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Results for "

Iron homeostasis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Ferroportin (1) ACSL Family (1) Akt (5) AMPK (5) Angiotensin-converting Enzyme (ACE) (1) Apoptosis (6) Atg8/LC3 (2) Bacterial (4) Cathepsin (2) Endogenous Metabolite (6) Ferroptosis (12) Fungal (1) Glutathione Peroxidase (2) Heme Oxygenase (HO) (1) Interleukin Related (5) JAK (5) JNK (6) Keap1-Nrf2 (2) MMP (2) NF-κB (5) p38 MAPK (6) PERK (1) PI3K (5) PROTACs (1) Reactive Oxygen Species (ROS) (5) Reference Standards (2) Sirtuin (5) STAT (5) TMPRSS6 (2) TNF Receptor (5) α-synuclein (1)
By Research Areas:	Cancer (5) Cardiovascular Disease (4) Infection (5) Inflammation/Immunology (7) Metabolic Disease (6) Neurological Disease (6)
Oligonucleotides:	Antisense Oligonucleotides (2)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Oligonucleotides

Targets Recommended: Ferroportin

Cat. No.	상품명	Target	연구분야	Chemical Structure

HY-113402

Gamma-glutamylcysteine 4 Publications Verification γ-Glu-Cys	Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-P4373A

Hepcidin-1 (mouse) TFA 1 Publications Verification	Cathepsin MMP	Inflammation/Immunology
Hepcidin-1 (mouse) TFA is an endogenous peptide hormone involved in the regulation of iron homeostasis. Hepcidin-1 (mouse) TFA upregulates mRNA levels of TRAP, cathepsin K, and MMP-9 and increases TRAP-5b protein secretion. Hepcidin-1 (mouse) TFA downregulates the level of FPN1 protein and increases intracellular iron. Hepcidin-1 (mouse) TFA facilitates osteoclast differentiation .

HY-177662

Sapablursen IONIS-TMPRSS6-Lrx; ISIS 702843	TMPRSS6	Metabolic Disease
Sapablursen, an antisense oligonucleotide, is designed to reduce the production of TMPRSS6 resulting in increased expression of hepcidin, which is the key regulator of iron homeostasis. Sapablursen can be used in the research of blood diseases such as pol

HY-175209

Nrf2-IN-4	Keap1-Nrf2 Ferroptosis Reactive Oxygen Species (ROS) Atg8/LC3	Cancer
Nrf2-IN-4 is a Nrf2 inhibitor. Nrf2-IN-4 induces ferroptosis via NRF2 inhibition. Nrf2-IN-4 disrupts cellular iron homeostasis, facilitates ferritin degradation, and ultimately triggers ferroptosis. Nrf2-IN-4 induces lysosome activation by promoting iron-dependent ROS production and lysosomal acidification. Nrf2-IN-4 demonstrates significant antitumor efficacy. Nrf2-IN-4 can be used for the study of breast cancer .

HY-P4373

Hepcidin-1 (mouse)	Cathepsin MMP	Metabolic Disease
Hepcidin-1 (mouse) is an endogenous peptide hormone involved in the regulation of iron homeostasis. Hepcidin-1 (mouse) upregulates mRNA levels of TRAP, cathepsin K, and MMP-9 and increases TRAP-5b protein secretion. Hepcidin-1 (mouse) downregulates the level of FPN1 protein and increases intracellular iron. Hepcidin-1 (mouse) facilitates osteoclast differentiation .

HY-113402R

Gamma-glutamylcysteine (Standard) γ-Glu-Cys (Standard)	Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Inflammation/Immunology
Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

HY-177662A

Sapablursen sodium IONIS-TMPRSS6-Lrx sodium; ISIS 702843 sodium	TMPRSS6	Metabolic Disease
Sapablursen sodium, an antisense oligonucleotide, is designed to reduce the production of TMPRSS6 resulting in increased expression of hepcidin, which is the key regulator of iron homeostasis. Sapablursen sodium can be used in the research of blood diseas

HY-175209A

Nrf2-IN-4 hydrobromide	Keap1-Nrf2 Ferroptosis Reactive Oxygen Species (ROS) Atg8/LC3	Cancer
Nrf2-IN-4 (Compound PhcY) hydrobromide is a Nrf2 inhibitor. Nrf2-IN-4 hydrobromide induces ferroptosis via NRF2 inhibition. Nrf2-IN-4 hydrobromide disrupts cellular iron homeostasis, facilitates ferritin degradation, and ultimately triggers ferroptosis. Nrf2-IN-4 hydrobromide induces lysosome activation by promoting iron-dependent ROS production and lysosomal acidification. Nrf2-IN-4 hydrobromide demonstrates significant antitumor efficacy. Nrf2-IN-4 hydrobromide can be used for the study of breast cancer .

HY-174867

AY-4	PROTACs Ferroptosis	Cancer
AY-4 (Compound AY-4) is an efficient PROTAC degrader targeting FTH1 (K_d = 3.17 nM). AY-4 effectively upregulates the levels of ferrous (Fe ²⁺) and ferric (Fe ³⁺) ions in cells. AY-4 is a potential anticancer candidate compound that regulates iron homeostasis through ferritin degradation and enhances the efficacy of existing drugs. AY-4 can effectively reduce the level of FTH1 in breast cancer cells (Pink: FTH1 ligand AY-2 (HY-174871); Blue: E3 ligand Pomalidomide (HY-10984); Black: Linker, Pomalidomide-PEG3-acid (HY-174872)) .

HY-175869

Ferroptosis-IN-22	Ferroptosis	Metabolic Disease Inflammation/Immunology
Ferroptosis-IN-22 is a selective ferroptosis inhibitor by targeting NCOA4 and disrupting its interaction with ferritin with an EC₅₀ of 520 nM and a K_d of 0.78 μM. Ferroptosis-IN-22 has a strong inhibitory activity against ferroptosis induced by multiple ferroptosis inducers (RSL3 (HY-100218A), Erastin (HY-15763), ML210 (HY-100003), FIN56 (HY-103087)), but does not inhibit necrosis induced by H₂O₂ or apoptosis induced by STS (HY-15141). Ferroptosis-IN-22 effectively ameliorates Concanavalin A (HY-P2149)-induced acute liver injury. Ferroptosis-IN-22 can be used for the study of ferroptosis-related diseases .

HY-121858

Nicotianamine	Angiotensin-converting Enzyme (ACE)	Metabolic Disease
Nicotianamine can be isolated from the leaves of Nicotiana Tabacum L.. Nicotianamine is a key biosynthetic precursor of phytosiderophores. Nicotianamine is an iron chelating agent and can promote the transport of iron. Nicotianamine is an angiotensin-converting enzyme (ACE) inhibitor with IC₅₀ values of 76 nM and 59 nM for rhACE2 and rhACE, respectively. Nicotianamine is vital in metal nutrition and metal homeostasis of flowering plants .

HY-125288

DS42450411	Ferroportin	Metabolic Disease
DS42450411 is an orally active hepcidin production inhibitor with an IC₅₀ of 32 nM. DS42450411 in an acute inflammatory mouse model induced by IL-6, DS42450411 significantly reduces serum hepcidin levels. DS42450411 can be used for studying iron homeostasis .

HY-106159

SB-T-101141	Reactive Oxygen Species (ROS) p38 MAPK JNK PERK Ferroptosis	Cancer
SB-T-101141 is a novel taxane. SB-T-101141 effectively induces a noncanonical ferroptosis to overcome Paclitaxel (HY-B0015) resistance of breast cancer. SB-T-101141 facilitates the production of iron and ferrous ions and ROS. SB-T-101141 stably binds to KHSRP to inhibit the iron-dependent expression of CISD1 related to iron homeostasis. SB-T-101141 synergistically enhances the iron-dependent activation of JNK and PERK pathways via KHSRP. SB-T-101141 suppresses breast tumor growth in MCF-7(PR)/MDA-MB-231(PR) or KHSRP knock-down MCF-7 xenograft mice model .

HY-136861

Antibacterial agent 192	Bacterial	Infection
Antibacterial agent 192 is an antibacterial agent that can disrupt iron homeostasis in E. coli .

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-156439

Antibiofilm agent-2	Bacterial	Infection
Antibiofilm agent-2 (compound 4T) is a potent biofilm inhibitor with an IC₅₀ of 3.6 μM. Antibiofilm agent-2 inhibits the quorum sensing system and iron homeostasis as antibacterial synergists against Pseudomonas aeruginosa .

HY-113402AR

Gamma-glutamylcysteine TFA (Standard) γ-Glu-Cys TFA (Standard)	Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

HY-173428

Antifungal agent 130	Fungal	Infection
Antifungal agent 130 (Compound A7) is an orally active antifungal agent. Antifungal agent 130 has good antifungal activity against Candida albicans (MIC = 0.12 ng/mL) and Cryptococcus neoformans (MIC = 0.12 ng/mL) and has excellent antivirulence effect. Antifungal agent 130 exerts its antifungal effect by disrupting the iron homeostasis of fungal cells and inducing oxidative stress damage. Antifungal agent 130 can inhibit the formation of fungal virulence factors (such as biofilm, capsule, urease and melanin). Antifungal agent 130 has good antifungal effect and can be used in the study of drug-resistant fungal infections .

HY-113402B

Gamma-glutamylcysteine ammonium γ-Glu-Cys ammonium	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-183711

Antibacterial agent 344	Bacterial Heme Oxygenase (HO)	Infection
Antibacterial agent 344 is an antibacterial agent with potent biofilm inhibition (IC₅₀ = 0.27 μM). Antibacterial agent 344 inhibits heme oxygenase (HemO), impairs iron homeostasis, virulence factor production, and motility. Antibacterial agent 344 synergizes with Ciprofloxacin (HY-B0356) and Tobramycin (HY-B0441), enhancing their efficacy and delaying the development of resistance. Antibacterial agent 344 improves bacterial-infected Galleria mellonella survival, and reduces bacterial load in mice wounds. Antibacterial agent 344 can be used for the research of Pseudomonas aeruginosa infections .

HY-181665

Ferroptosis-IN-23	Ferroptosis Glutathione Peroxidase Reactive Oxygen Species (ROS) Apoptosis	Neurological Disease
Ferroptosis-IN-23 is an inhibitor of ferroptosis. Ferroptosis-IN-23 exerts a synergistic effect by simultaneously activating Steap4 and glutathione peroxidase 4 (GPX4), thereby maintaining iron metabolism homeostasis. Ferroptosis-IN-23 reverses neuronal ferroptosis and inhibits lipid ROS accumulation in cells. Ferroptosis-IN-23 inhibits ferroptosis in zebrafish, alleviates neuronal apoptosis, ROS accumulation, and dopaminergic neuron damage in a zebrafish model of Parkinson's disease. Ferroptosis-IN-23 can be used for research on Parkinson's disease .

HY-W722245

Pyochelin	Endogenous Metabolite Bacterial	Infection
Pyochelin is a salicylate-based nonribosomal peptide siderophore produced by Pseudomonas aeruginosa. Pyochelin chelates Fe ³⁺ and transports it back into bacterial cells, providing the iron essential for bacterial survival. Pyochelin can also chelate other metals such as Zn ²⁺, Co ²⁺, and Ni ²⁺, which helps bacteria maintain intracellular metal ion homeostasis by chelating and excreting excess metals in response to toxic metal stress. Pyochelin can be used in studies related to Pseudomonas aeruginosa infection .

HY-125984

Syn-516	α-synuclein	Neurological Disease
Syn-516 is an inhibitor of α-synuclein (α-Syn). Syn-516 targets the 5' untranslated region (5'UTR) of α-Syn mRNA, with an IC₅₀ value of 1.8 μM, thereby inhibiting the translation process of α-Syn. Syn-516 improves motor dysfunction and colonic motility abnormalities associated with α-Syn overexpression in mouse models. α-Syn can be used to study diseases such as Parkinson's disease and Lewy body dementia .

Cat. No.	상품명

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.

HY-L045

Oxygen Sensing Compound Library	4,029 compounds
Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis. A variety of HF-1 target genes have been identified thus far which encode proteins that play key roles in critical developmental and physiological processes including angiogenesis/vascular remodeling, erythropoiesis, glucose transport, glycolysis, iron transport, and cell proliferation/survival. HIF-1 is a heterodimeric transcription factor consisting of a constitutively expressed β-subunit and an oxygen-regulated α-subunit. The unique feature of HIF-1 is the regulation of HIF-1α expression and activity based upon the cellular O₂ concentration. Under normoxic conditions, hydroxylation of HIF-1α on these different proline residues is essential for HIF proteolytic degradation by promoting interaction with the von Hippel-Lindau tumor-suppressor protein (pVHL) through hydrogen bonding to the hydroxyproline-binding pocket in the pVHL β-domain. As oxygen levels decrease, hydroxylation of HIF decreases; HIF-1α then no longer binds pVHL, and becomes stabilized, allowing more of the protein to translocate to the cell’s nucleus, where it acts as a transcription factor, upregulating (often within minutes) the production of proteins that stimulate blood perfusion in tissues and thus tissue oxygenation. MCE offers a unique collection of 4,029 oxygen sensing related compounds targeting HIF/HIF Prolyl-Hydroxylase, MAPK/ERK, PI3K/AKT signaling pathways, etc. MCE Oxygen Sensing Compound Library is a useful tool to study hypoxia, oxidative stress and discover new anti-cancer drugs.

Oxygen Sensing Compound Library

4,029 compounds

Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression.

Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis. A variety of HF-1 target genes have been identified thus far which encode proteins that play key roles in critical developmental and physiological processes including angiogenesis/vascular remodeling, erythropoiesis, glucose transport, glycolysis, iron transport, and cell proliferation/survival.

HIF-1 is a heterodimeric transcription factor consisting of a constitutively expressed β-subunit and an oxygen-regulated α-subunit. The unique feature of HIF-1 is the regulation of HIF-1α expression and activity based upon the cellular O₂ concentration. Under normoxic conditions, hydroxylation of HIF-1α on these different proline residues is essential for HIF proteolytic degradation by promoting interaction with the von Hippel-Lindau tumor-suppressor protein (pVHL) through hydrogen bonding to the hydroxyproline-binding pocket in the pVHL β-domain. As oxygen levels decrease, hydroxylation of HIF decreases; HIF-1α then no longer binds pVHL, and becomes stabilized, allowing more of the protein to translocate to the cell’s nucleus, where it acts as a transcription factor, upregulating (often within minutes) the production of proteins that stimulate blood perfusion in tissues and thus tissue oxygenation.

MCE offers a unique collection of 4,029 oxygen sensing related compounds targeting HIF/HIF Prolyl-Hydroxylase, MAPK/ERK, PI3K/AKT signaling pathways, etc. MCE Oxygen Sensing Compound Library is a useful tool to study hypoxia, oxidative stress and discover new anti-cancer drugs.

Cat. No.	상품명	Target	Research Area