Kremen-2 Activators

Lithium Chloride fosters an environment where beta-catenin can accumulate, potentially compensating for Kremen-2 mediated inhibition of the signaling cascade. GSK-3 Inhibitor IX, GSK-3 Inhibitor XVI, and QS 11, provide a boost to beta-catenin signaling that can overshadow the suppressive effects Kremen-2 typically exerts on the pathway. Valproic Acid operates through a different mode, acting as an HDAC inhibitor to broaden the spectrum of gene expression, which may touch upon components of the Wnt pathway and inadvertently influence Kremen-2's function.

A direct Wnt signaling agonist creates an influx of ligands that may increase the activation of Kremen-2 by saturating its inhibitory role. Conversely, tankyrase inhibitors like XAV939 and JW55 work to stabilize Axin, thereby promoting the degradation of beta-catenin and subtly shifting the signaling equilibrium that Kremen-2 is a part of. Other compounds such as IWR-1 and IWP-2 selectively manipulate the production and activity of Wnt ligands, which can lead to an altered interaction with Kremen-2, thus affecting its activity. Similarly, Skp2 Inhibitor, C1, operates by increasing p27 levels, which may indirectly influence the cell cycle and Wnt signaling, further affecting the functional landscape of Kremen-2.