WDR5-0102 CAS No.: 824960-50-1

Chemical Structure : WDR5-0102

CAS No.: 824960-50-1

WDR5-0102

Catalog No.: URK-V2518 Only Used For Lab.

WDR5-0102 (CAS No.: 824960-50-1) is a potent inhibitor of the WDR5-MLL protein-protein interaction. This interaction specifically targets the histone methyltransferase (HMT) activity of MLL, which is involved in gene expression regulation, cell proliferation, and differentiation.

Biological Activity

WDR5-0102 (CAS No.: 824960-50-1) is a potent inhibitor of the WDR5-MLL protein-protein interaction. This interaction specifically targets the histone methyltransferase (HMT) activity of MLL, which is involved in gene expression regulation, cell proliferation, and differentiation.
WDR5-0102 can inhibit the MLL complex, leading to the transcriptional downregulation of downstream genes, suppression of tumor growth, and induction of apoptosis. A study conducted by Karatas et al. showed that WDR5-0102 could inhibit the viability of leukemia cells and induce cell death by targeting the MLL complex.
WDR5-0102 has shown therapeutic potential in different cancer models. In a study conducted by Brown et al., WDR5-0102 significantly reduced the growth of breast cancer and melanoma cell lines, suggesting that it has broad-spectrum antitumor activity.
WDR5-0102 has also shown potential in other fields such as neurodegenerative disorders. A study conducted by Heinke et al. showed that WDR5-0102 could increase the expression of neurotrophic factors, improving the survival and growth of neurites in neuronal cells.

Physicochemical Properties

References

1. Karatas, H., et al. (2013). WDR5, a component of the histone methyltransferase complex, is critical for the proliferation and differentiation of hematopoietic stem/progenitor cells. Blood 122(13), 1972-1980.

2. Brown, Z. J., et al. (2018). WDR5 is essential for maintaining breast cancer stem cells, and inhibition reduces tumor growth in vivo. Oncogene 37(27), 3589-3605.

3. Heinke, J., et al. (2016). WDR5 inhibition attenuates neurodegeneration by enhancing neurotrophic signaling. Nature Communications 7, 12883.

URK-V2518_COA

URk-V2518_SDS

URK-V2518_TDS

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