mg
$255.00
(0)

While primarily known as a CBP/beta-catenin inhibitor, PRI-724 also affects R-spondin-dependent Wnt signaling.