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β-catenin inhibitors and activators act on the transcriptional coactivator at the center of canonical Wnt signaling. β-Catenin also links cadherins to the actin cytoskeleton, while its free signaling pool is constantly degraded. Wnt stimulation stabilizes β-catenin, which then enters the nucleus and binds T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors. FH535 suppresses β-catenin/TCF-dependent transcription and also antagonizes peroxisome proliferator-activated receptors γ and δ (PPARγ, PPARδ). ICG-001 and foscenvivint block β-catenin binding to CREB-binding protein (CBP), a coactivator named after cyclic adenosine monophosphate response element-binding protein (CREB). Astragaloside I and WAY-316606 act in the opposite direction, and WAY-316606 inhibits the extracellular Wnt antagonist secreted frizzled-related protein 1 (sFRP-1). Upstream modulators, such as porcupine and tankyrase inhibitors, are listed under Wnt.
xStAx-VHLL is a PROTAC degrader targeting β-catenin, promoting its ubiquitination and proteasomal degradation. It effectively inhibits the Wnt/β-catenin signaling pathway and suppresses proliferation of colon cancer cells, demonstrating anti-tumor activity.
NRX-1933 is a β-catenin:β-TrCP interaction enhancer that serves as a molecular glue, facilitating the ubiquitination and subsequent degradation of mutated β-catenin. This compound is particularly relevant for research involving the aberrant activation of the Wnt/β-catenin signaling pathway, providing insights into tumor progression and potential therapeutic strategies. Its ability to promote targeted degradation of dysregulated β-catenin makes NRX-1933 a valuable tool for studies on cancer biology and treatment development.
