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Results for "

iron death

" in MedChemExpress (MCE) Product Catalog:

By Targets:	ACSL Family (2) ADC Payload (1) Apoptosis (3) Bacterial (1) Carbonic Anhydrase (1) Fatty Acid Synthase (FASN) (1) Ferroptosis (10) Fluorescent Dye (1) Glutathione Peroxidase (4) MDM-2/p53 (1) Mitochondrial Metabolism (2) Necroptosis (2) NO Synthase (1) Reactive Oxygen Species (ROS) (3) Reference Standards (1) RIP kinase (1)
By Research Areas:	Cancer (16) Cardiovascular Disease (2) Inflammation/Immunology (3) Neurological Disease (2)
Click Chemistry:	Alkynes (1)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Click Chemistry

Targets Recommended: Ferroportin DAPK Programmed Cell Death 4 (PDCD4) PD-1/PD-L1

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-111914A

Ferroheme 1 Publications Verification	NO Synthase Fatty Acid Synthase (FASN)	Cardiovascular Disease
Ferroheme is the ferrous form of heme in hemoglobin, reversibly binding oxygen as an oxygen carrier. Its free form induces oxidative stress and ferroptosis by releasing iron ions, which catalyze reactive oxygen species generation via Fenton reactions, leading to lipid peroxidation and cell death. This mechanism is critical in pathological contexts like intracerebral hemorrhage and neurodegenerative diseases, making it a target for studying iron-overload disorders and ferroptosis-related pathologies[1][2][3].

HY-153629

FSEN1 2 Publications Verification	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-175615

RSL3-NH2	ADC Payload Glutathione Peroxidase Ferroptosis	Cancer
RSL3-NH2 is a GPX4 inhibitor and ferroptosis inducer. RSL3-NH2 triggers the iron-dependent cell death pathway associated with lipid peroxidation by inhibiting GPX4 activity. RSL3-NH2 exhibits significant cytotoxicity against colorectal cancer cells and effectively induces their ferroptosis. RSL3-NH2 can serve as a ADC payload for synthesizing antibody-drug conjugates (ADC) and be used in colorectal cancer-related research .

HY-108894

Ferumoxytol	Ferroptosis Reactive Oxygen Species (ROS)	Cardiovascular Disease Inflammation/Immunology Cancer
Ferumoxytol is an FDA-approved ultrasmall superparamagnetic iron oxide preparation and iron replacement agent that exerts selective activity against leukemia cells with low ferroportin expression. Ferumoxytol increases intracellular iron levels, induces reactive oxygen species (ROS) production via the Fenton reaction, and triggers oxidative stress and cell death. Ferumoxytol reduces disease burden in mouse models and patient-derived leukemia models. As an MRI contrast agent, Ferumoxytol enables imaging of vascular lesions, tumors and lymph nodes. Ferumoxytol can be used in research related to acute myeloid leukemia and blast-phase chronic myeloid leukemia .

HY-100887

Piperazine Erastin Maximum Cited Publications 9 Publications Verification	Ferroptosis	Cancer
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-112063

CIL56 4 Publications Verification	Ferroptosis	Cancer
CIL56 is a potent and selective ferroptosis inducer. Ferroptosis is an iron-dependent form of regulated cell death (RCD).

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-174345

Ferroptosis inducer-8	ACSL Family Ferroptosis Glutathione Peroxidase Reactive Oxygen Species (ROS)	Cancer
Ferroptosis inducer-8 is a ferroptosis inducer with high selectivity for other cell death mechanism. Ferroptosis inducer-8 induces ferroptosis by affecting ACSL4, GPX4, and FTH1, thereby disrupting intracellular iron homeostasis and the GSH/GPX4 antioxidant defense system, ultimately leading to the accumulation of lipid peroxidation. Ferroptosis inducer-8 also induces ROS production. Ferroptosis inducer-8 inhibits tumor growth and can be used for research of triple-negative breast cancer (TNBC) .

HY-119325A

Lanperisone hydrochloride NK433	Apoptosis	Cancer
Lanperisone hydrochloride is a novel oral muscle relaxant with anticancer activity. Lanperisone hydrochloride produces non-apoptotic cell death by inhibiting monosynaptic and polysynaptic reflex potentials. Lanperisone hydrochloride is also believed to play an important role in the dysregulation of iron metabolism and antioxidant systems to modulate processes associated with ischemic stroke .

HY-119325

Lanperisone NK433 free base	Apoptosis	Cancer
Lanperisone is a novel oral muscle relaxant with anticancer activity. Lanperisone produces non-apoptotic cell death by inhibiting monosynaptic and polysynaptic reflex potentials. Lanperisone is also believed to play an important role in the dysregulation of iron metabolism and antioxidant systems to modulate processes associated with ischemic stroke .

HY-155851

Lepadin E	Ferroptosis MDM-2/p53 Glutathione Peroxidase ACSL Family	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 .

HY-162867

Photosensitizer-5	Ferroptosis	Cancer
Photosensitizer-5 is a photosensitizer. Photosensitizer-5 has cytotoxicity against HeLa and HepG2 cells, with IC₅₀ values of 10.4 nM and 6.9 nM, respectively. Photosensitizer-5 can lead to lipid peroxidation and induces cell death through an iron-independent ferroptosis-like pathway. Photosensitizer-5 shows anti-tumor activity in HeLa tumor-bearing mice .

HY-178475

CA IX/GPX4-IN-1	Carbonic Anhydrase Glutathione Peroxidase Ferroptosis	Cancer
CA IX/GPX4-IN-1 (Compound 22abcb) is a dual targeted inhibitor of CA IX and GPX4 activity. CA IX/GPX4-IN-1 can effectively kill SUM159PT cells (IC₅₀ = 416 nM) by inducing iron death under hypoxic conditions. CA IX/GPX4-IN-1 has an IC₅₀ of 663 nM to CA IX in SUM159PT-CAIX-FL cells. CA IX/GPX4-IN-1 can significantly inhibit tumor growth and can be reversed by ferroptosis inhibitors. CA IX/GPX4-IN-1 can be used for research on breast cancer and other cancers .

HY-138185

Collismycin A SF 2738A	Bacterial Apoptosis	Cancer
Collismycin A is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities, including antibacterial, antiproliferative, and neuroprotective properties. It is active against a variety of bacteria (MICs=6.25 and 100 μg/mL) and fungi (MICs=12.5-100 μg/mL). It inhibits proliferation of A549 lung, HCT116 colon, and HeLa cervical cancer cells (IC₅₀s=0.3, 0.6, and 0.3 μM, respectively) and NIH373 fibroblasts (IC₅₀=56.6 μM) but not MDA-MD-231 breast cancer cells (IC₅₀=>100 μM). Collismycin A forms a complex with Fe(II) and Fe(III) at a 2:1 ratio, and the addition of iron ions inhibits the antiproliferative effect of collismycin A on HeLa cells, an effect that does not occur with the addition of zinc, manganese, copper, or magnesium ions.3 Collismycin A (1 μM) prevents apoptosis in the brain region of zebrafish larvae in a model of neuronal cell death induced by all-trans retinoic acid.

HY-183232

SRS6-11	Necroptosis	Cancer
SRS6-11 is an iron death-independent necrotic cell death (Necrosis) inducer. SRS6-11 retains significant lethality in the presence of α-tocopherol (HY-W020044). SRS6-11 can be used in fibrosarcoma research .

HY-100887R

Piperazine Erastin (Standard)	Ferroptosis Reference Standards	Cancer
Piperazine Erastin (Standard) is the analytical standard of Piperazine Erastin (HY-100887). This product is intended for research and analytical applications. 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-181688

2α-Ferrocenylmethyl-DHT	Reactive Oxygen Species (ROS)	Cancer
2α-Ferrocenylmethyl-DHT is a dihydrotestosterone-derived ferrocene-steroid conjugate. 2α-Ferrocenylmethyl-DHT inhibits the growth of various cancer cells. 2α-Ferrocenylmethyl-DHT induces S-phase cell cycle arrest in ovarian cancer cells, elevates intracellular iron levels, triggers ROS-dependent cell death, and disrupts the integrity of multicellular tumor spheroids of ovarian cancer cells. 2α-Ferrocenylmethyl-DHT can be used in the research of prostate cancer and ovarian cancer .

HY-P11638

Mitochondrial-targeted peptide BP29	Mitochondrial Metabolism	Neurological Disease Inflammation/Immunology
Mitochondrial-targeted peptide BP29 is a mitochondria-targeted iron chelator linked to a mitochondria-homing SS-peptide. Mitochondrial-targeted peptide BP29 protects human primary skin fibroblasts against ultraviolet A-induced oxidative damage to mitochondrial membranes, ATP depletion, and necrotic cell death. Mitochondrial-targeted peptide BP29 prevents hydrogen peroxide-induced oxidative stress and cytotoxicity in both healthy and Friedreich's ataxia skin fibroblasts. Mitochondrial-targeted peptide BP29 can be used for the research of Friedreich's ataxia .

HY-P11638A

Mitochondrial-targeted peptide BP29 acetate	Mitochondrial Metabolism	Neurological Disease Inflammation/Immunology
Mitochondrial-targeted peptide BP29 acetate is a mitochondria-targeted iron chelator linked to a mitochondria-homing SS-peptide. Mitochondrial-targeted peptide BP29 acetate protects human primary skin fibroblasts against ultraviolet A-induced oxidative damage to mitochondrial membranes, ATP depletion, and necrotic cell death. Mitochondrial-targeted peptide BP29 acetate prevents hydrogen peroxide-induced oxidative stress and cytotoxicity in both healthy and Friedreich's ataxia skin fibroblasts. Mitochondrial-targeted peptide BP29 acetate can be used for the research of Friedreich's ataxia .

Cat. No.	Product Name

HY-L051

Ferroptosis Compound Library	1,177 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 1,177 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

1,177 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 1,177 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	403 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 403 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

403 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 403 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	Target	Research Area