necroptosis pathway

Pathways Recommended:	MAPK/ERK Pathway

By Targets:	Necroptosis (5) Apoptosis (2) Atg8/LC3 (2) Autophagy (5) Endogenous Metabolite (2) ERK (2) Fungal (2) HIV (2) Keap1-Nrf2 (2) Mixed Lineage Kinase (1) p62 (2) PI3K (2) Reactive Oxygen Species (4) RIP kinase (4) TNF Receptor (2)
By Research Areas:	Cancer (7) Cardiovascular Disease (2) Infection (2) Inflammation/Immunology (4) Neurological Disease (4)

Targets Recommended: Necroptosis

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-17363

Dimethyl fumarate Maximum Cited Publications 28 Publications Verification	Keap1-Nrf2 Reactive Oxygen Species HIV Autophagy Endogenous Metabolite	Infection Neurological Disease Inflammation/Immunology Cancer
Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research .

HY-17363R

Dimethyl fumarate (Standard)	Keap1-Nrf2 Reactive Oxygen Species HIV Autophagy Endogenous Metabolite	Infection Neurological Disease Inflammation/Immunology Cancer
Dimethyl fumarate (Standard) is the analytical standard of Dimethyl fumarate. This product is intended for research and analytical applications. Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research .

HY-W010201

Citronellol 2 Publications Verification (±)-Citronellol; (±)-β-Citronellol	Reactive Oxygen Species ERK PI3K TNF Receptor Atg8/LC3 p62 Apoptosis Necroptosis Autophagy Fungal	Cardiovascular Disease Neurological Disease Cancer
Citronellol ((±)-Citronellol) is an orally active inducer of apoptosis. Citronellol can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol can induce *necroptosis* in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis .

HY-144828

RIP1/RIP3/MLKL activator 1 2 Publications Verification	RIP kinase Mixed Lineage Kinase Necroptosis	Cancer
RIP1/RIP3/MLKL activator 1 (Compound 6i) is a potent anti-glioma agent. RIP1/RIP3/MLKL activator 1 induces *necroptosis* through RIP1/RIP3/MLKL pathway. RIP1/RIP3/MLKL activator 1 exerts acceptable BBB permeability .

HY-146757

RIPK1-IN-13	RIP kinase	Inflammation/Immunology
RIPK1-IN-13 (Compound 8) is a potent inhibitor of RIPK1 with an IC₅₀ value of 1139 nM. RIPK1-IN-13 blocks the activation of the necroptosis pathway via the inhibition of RIPK1. RIPK1-IN-13 has the potential for the research of inflammation diseases .

HY-156920

VDX-111	Necroptosis RIP kinase	Inflammation/Immunology Cancer
VDX-111 is an analog of vitamin D. VDX-111 exhibits cytotoxicity in ovarian cancer cells through upregulation of RIPK1/RIPK3 pathway and induction of *necroptosis*. VDX-111 promotes expressions of cytokines and exhibits antitumor activity in mouse model .

HY-W010201R

Citronellol (Standard) (±)-Citronellol (Standard); (±)-β-Citronellol (Standard)	Reactive Oxygen Species ERK PI3K TNF Receptor Atg8/LC3 p62 Apoptosis Necroptosis Autophagy Fungal	Cardiovascular Disease Neurological Disease Cancer
Citronellol (Standard) is the analytical standard of Citronellol. Citronellol (Standard) is an orally active inducer of apoptosis. Citronellol (Standard) can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol (Standard) can induce *necroptosis* in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol (Standard) can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol (Standard) exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis .

HY-168640

RIP3 activator 1	Autophagy Necroptosis RIP kinase	Cancer
RIP3 activator 1 (compound C8) is a potent RIP3 activator. RIP3 activator 1 inhibits cell growth. RIP3 activator 1 induces *necroptosis* through the RIP3/p62/Keap1 signaling pathway. RIP3 activator 1 increases the protein expression of p-MLKL. RIP3 activator 1 induces autophagy. RIP3 activator 1 increases accumulation of LC3-II and p62 protein expression .

Cat. No.	Product Name

HY-L059

Pyroptosis Compound Library	1,430 compounds
Programmed cell death pathways, including apoptosis, pyroptosis and necroptosis, are regulated by unique sets of host proteins that coordinate a variety of biological outcomes. Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response. This process promotes the rapid clearance of various bacterial, viral, fungal and protozoan infections by removing intracellular replication niches and enhancing the host's defensive responses. Pyroptosis has been widely studied in inflammatory and infection disease models. Recently, there are growing evidences that pyroptosis also plays an important role in the development of cancer, cardiovascular diseases and Metabolic disorder, etc. MCE designs a unique collection of 1,430 pyroptosis-related compounds mainly focusing on the key targets in the pyroptosis signaling pathway and can be used in the research of pyroptosis signal pathway and related diseases.

Pyroptosis Compound Library

1,430 compounds

Programmed cell death pathways, including apoptosis, pyroptosis and necroptosis, are regulated by unique sets of host proteins that coordinate a variety of biological outcomes. Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response. This process promotes the rapid clearance of various bacterial, viral, fungal and protozoan infections by removing intracellular replication niches and enhancing the host's defensive responses. Pyroptosis has been widely studied in inflammatory and infection disease models. Recently, there are growing evidences that pyroptosis also plays an important role in the development of cancer, cardiovascular diseases and Metabolic disorder, etc.

MCE designs a unique collection of 1,430 pyroptosis-related compounds mainly focusing on the key targets in the pyroptosis signaling pathway and can be used in the research of pyroptosis signal pathway and related diseases.

HY-L051

Ferroptosis Compound Library	1,053 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 1,053 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

1,053 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 1,053 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	233 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 233 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

233 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 233 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.

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-17363

Dimethyl fumarate Maximum Cited Publications 28 Publications Verification	Infection Structural Classification Natural Products Neurological Disease Classification of Application Fields Source classification Endogenous metabolite Inflammation/Immunology Disease Research Fields	Keap1-Nrf2 Reactive Oxygen Species HIV Autophagy Endogenous Metabolite
Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research .

HY-17363R

Dimethyl fumarate (Standard)	Structural Classification Natural Products Source classification Endogenous metabolite	Keap1-Nrf2 Reactive Oxygen Species HIV Autophagy Endogenous Metabolite
Dimethyl fumarate (Standard) is the analytical standard of Dimethyl fumarate. This product is intended for research and analytical applications. Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research .

HY-W010201

Citronellol 2 Publications Verification (±)-Citronellol; (±)-β-Citronellol	Structural Classification Other Monoterpenes Microorganisms Classification of Application Fields Terpenoids Source classification Plants Geraniaceae Disease Research Fields Cancer	Reactive Oxygen Species ERK PI3K TNF Receptor Atg8/LC3 p62 Apoptosis Necroptosis Autophagy Fungal
Citronellol ((±)-Citronellol) is an orally active inducer of apoptosis. Citronellol can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol can induce *necroptosis* in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis .

HY-W010201R

Citronellol (Standard) (±)-Citronellol (Standard); (±)-β-Citronellol (Standard)	Structural Classification Other Monoterpenes Microorganisms Classification of Application Fields Terpenoids Source classification Plants Geraniaceae Disease Research Fields Cancer	Reactive Oxygen Species ERK PI3K TNF Receptor Atg8/LC3 p62 Apoptosis Necroptosis Autophagy Fungal
Citronellol (Standard) is the analytical standard of Citronellol. Citronellol (Standard) is an orally active inducer of apoptosis. Citronellol (Standard) can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol (Standard) can induce *necroptosis* in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol (Standard) can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol (Standard) exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis .

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necroptosis pathway

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