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Results for "

iron death

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Ferroptosis (3) Fluorescent Dye (1) Glutathione Peroxidase (1) MDM-2/p53 (1) Necroptosis (1) RIP kinase (1)
By Research Areas:	Cancer (4)

Inhibitors & Agonists

Screening Libraries

Natural
Products

Targets Recommended: DAPK Ferroportin PD-1/PD-L1

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-153629

FSEN1	Ferroptosis	Cancer
FSEN1 is a potent and non-competitive FSP1 inhibitor with an IC₅₀ value of 313 nM. FSEN1 triggers iron death in cancer cells by inhibiting FSP1. FSEN1 can be used in research of cancer .

HY-112063

CIL56

1 Publications Verification

Ferroptosis Cancer

CIL56 is a potent and selective ferroptosis inducer. Ferroptosis is an iron-dependent form of regulated cell death (RCD).

CIL56 1 Publications Verification	Ferroptosis	Cancer
CIL56 is a potent and selective ferroptosis inducer. Ferroptosis is an iron-dependent form of regulated cell death (RCD).

HY-100887

Piperazine Erastin 5+ Cited Publications
Piperazine erastin is an analog of erastin which induces an iron-dependent form of non-apoptotic cell death, termed ferroptosis. Piperazine erastin can be used in cancer research .

HY-153435

RIP1 kinase inhibitor 5	RIP kinase Necroptosis	Cancer
RIP1 kinase inhibitor 5 (example 1) is a potent inhibitor of RIP1, which is used as a checkpoint kinase to control tumor immunity . RIP1 kinase inhibitor 5 is similar with SIR1-365 (compound 13), which inhibits necrosis and iron death activity .

HY-149028

Mem-C1C18	Fluorescent Dye	Others
Mem-C1C18 is a polarity-sensitive fluorescent probe with excellent plasma membrane anchoring, high brightness and a sensitive response to environmental polarity by altering the fluorescence lifetime. Mem-C1C18 can be used to quantify changes in the polarity of the plasma membrane during iron death .

HY-155851

Lepadin E	Ferroptosis MDM-2/p53 Glutathione Peroxidase	Cancer
Lepadin E is a significantly cytotoxic ferroptosis inducer that induces iron death through the classical p53-SLC7A11-GPX4 pathway. Lepadin E promoted p53 expression, decreases SLC7A11 and GPX4 levels, and leads to increased ROS and lipid peroxide production, and upregulated ACSL4 expression, thus causes cell death. Lepadin E has significant antitumor effect .

Cat. No.	Product Name

HY-L051

Ferroptosis Compound Library	925 compounds
Ferroptosis is a novel type of cell death program that is distinct from apoptosis, necroptosis and autophagy. It is dependent on iron and reactive oxygen species (ROS) and is characterized by lipid peroxidation. As a novel type of cell death, ferroptosis has distinct properties and recognizing functions involved in physical conditions or various diseases including cancers, neurodegenerative diseases, acute renal failure, etc. MCE carefully collected a unique collection of 925 ferroptosis signaling pathway related compounds with ferroptosis-inducing or -inhibitory activity. MCE Ferroptosis Compound Library is a useful tool to study ferroptosis mechanism as well as related diseases.

Ferroptosis Compound Library

925 compounds

Ferroptosis is a novel type of cell death program that is distinct from apoptosis, necroptosis and autophagy. It is dependent on iron and reactive oxygen species (ROS) and is characterized by lipid peroxidation. As a novel type of cell death, ferroptosis has distinct properties and recognizing functions involved in physical conditions or various diseases including cancers, neurodegenerative diseases, acute renal failure, etc.

MCE carefully collected a unique collection of 925 ferroptosis signaling pathway related compounds with ferroptosis-inducing or -inhibitory activity. MCE Ferroptosis Compound Library is a useful tool to study ferroptosis mechanism as well as related diseases.

HY-L133

Cuproptosis Compound Library	187 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 187 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

187 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 187 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.

Lepadin E	Structural Classification Alkaloids Animals Source classification Marine natural products Other marine organisms Quinoline Alkaloids	Ferroptosis MDM-2/p53 Glutathione Peroxidase
Lepadin E is a significantly cytotoxic ferroptosis inducer that induces iron death through the classical p53-SLC7A11-GPX4 pathway. Lepadin E promoted p53 expression, decreases SLC7A11 and GPX4 levels, and leads to increased ROS and lipid peroxide production, and upregulated ACSL4 expression, thus causes cell death. Lepadin E has significant antitumor effect .

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