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Results for "

Cuproptosis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Cuproptosis (4) Aldehyde Dehydrogenase (ALDH) (1) Apoptosis (3) Bacterial (1) Fungal (1) Interleukin Related (1) Proton Pump (1) Pyroptosis (1) Reactive Oxygen Species (1) Topoisomerase (1)
By Research Areas:	Cancer (3) Infection (1) Metabolic Disease (2)

Inhibitors & Agonists

Screening Libraries

Targets Recommended: Cuproptosis

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-12040

Elesclomol 20+ Cited Publications STA-4783	Reactive Oxygen Species Apoptosis Cuproptosis	Cancer
Elesclomol (STA-4783) is a potent copper ionophore and promotes copper-dependent cell death (cuproptosis). Elesclomol specifically binds ferredoxin 1 (FDX1) α2/α3 helices and β5 strand. Elesclomol inhibits FDX1-mediated Fe-S cluster biosynthesis. Elesclomol is an oxidative stress inducer that induces cancer cell apoptosis. Elesclomol is a reactive oxygen species (ROS) inducer. Elesclomol can be used for Menkes and associated disorders of hereditary copper deficiency research .

HY-B0572

Zinc Pyrithione 4 Publications Verification	Cuproptosis Proton Pump Bacterial Fungal	Infection Metabolic Disease
Zinc Pyrithione is an antifungal and antibacterial agent disrupting membrane transport by blocking the proton pump . Zinc Pyrithione is also a copper ionophore that delivers copper into cells and is a useful tool for studying cuproptosis .

HY-156376

Cu(II)-Elesclomol	Cuproptosis Apoptosis Topoisomerase	Cancer
Cu(II)-Elesclomol is a Cu ²⁺ complex of Elesclomol (HY-12040). Cu(II)-Elesclomol induces *cuproptosis. Cu(II)-Elesclomol also inducesapoptosis, causes a G1 cell cycle block and induces DNA double strand breaks in K562 cells. Cu(II)-Elesclomol also weakly inhibits DNA topoisomerase I*. Cu(II)-Elesclomol has anticancer activity .

HY-B0240

Disulfiram Maximum Cited Publications 47 Publications Verification Tetraethylthiuram disulfide; TETD	Aldehyde Dehydrogenase (ALDH) Interleukin Related Pyroptosis Apoptosis Cuproptosis	Metabolic Disease Cancer
Disulfiram (Tetraethylthiuram disulfide) is a specific inhibitor of aldehyde-dehydrogenase (ALDH1), used for the treatment of chronic alcoholism by producing an acute sensitivity to alcohol. Disulfiram inhibits gasdermin D (GSDMD) pore formation in liposomes and inflammasome-mediated pyroptosis and IL-1β secretion in human and mouse cells. Disulfiram, a copper ion carrier, with Cu ²⁺ increases intracellular ROS levels and induces cuproptosis .

Cat. No.	Product Name

HY-L133

Cuproptosis Compound Library	188 compounds
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 cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism. Targeted regulation of cuproptosis 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 cuproptosis. MCE supplies a unique collection of 188 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.

Cuproptosis Compound Library

188 compounds

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 cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism.

Targeted regulation of cuproptosis 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 cuproptosis.

MCE supplies a unique collection of 188 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.

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