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Cuproptosis Compound Library

MCE 站：Cuproptosis Compound Library

Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis". The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, ａnd ferroptosis. Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation ａnd subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress ａnd cell death. Studies have shown that the necessary factors for copper death include the presence of glutathione, mitochondrial metabolism of galactose ａnd pyruvate, glutamine metabolism, ａnd glutamine metabolism. Targeted regulation of copper death is a potential choice to treat cancer, rheumatoid arthritis, ａnd other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence ａnd development of tumors by destroying TCA in mitochondria ａnd then inducing copper death. MCE supplies a unique collection of 144 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis ａnd may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, ａnd other diseases.

Description & Advantages:

    A unique collection of 144 cuproptosis-related compounds for high throughput screening (HTS) ａnd high content screening (HCS).

    A useful tool to screen new inhibitors or inducers of cuproptosis.

   Target diverse, medicinally active ａnd cell permeable.

   Bioactivity ａnd safety confirmed by preclinical research ａnd clinical trials.

   More detailed compound information with structure, IC50, ａnd other chemical & biological data.

   High purity ａnd quality validated by NMR ａnd LC/MS.

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