Date published: 2025-9-18

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LOXL1 Inhibitors

The chemical class of LOXL1 inhibitors comprises a diverse array of compounds that exert their inhibitory effects through intricate interactions with specific cellular signaling pathways. These pathways play crucial roles in regulating LOXL1 expression and enzymatic activity, ultimately influencing its impact on extracellular matrix remodeling processes. Nordihydroguaiaretic acid, for instance, targets the NF-κB signaling pathway, disrupting the activation of transcription factors involved in LOXL1 gene expression. Luteolin, on the other hand, acts as an indirect inhibitor by modulating the TGF-β signaling pathway. It interferes with Smad protein phosphorylation, hindering the transcriptional activation of LOXL1 and contributing to the downregulation of its expression. This theme continues with gallic acid, which targets the PI3K/Akt signaling pathway. By impeding Akt phosphorylation, gallic acid disrupts the downstream activation of transcription factors responsible for LOXL1 gene expression.

Resveratrol, quercetin, baicalein, and genistein showcase the versatility of indirect inhibition, each targeting distinct pathways such as JAK/STAT, MAPK/ERK, Wnt/β-catenin, and Notch, respectively. These compounds interfere with critical steps in these signaling cascades, resulting in diminished LOXL1 activity and expression. The chemical class also includes compounds like ursolic acid, ellagic acid, piceatannol, curcumin, and chrysin, which influence Hedgehog, Hippo, mTOR, Nrf2, and AMPK signaling pathways, respectively. These interactions showcase the intricate web of cellular processes that can be modulated to regulate LOXL1 activity indirectly. In summary, the chemical class of LOXL1 inhibitors encompasses a spectrum of compounds, each with a unique mechanism of action targeting specific signaling pathways. This targeted approach provides a nuanced understanding of how these inhibitors interfere with cellular processes to ultimately regulate LOXL1 expression and function in the context of extracellular matrix remodeling.

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