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Impaired Copper Metabolism and Human Diseases

Metabolic Diseases Mitochondrial Dysfunction Oxidative Stress Neurodegeneration

Copper is an essential redox-active micronutrient used by enzymes that support respiration, antioxidant defense, connective tissue, pigmentation, neurotransmitter synthesis, and iron handling. Its reactivity also makes free copper dangerous, so absorption, chaperoning, storage, incorporation into enzymes, and biliary excretion must be tightly coordinated. Impaired copper metabolism can mean deficiency, toxic accumulation, or incorrect intracellular distribution. Research historically centered on Menkes and Wilson diseases; recent work connects copper to mitochondrial metabolism, proteotoxic stress, neurodevelopment, cancer, and the regulated death process cuproptosis. The central biological problem is therefore loss of spatial control rather than copper concentration alone[1][2][3].

Dietary copper enters intestinal cells through transport systems, is handed to chaperones, and reaches secretory-pathway enzymes through ATP7A or ATP7B. ATP7A supports export from enterocytes and delivery to peripheral tissues, whereas hepatic ATP7B loads copper into ceruloplasmin and promotes biliary excretion. ATP7B mutations cause Wilson disease, with copper accumulation in liver, brain, and other organs. At the cellular level, excess copper can bind lipoylated tricarboxylic-acid-cycle proteins, drive their aggregation, deplete iron-sulfur-cluster proteins, and produce proteotoxic stress characteristic of cuproptosis. Deficiency instead compromises cuproenzymes, mitochondrial function, vascular and neural development, and redox balance[1][2][3].

Clinical intervention is established for Wilson disease through copper chelation, zinc-mediated reduction of absorption, and liver transplantation in selected patients; newer chelators and genetic approaches remain under study. Cancer programs attempt the opposite manipulation by delivering copper or increasing mitochondrial copper stress in susceptible tumors, while other diseases may require chelation or restoration. A 2026 study linked low copper to impaired oligodendrocyte maturation in autism-spectrum-disorder cohorts and models; copper deficiency activated a HIF1α-BNIP3 mitophagy program, suppressed mTOR, and caused hypomyelination, while restoring mTOR improved oligodendrocyte maturation and behavior in mice. This finding is mechanistically important but does not justify unsupervised copper supplementation[2][3][4].

Copper homeostasis is intertwined with other nutrients and proteins. Ceruloplasmin connects copper handling to iron export, metallothioneins buffer intracellular metal, and ATOX1 and mitochondrial chaperones deliver copper to selected enzymes rather than allowing uncontrolled diffusion. Inherited ATP7A defects cause systemic deficiency despite dietary availability, whereas ATP7B defects impair hepatic export and cause accumulation. Acquired imbalance can arise from malabsorption, excessive supplementation, liver disease, inflammation, or drugs. These states can produce similar circulating measurements but demand opposite treatment. Cancer adds another layer because copper supports angiogenesis and mitochondrial enzymes while excessive mitochondrial copper can become lethal. Direct measurement of flux and compartmentalization is therefore necessary before a copper-modulating drug is classified as replacement, redistribution, chelation, or cuproptosis induction. Major gaps include reliable measures of bioavailable copper, tissue-specific thresholds, and separation of cause from consequence. Serum copper or ceruloplasmin can miss intracellular misdistribution, inflammation can alter circulating markers, and organs differ in vulnerability. Cuproptosis markers require validation in human tissue and should not be inferred from expression signatures alone. Future work should integrate isotope tracing, metalloproteomics, organoids, imaging, and genetic transport models to map copper flux. Therapeutic studies must monitor iron interactions, mitochondrial function, liver and neurological toxicity, and effects on normal cuproenzymes. Patient selection should distinguish inherited transporter defects, nutritional deficiency, inflammatory redistribution, and tumor-specific copper dependence so that chelation, replacement, transport correction, or death induction is applied to the correct biological state[1][2][3][4].

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Cat. No. Product Name Information Application Publication
HY-10219 Rapamycin
Rapamycin (Sirolimus; AY 22989) is a potent and specific blood-brain barrier-transmissible mTOR inhibitor with an IC50 of 0.1 nM in HEK293 cells. Rapamycin is a molecular glue that binds FKBP12 and mTOR proteins together, thereby inhibiting mTOR kinase activity. Rapamycin binds to FKBP12 and specifically acts as an allosteric inhibitor of mTORC1. Rapamycin is an autophagy activator, an immunosuppressant.

Source: Streptomyces hygroscopicus

mTOR   FKBP   Molecular Glues   Fungal   Autophagy   Endogenous Metabolite   Antibiotic   Bacterial  
Breast Cancer   Colorectal Cancer   Prostate Cancer   Gastric Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Viral Infection   Bacterial Infection   Fungal Infection   Pain   Non-Small Cell Lung Cancer   Lung Adenocarcinoma   SARS-CoV-2 Infection   Obesity   Lung Fibrosis  
1475
HY-100523 ML385
ML385 is a potent and selective Nrf2 inhibitor with an IC50 of 1.9 μM. ML385 directly binds to the Neh1 domain of NRF2, interferes with the binding of the MAFG-NRF2 protein complex to the antioxidant response element (ARE) DNA sequence, thereby blocking the expression of downstream target genes of NRF2. ML385 can be used in studies related to adult T-cell leukemia, breast cancer, myocardial ischemia/reperfusion injury, non-small cell lung cancer, esophageal squamous cell carcinoma, head and neck squamous cell carcinoma, and lung squamous cell carcinoma.
Keap1-Nrf2   Ferroptosis   Apoptosis   mTOR  
Breast Cancer   Colorectal Cancer   Cardiovascular Disease   Non-Small Cell Lung Cancer   Lung Squamous Cell Carcinoma   Squamous Cell Carcinoma   Esophageal Cancer  
645
HY-10071 Y-27632
Y-27632 is a ROCK inhibitor with Ki values of 220 nM and 300 nM for ROCK1 and ROCK2, respectively. Y-27632 exerts anti-inflammatory and immunomodulatory effects in systemic lupus erythematosus models by inhibiting the ROCK/NF-κB pathway. Y-27632 enhances autophagy by inhibiting the AKT/mTOR pathway, thereby inducing apoptosis apoptosis in oral squamous cell carcinoma. Y-27632 induces the formation of tunneling nanotubes in ARPE-19 cells and significantly enhances mitochondrial transfer through these channels. Y-27632 promotes neurite outgrowth in PC12 cells by activating the Rac1/NOX1/ROS/AKT/PAK1 signaling cascade.
ROCK   Reactive Oxygen Species (ROS)   Akt   Ras   mTOR   Apoptosis   PAK   NADPH Oxidase   NF-κB   Autophagy  
Cancer   Digestive System Disease   Digestive System Inflammation   Lung Fibrosis  
607
HY-10358 MK-2206 dihydrochloride
MK-2206 dihydrochloride (MK-2206 2HCl) is an orally active pan-AKT inhibitor, with IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 dihydrochloride inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia.
Bcl-2 Family   Akt   mTOR   Apoptosis   GSK-3  
Colorectal Cancer   Prostate Cancer   Gastric Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Large Cell Lung Carcinoma   Metastatic Breast Cancer   Lung Fibrosis  
496
HY-10201 Sorafenib
Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
Raf   VEGFR   FLT3   Autophagy   Apoptosis   STAT   Akt   MMP   Cadherin   p38 MAPK   ERK   MEK   PI3K   PARP   Bcl-2 Family   Ephrin Receptor   PDGFR  
Gastric Cancer   Liver Cancer   Ovarian Cancer   Digestive System Inflammation   Small Cell Lung Cancer   Non-Small Cell Lung Cancer   Metastatic Breast Cancer   Metastatic Colorectal Cancer   Metastatic Prostate Cancer   Multiple Myeloma   Metastatic Pancreatic Cancer   SARS-CoV-2 Infection   Alzheimer's Disease   Parkinson's Disease   Obesity   Lung Fibrosis  
317
HY-15531 Venetoclax
Venetoclax (ABT-199; GDC-0199) is a highly potent, selective and orally bioavailable Bcl-2 inhibitor with a Ki of less than 0.01 nM. Venetoclax induces autophagy.
Bcl-2 Family   Autophagy  
Prostate Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Glucose Metabolism   SARS-CoV-2 Infection  
260
HY-B0795 MHY1485
MHY1485 is a potent cell-permeable mTOR activator that targets the ATP domain of mTOR. MHY1485 inhibits autophagy by suppression of fusion between autophagosomes and lysosomes.
mTOR   Autophagy  
Breast Cancer   Pancreatic Cancer   Depression   Pain  
223
HY-17471A Metformin hydrochloride
Metformin (1,1-Dimethylbiguanide) hydrochloride inhibits the mitochondrial respiratory chain in the liver, leading to AMPK activation and enhancing insulin sensitivity, and can be used in the study of type 2 diabetes. Metformin hydrochloride exerts central glucose-lowering effects by inhibiting Ras-related protein 1 (Rap1) in SF1 hypothalamic neurons. Metformin hydrochloride also inhibits liver oxidative stress, nitrosative stress, inflammation, and apoptosis caused by liver ischemia/reperfusion injury. In addition, Metformin hydrochloride regulates the expression of autophagy-related proteins by activating AMPK and inhibiting the mTOR signaling pathway, thereby inducing tumor cell autophagy and inhibiting the growth of renal cell carcinoma in vitro and in vivo.
AMPK   Autophagy   Mitophagy   Apoptosis   mTOR  
Colorectal Cancer   Prostate Cancer   Gastric Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Viral Infection   Digestive System Inflammation   Cardiovascular Disease   Glucose Metabolism   Non-Small Cell Lung Cancer   Lung Adenocarcinoma   Large Cell Lung Carcinoma   HER-2 Positive Breast Cancer   Triple-Negative Breast Cancer   Metastatic Breast Cancer   SARS-CoV-2 Infection   Parkinson's Disease   Chronic Pain   Obesity  
213
HY-B0627 Metformin
Metformin (1,1-Dimethylbiguanide) inhibits the mitochondrial respiratory chain in the liver, leading to AMPK activation and enhancing insulin sensitivity, and can be used in the study of type 2 diabetes. Metformin exerts central glucose-lowering effects by inhibiting Ras-related protein 1 (Rap1) in SF1 hypothalamic neurons. Metformin also inhibits liver oxidative stress, nitrosative stress, inflammation, and apoptosis caused by liver ischemia/reperfusion injury. In addition, Metformin regulates the expression of autophagy-related proteins by activating AMPK and inhibiting the mTOR signaling pathway, thereby inducing tumor cell autophagy and inhibiting the growth of renal cell carcinoma in vitro and in vivo.
AMPK   Autophagy   Mitophagy   Apoptosis   mTOR  
Colorectal Cancer   Prostate Cancer   Gastric Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Viral Infection   Pain   Digestive System Inflammation   Cardiovascular Disease   Glucose Metabolism   Non-Small Cell Lung Cancer   Lung Adenocarcinoma   Large Cell Lung Carcinoma   HER-2 Positive Breast Cancer   Triple-Negative Breast Cancer   Metastatic Breast Cancer   Parkinson's Disease   Obesity   Lung Fibrosis  
213
HY-10087 Navitoclax
Navitoclax (ABT-263) is a potent and orally active Bcl-2 family protein inhibitor that binds to multiple anti-apoptotic Bcl-2 family proteins, such as Bcl-xL, Bcl-2 and Bcl-w, with a Ki of less than 1 nM.
Bcl-2 Family  
Prostate Cancer   Leukemia/Lymphoma/Myeloma   Ovarian Cancer   SARS-CoV-2 Infection  
162
HY-B0240 Disulfiram
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 Cu2+ increases intracellular ROS levels and induces cuproptosis.
Aldehyde Dehydrogenase (ALDH)   Interleukin Related   Pyroptosis   Apoptosis   Cuproptosis  
Metabolic or Endocrine Disease   Breast Cancer   Prostate Cancer   Pancreatic Cancer   Ovarian Cancer   Viral Infection   Depression   Pain   Autoimmune Disease   Digestive System Inflammation   SARS-CoV-2 Infection  
162
HY-13003 Torin 1
Torin 1 is a potent inhibitor of mTOR with an IC50 of 3 nM. Torin 1 inhibits both mTORC1/2 complexes with IC50 values between 2 and 10 nM. Torin 1 is an effective inducer of autophagy.
mTOR   Autophagy  
Lung Cancer   Breast Cancer   Colorectal Cancer   Prostate Cancer   Gastric Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Pain   Obesity   Lung Fibrosis  
141
HY-12040 Elesclomol
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.
Reactive Oxygen Species (ROS)   Apoptosis   Cuproptosis  
Digestive System Disease   Prostate Cancer   Digestive System Inflammation   SARS-CoV-2 Infection   Parkinson's Disease  
131
HY-10218 Everolimus
Everolimus (RAD001) is a Rapamycin (HY-10219) derivative and a potent, selective, orally active, blood-brain barrier-permeable mTOR1 inhibitor. Everolimus binds to FKBP-12 to generate an immunosuppressive complex. Everolimus inhibits tumor cells proliferation and induces cell apoptosis and autophagy. Everolimus has potent immunosuppressive and anticancer activities.
mTOR   FKBP   Autophagy   Apoptosis   Bacterial  
Colorectal Cancer   Prostate Cancer   Gastric Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Bacterial Infection   Pain   Digestive System Inflammation   Non-Small Cell Lung Cancer   Luminal Breast Cancer   HER-2 Positive Breast Cancer   Triple-Negative Breast Cancer   Metastatic Breast Cancer   Cytomegalovirus Infection   SARS-CoV-2 Infection   Obesity   Lung Fibrosis  
126
HY-100741 S63845
S63845 is a potent and selective myeloid cell leukemia 1 (MCL1) inhibitor with a Kd of 0.19 nM for human MCL1.
Bcl-2 Family  
Leukemia/Lymphoma/Myeloma   Ovarian Cancer  
115
HY-L089 Mitochondria-Targeted Compound Library
Mitochondria plays an important role in many vital processes in cells, including energy production, fatty-acid oxidation and the Tricarboxylic Acid (TCA) cycle, calcium signaling, permeability transition, apoptosis and heat production. At present, it is recognized that many diseases are associated with impaired mitochondrial function, such as increased accumulation of ROS and decreased OXPHOS and ATP production. Mitochondria are recognized as one of the most important targets for new drug design in cancer, cardiovascular, and neurological diseases, etc. Some small molecule drugs or biologics can act on mitochondria through various pathways, including ETC inhibition, OXPHOS uncoupling, mitochondrial Ca2+ modulation, and control of oxidative stress via decrease or increase of mitochondrial ROS accumulation. MCE supplies a unique collection of 1,182 mitochondria-targeted compound that mainly targeting Mitochondrial Metabolism, ATP Synthase, Mitophagy, Reactive Oxygen Species, etc. MCE Mitochondria-Targeted Compound Library is a useful tool for mitochondria-targeted drug discovery and related research.

Signaling Pathway Targeting Libraries

89
HY-L034 Anti-Aging Compound Library
Aging is a complex biological process characterized by functional decline of tissues and organs, structural degeneration, and reduced adaptability and resistance, all of which contribute to an increase in morbidity and mortality caused by multiple chronic diseases, such as Alzheimer's disease, cancer, and diabetes. Many theories, which fall into two main categories: programmed and error theories, have been proposed to explain the process of aging, but neither of them appears to be fully satisfactory. The programmed theories imply that aging relies on specific gene regulation, and the error theories emphasize the internal and environmental damages accumulated to living organisms. The damage theories proposed the nine hallmarks that were generally considered to contribute to the aging process: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. MCE Anti-Aging Compound Library contains 7,771 compounds, mainly targeting Sirtuin, mTOR, IGF-1R, AMPK, p53, Telomerase, Mitophagy, Mitochondrial Metabolism, COX, Cytochrome P450, Oxidase, etc. This library is a useful tool for anti-aging research.

Disease Focused Libraries

84
HY-L034M Anti-Aging Compound Library Mini
Research has shown that drugs targeting aging pathways demonstrate promising potential in models of age-related diseases such as Alzheimer's disease, cardiovascular diseases, metabolic syndrome, osteoarthritis, and various malignancies. This suggests that intervening in the biological processes of aging may enable synergistic prevention and treatment of multiple chronic diseases. Against the backdrop of the gradual elucidation of core aging mechanisms-including cellular senescence, telomere attrition, epigenetic dysregulation, and chronic inflammation anti-aging research has shifted from traditional phenotypic interventions toward targeting key pathways that regulate biological age. The MCE Anti-Aging Compound Library Mini is precisely built upon this cutting-edge concept. It focuses on aging-related targets validated through genetic or functional studies, comprising 381 compounds designed to provide systematic research tools for aging biology and intervention strategy development. The library covers core mechanisms such as mTOR, SIRT, energy metabolism, clearance of senescent cells, optimization of mitochondrial function, and telomere maintenance. For each target, 1-5 compounds with clear activity and strong representativeness have been carefully selected, spanning the entire translational spectrum from preclinical tool molecules to clinically investigational drugs.

Disease Focused Libraries

83
HY-L064 Glutamine Metabolism Compound Library
Glutamine is an important metabolic fuel that helps rapidly proliferating cells meet the increased demand for ATP, biosynthetic precursors, and reducing agents. Glutamine Metabolism pathway involves the initial deamination of glutamine by glutaminase(GLS), yielding glutamate and ammonia. Glutamate is converted to the TCA cycle intermediate α-ketoglutarate (α-KG) by either glutamate dehydrogenase (GDH) or by the alanine or aspartate transaminases (TAs), to produce both ATP and anabolic carbons for the synthesis of amino acids, nucleotides and lipids. During periods of hypoxia or mitochondrial dysfunction, α-KG can be converted to citrate in a reductive carboxylation reaction catalyzed by IDH2. The newly formed citrate exits the mitochondria where it is used to synthesize fatty acids and amino acids and produce the reducing agent, NADPH. Cancer cells display an altered metabolic circuitry that is directly regulated by oncogenic mutations and loss of tumor suppressors. Mounting evidence indicates that altered glutamine metabolism in cancer cells has critical roles in supporting macromolecule biosynthesis, regulating signaling pathways, and maintaining redox homeostasis, all of which contribute to cancer cell proliferation and survival. Thus, intervention in glutamine metabolic processes could provide novel approaches to improve cancer treatment. MCE owns a unique collection of 1,827 compounds targeting the mainly proteins and enzymes involved in glutamine metabolism pathway. Glutamine Metabolism compound library is a useful tool for intervention in glutamine metabolic processes.

Signaling Pathway Targeting Libraries

83
HY-L133 Cuproptosis Compound Library
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 446 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.

Signaling Pathway Targeting Libraries

83
HY-L155 Mitochondrial Toxicity Compound Library
Mitochondria, as the main place of energy supply in life, is essential to maintain normal life activities. Mitochondrial dysfunction is associated with common diseases, such as cardiovascular diseases, neurodegenerative diseases, diabetes and cancer. The heart, brain and liver rely heavily on mitochondrial function as the main organs for drug metabolism. In addition, mitochondria is also a target of many drugs, some of which induce organotoxicity by inducing mitochondrial toxicity. MCE contains 545 mitochondrial toxic compounds, which can be used as tool compounds for drug development and disease mechanism research.

Compound Characteristic Classified Libraries Signaling Pathway Targeting Libraries

83
HY-L162M Cell Death Inhibitor Library Mini
Cell death is a core biological process that maintains homeostasis in multicellular organisms, playing a dual role in life activities. On one hand, cell death participates in physiological processes such as cell renewal and damage repair through precise regulation; on the other hand, it actively eliminates damaged, infected, or cancerous cells, thereby blocking pathological progression and preserving organism health. Cell death not only ensures the normal development and growth regulation of organisms but is also closely associated with the occurrence and development of various diseases. Numerous studies have shown that specific types of programmed cell death play critical roles in disease progression, providing an important theoretical basis for developing novel therapeutic strategies by regulating cell death pathways. MCE offers 23 types of commonly used cell death inhibitors, such as apoptosis, ferroptosis, pyroptosis, and cuproptosis, suitable for use as positive controls in the study of novel cell death mechanisms.

Signaling Pathway Targeting Libraries

83
HY-L227 Amino Acid Metabolite Compound Library
Amino acids are the fundamental components that sustain life activities, playing roles in ATP generation, promoting nucleotide synthesis, and maintaining cellular redox balance. Moreover, dysregulation of amino acid consumption is a significant potential regulatory mechanism leading to impaired anti-tumor immunity in immune cells. The normal functioning of immune cells relies on amino acid metabolic pathways to obtain energy and materials, and upon activation, they reprogram their metabolism to support growth, proliferation, and effector functions. Additionally, metabolic disorders of specific amino acids (such as branched-chain amino acids, glutamine, and arginine) can exacerbate mitochondrial dysfunction and oxidative stress, thereby promoting myocardial fibrosis and cardiac cell damage. Therefore, conducting research related to amino acid metabolism holds promise for discovering potential drugs for diseases related to cancer, immunity, and metabolism. MCE can provide 195 kinds of metabolites of amino acid metabolic pathways, which can be used for drug screening in various diseases such as cancer, immune disorders, metabolic diseases, mitochondrial-targeted diseases

Metabolism Focused Libraries

83
HY-L263 Energy Metabolites Library
Energy metabolism is the most fundamental biochemical process in living organisms, encompassing glycolysis, the TCA cycle, oxidative phosphorylation, the pentose phosphate pathway, and fatty acid oxidation. These core pathways directly regulate cell survival, proliferation, differentiation, and apoptosis. Dysregulation of energy metabolism is closely linked to major diseases including cancer, diabetes, obesity, cardiovascular diseases, neurodegenerative disorders, and ischemia‑reperfusion injury. Targeting these metabolic pathways has become a frontier in drug discovery and mechanistic research. The MCE Energy Metabolite Compound Library features 89 structurally defined small‑molecule compounds. It covers energy substrates, pathway intermediates, coenzymes and redox carriers, nucleotide derivatives, and microenvironmental modulators. This library is applicable to research areas including tumor metabolism, insulin resistance, mitochondrial dysfunction, oxidative stress, neuroprotection, and cardiometabolic diseases, providing a high‑quality tool for mechanistic studies, biomarker discovery, and high‑throughput drug screening.

Signaling Pathway Targeting Libraries

83
HY-13755 Sulforaphane
Sulforaphane is an orally active inducer of the Keap1/Nrf2/ARE pathway. Sulforaphane promotes the transcription of tumor-suppressing proteins and effectively inhibits the activity of HDACs. Through the activation of the Keap1/Nrf2/ARE pathway and further induction of HO-1 expression, Sulforaphane protects the heart. Sulforaphane suppresses high glucose-induced pancreatic cancer through AMPK-dependent signal transmission. Sulforaphane exhibits both anticancer and anti-inflammatory properties.
HDAC   Keap1-Nrf2   Apoptosis   Bcl-2 Family   Caspase   Reactive Oxygen Species (ROS)  
Inflammation or Immune System Disease  
79
HY-50907 ABT-737
ABT-737, a BH3 mimetic, is a potent Bcl-2, Bcl-xL and Bcl-w inhibitor with EC50s of 30.3 nM, 78.7 nM, and 197.8 nM, respectively. ABT-737 induces the disruption of the BCL-2/BAX complex and BAK-dependent but BIM-independent activation of the intrinsic apoptotic pathway. ABT-737 induces autophagy and has the potential for acute myeloid leukemia (AML) research.
Bcl-2 Family   Apoptosis   Autophagy   Mitophagy  
Digestive System Disease   Prostate Cancer   Leukemia/Lymphoma/Myeloma   Ovarian Cancer   Digestive System Inflammation  
75
HY-107202 Polyinosinic-polycytidylic acid
Polyinosinic-polycytidylic acid (Poly(I:C)) is a synthetic analog of double-stranded RNA and an agonist of toll-like receptor 3 (TLR3) and retinoic acid inducible gene I (RIG-I)-like receptors (RIG-I and MDA5). Polyinosinic-polycytidylic acid can be used as a vaccine adjuvant to enhance innate and adaptive immune responses, and to alter the tumor microenvironment. Polyinosinic-polycytidylic acid can directly trigger cancer cells to undergo apoptosis.
RIG-I-like receptor (RLR)   Toll-like Receptor (TLR)   PKD   HSP   Bcl-2 Family   Interleukin Related   Apoptosis  
Infection   Digestive System Disease   Prostate Cancer   Pain   Digestive System Inflammation   Lung Fibrosis   Rheumatoid Arthritis  
73
HY-50876 Daporinad
Daporinad (FK866) is a non-competitive inhibitor of nicotinamide phosphoribosyltransferase (Nampt), with a Ki value of 0.3 nM. Daporinad depletes NAD+ and ATP levels, inhibits mTORC1 and MAPK/ERK pathways, and activates TFEB to induce autophagy. Daporinad causes the depletion of the endoplasmic reticulum Ca²⁺ pool, ultimately weakening the mitogen-induced Ca²⁺ signal and the activation and function of T cells. Daporinad induces cell cycle arrest and apoptosis, and inhibits cell proliferation. Daporinad can be used for the study of myeloma, liver cancer, and immunosuppression.
NAMPT   Autophagy   Apoptosis   mTOR   p38 MAPK   ERK  
Cancer  
67
HY-114118C Semaglutide sodium
Semaglutide sodium is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide sodium promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide sodium also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide sodium has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide sodium can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
GLP Receptor   Insulin Receptor   α-synuclein   Apoptosis   p38 MAPK   Autophagy   Bcl-2 Family  
Cancer   Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
50
HY-114118B Semaglutide acetate
Semaglutide acetate is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
GLP Receptor   Apoptosis   Bcl-2 Family   α-synuclein   Autophagy   Insulin Receptor   p38 MAPK  
Cancer   Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
50
HY-114118A Semaglutide TFA
Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
GLP Receptor   Apoptosis   Bcl-2 Family   α-synuclein   Autophagy   Insulin Receptor   p38 MAPK  
Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
50
HY-114118 Semaglutide
Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
GLP Receptor   Apoptosis   Bcl-2 Family   α-synuclein   Autophagy   Insulin Receptor   p38 MAPK  
Cancer   Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
50
HY-N0171A Beta-Sitosterol (purity>98%)
Beta-Sitosterol (purity>98%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc.
Bacterial   Apoptosis   Reactive Oxygen Species (ROS)   MDM-2/p53   Caspase   PARP   MMP   Bcl-2 Family   HIF/HIF Prolyl-Hydroxylase   TNF Receptor   Interleukin Related   NF-κB   mTOR   Lactate Dehydrogenase   CDK   Glutathione Peroxidase   SOD  
Lung Cancer   Breast Cancer   Prostate Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Bacterial Infection   Depression   Pain   Digestive System Inflammation   Cardiovascular Disease   Glucose Metabolism   Obesity   Lung Fibrosis   Rheumatoid Arthritis  
25
HY-W105518 L-Carnitine tartrate
L-Carnitine tartrate is a highly polar, small zwitterion. L-Carnitine tartrate is an essential co-factor for the mitochondrial β-oxidation pathway. L-Carnitine tartrate functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation. L-Carnitine tartrate is an antioxidant. L-Carnitine tartrate can ameliorate metabolic imbalances in many inborn errors of metabolism[3].
Endogenous Metabolite  
Neurological, Eye or Ear Disease  
22
HY-B2246 L-Carnitine hydrochloride
L-Carnitine hydrochloride ((R)-Carnitine hydrochloride), a highly polar, small zwitterion, is an essential co-factor for the mitochondrial β-oxidation pathway. L-Carnitine hydrochloride functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation. L-Carnitine hydrochloride is an antioxidant. L-Carnitine hydrochloride can ameliorate metabolic imbalances in many inborn errors of metabolism.
Endogenous Metabolite  
Metabolic or Endocrine Disease   Pancreatic Cancer   Viral Infection  
22
HY-B0399 L-Carnitine
L-Carnitine ((R)-Carnitine), a highly polar, small zwitterion, is an essential co-factor for the mitochondrial β-oxidation pathway. L-Carnitine functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation. L-Carnitine is an antioxidant. L-Carnitine can ameliorate metabolic imbalances in many inborn errors of metabolism.
Endogenous Metabolite  
Neurological, Eye or Ear Disease   Pancreatic Cancer   Viral Infection  
22
HY-B0572 Zinc Pyrithione
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.
Environmental Pollutants   Proton Pump   Cuproptosis   Bacterial   Fungal  
Metabolic or Endocrine Disease   Bacterial Infection   Fungal Infection  
12
HY-B0158 Cytidine
Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function.

Source: Widespread

Nucleoside Antimetabolite/Analog   Endogenous Metabolite  
Neurological, Eye or Ear Disease   Lung Cancer   Leukemia/Lymphoma/Myeloma   SARS-CoV-2 Infection  
8
HY-112220 VIT-2763
VIT-2763, an oral ferroportin inhibitor, inhibits hepcidin binding to ferroportin and blocks iron efflux. VIT-2763 has the potential in the treatment of β-thalassemia.
Ferroportin  
Metabolic or Endocrine Disease  
7
HY-156376 Cu(II)-Elesclomol
Cu(II)-Elesclomol is a complex formed by Elesclomol (HY-12040) and Cu2+ (copper ions). Cu(II)-Elesclomol is also a weak inhibitor of DNA topoisomerase I. Cu(II)-Elesclomol exerts anticancer effects by inducing oxidative stress and DNA damage through copper chelation. Cu(II)-Elesclomol can inhibit tumor cell proliferation and induce cell cycle arrest and apoptosis. Cu(II)-Elesclomol can be used in the study of cancer.
Cuproptosis   Apoptosis   Topoisomerase   Reactive Oxygen Species (ROS)  
Digestive System Disease   Lung Cancer   Digestive System Inflammation   Parkinson's Disease  
7
HY-N9933 Tauro-β-muricholic acid
Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis.

Source: rat

FXR   Apoptosis  
Cancer   Digestive System Disease   Neurodegenerative Disease   Digestive System Inflammation   Obesity  
6
HY-113224 Desmosterol
Desmosterol is a cholesterol-like molecule. In the Bloch pathway of cholesterol biosynthesis, Desmosterol is a direct precursor of cholesterol. As an endogenous metabolite, Desmosterol is used to study cholesterol metabolism . Desmosterol is an LXR activator and SREBP inhibitor, which can suppress macrophage inflammasome activation and prevent vascular inflammation and atherosclerosis. A reduction in Desmosterol promotes the production of mitochondrial reactive oxygen species (ROS) in macrophages and pyrin domain-dependent inflammasome activation of NLRP3. Desmosterol holds potential for research in inflammation, metabolism, and cardiovascular diseases .
Endogenous Metabolite   LXR   Fatty Acid Synthase (FASN)   Interleukin Related   Reactive Oxygen Species (ROS)   NOD-like Receptor (NLR)  
Inflammation or Immune System Disease   Blood or Cardio-cerebrovascular Disease   Metabolic or Endocrine Disease   Hepatitis C Virus Infection  
6
HY-N0327 Lobetyolin
Lobetyolin, a bioactive compound, is derived from Codonopsis pilosula. Lobetyolin has anti-inflammatory, anti-oxidative and xanthine oxidase inhibiting activities. Lobetyolin also induces the apoptosis via the inhibition of ASCT2-mediated glutamine metabolism. Lobetyolin is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
Apoptosis   Xanthine Oxidase  
Metabolic or Endocrine Disease   Digestive System Disease   Digestive System Inflammation  
4
HY-B0300 Penicillamine
Penicillamine (D-(-)-Penicillamine) is a penicillin metabolic degradation product, can be used as a heavy metal chelator. Penicillamine increases free copper and increases oxidative stress. Penicillamine has effect of seizures through nitric oxide/NMDA pathways. Penicillamine is a potential immune modulator. Penicillamine can be used for the research of Wilson disease, rheumatoid arthritis, and cystinuria.

Source: Penicillium

Cuproptosis   Drug Metabolite  
Lung Cancer   Breast Cancer   Neurodegenerative Disease   Rheumatoid Arthritis  
4
HY-126301 DMT1 blocker 1
DMT1 blocker 1 is an orally active blocker of divalent metal transporter 1 (DMT1) with an IC50 of 0.64 μM. DMT1 blocker 1 inhibits intestinal cell absorption of non-heme iron, thereby alleviating iron overload by blocking the DMT1 transporter. DMT1 blocker 1 demonstrates significant efficacy in rodent models of acute iron hyperabsorption. DMT1 blocker 1 is useful for studying iron overload disorders such as hereditary hemochromatosis and thalassemia.
Ferroportin  
Metabolic or Endocrine Disease  
3
HY-126302 DMT1 blocker 2
DMT1 blocker 2 is a direct inhibitor of divalent metal transporter 1 (DMT1), with an IC50 of 0.83 μM. DMT1 blocker 2 can block iron uptake by enterocytes in vivo.
Ferroportin  
Metabolic or Endocrine Disease  
3
HY-P1723A Spexin TFA
Spexin (Neuropeptide Q) TFA is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin TFA can function through both central and peripheral actions. Spexin TFA upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin TFA improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin TFA can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy.
Neuropeptide Y Receptor   Apoptosis   Ferroptosis   Autophagy  
Blood or Cardio-cerebrovascular Disease   Metabolic or Endocrine Disease  
2
HY-P1723 Spexin
Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy.
Neuropeptide Y Receptor   Apoptosis   Ferroptosis   Autophagy  
Neurological, Eye or Ear Disease   Blood or Cardio-cerebrovascular Disease  
2
HY-B0762 Acetyl-L-carnitine hydrochloride
Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression.
Caspase   Apoptosis  
Digestive System Disease   Prostate Cancer   Viral Infection   Depression   Digestive System Inflammation   Alzheimer's Disease   Parkinson's Disease  
2
HY-113218 Acetyl-L-carnitine
Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression.

Source: Homo sapiens

Caspase   Apoptosis  
Digestive System Disease   Viral Infection   Digestive System Inflammation   Alzheimer's Disease   Parkinson's Disease  
2
HY-W004563 Neocuproine
Neocuproine is an organic compound commonly used as a complexing reagent and copper ion detector. It can form stable complexes with copper ions, and can play a catalytic role in certain chemical reactions and analytical methods. In addition, this compound is also widely used in some biomedical fields, such as in the study of copper metabolism disorders and neurodegenerative diseases
Biochemical Assay Reagents  
2
HY-P4910 Baceridin
Baceridin is a proteasome inhibitor and a cyclic hexapeptide. Baceridin can be isolated from the culture medium of Epiphytic Bacillus. Baceridin can inhibit cell cycle progression and induce tumor cell apoptosis through a p53-independent pathway. Baceridin can be used in cancer research.
Proteasome   Apoptosis  
1
HY-13545 ABT-510
ABT-510 is an anti-angiogenic TSP peptide (Thrombospondin-1 analogue) that induces apoptosis and inhibits ovarian tumour growth in an orthotopic, syngeneic model of epithelial ovarian cancer. ABT-510 also reduces angiogenesis and inflammatory responses in a murine model of inflammatory bowel disease. ABT-510 can be used in studies of cancer (particularly epithelial ovarian cancer) and inflammatory bowel disease (IBD).
Apoptosis  
Cancer   Inflammation or Immune System Disease  
1
HY-119976 Boscalid
Boscalid is a succinate dehydrogenase (SDHI) inhibitor with antifungal activity. Boscalid binds to the ubiquinone-binding site of fungal mitochondrial complex II, blocks ATP production and aerobic respiration, exhibits good control efficacy against a variety of plant fungal diseases including gray mold, sclerotinia rot and powdery mildew, and is widely used for disease control in agriculture. Boscalid induces apoptosis, altered lipid metabolism, mitochondrial dysfunction, respiratory impairment, oxidative stress, ROS accumulation and neurodevelopmental disorders in zebrafish. Boscalid reduces foraging ability, shortens median death time and causes chronic toxicity in exposed honeybees. Boscalid also possesses genotoxicity, cytotoxicity, elevated mitochondrial superoxide levels and early-stage apoptosis.
Environmental Pollutants   Mitochondrial Metabolism   Fungal   Apoptosis   Succinate Dehydrogenase  
Fungal Infection  
1
HY-134238 Cardiolipin (Heart, Bovine) sodium
Cardiolipin (Heart, Bovine) sodium is a mitochondria-exclusive phospholipid that can be extracted from Bovine hear. Cardiolipin (Heart, Bovine) sodium can maintain mitochondrial function, regulate cellular metabolism and signaling and induce apoptosis and autophagy. Cardiolipin (Heart, Bovine) sodium can be coated on microtitre plates for ELISA assay. Cardiolipin (Heart, Bovine) sodium can be used for the researches of inflammation, immunology, cardiovascular and neurological disease.
Endogenous Metabolite   Mitochondrial Metabolism   Apoptosis   Autophagy  
Inflammation or Immune System Disease   Blood or Cardio-cerebrovascular Disease   Alzheimer's Disease   Parkinson's Disease  
1
HY-D3212 Crisp-17
Crisp-17 is a monovalent copper ion probe. Crisp-17 can be used to characterize cellular phenotypes associated with copper metabolism defects. Crisp-17 is applicable to research related to Menkes disease.
Fluorescent Dye  
Metabolic or Endocrine Disease  
/
HY-P10416 Q14
Q14 is a polypeptide derived from the USP30 (ubiquitin specific peptidase 30) transmembrane (TM) domain with the ability to inhibit the deubiquitination activity of USP30 (IC50=57.2 nM). Q14 reduces USP30 activity by inhibiting the interaction between the USP30 transmembrane domain and its catalytic domain. Q14 peptide contains the LC3 interaction region (LIR) motif, which enables it to bind to the LC3 and accelerate the formation of autophagosomes, thereby promoting mitophagy. Q14 can be used in the study of neurodegenerative diseases as well as mitochondrial quality control and cell metabolism.
Deubiquitinase   Mitophagy  
Neurological, Eye or Ear Disease  
/
HY-B0399G L-Carnitine (GMP)
L-Carnitine (GMP) is L-Carnitine (HY-B0399) produced by using GMP guidelines. GMP small molecules work appropriately as an auxiliary reagent for cell therapy manufacture. L-Carnitine, a highly polar, small zwitterion, is an essential co-factor for the mitochondrial β-oxidation pathway. L-Carnitine functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation. L-Carnitine is an antioxidant. L-Carnitine can ameliorate metabolic imbalances in many inborn errors of metabolism.
Endogenous Metabolite  
Cancer   Neurological, Eye or Ear Disease  
/
HY-W768207 Cytidine-1',2',3',4',5'-13C5
Cytidine-1',2',3',4',5'-13C5 is the 13C-labeled Cytidine (HY-B0158). Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function.
Isotope-Labeled Compounds   Endogenous Metabolite   Nucleoside Antimetabolite/Analog  
Neurological, Eye or Ear Disease  
/
HY-P11022 TL-119
TL-119 (A-3302-B) is a polypeptide. TL-119 can be isolated from the bacteria Micromonospora sp. MAG 9-7 and Saccharomonospora sp. CNQ-490. TL-119 inhibits TRPV-1. TL-119 exhibits antiviral activity against HSV-2. TL-119 possesses anticancer activity against gastric cancer and colorectal cancer.
Endogenous Metabolite   HSV   TRP Channel  
Colorectal Cancer   Gastric Cancer   Bacterial Infection   HSV Infection  
/
HY-P2120 Pseudobactin A
Pseudobactin A is a non-fluorescent extracellular iron carrier produced by the plant growth-promoting bacterium Pseudomonas B10.
Bacterial  
/
HY-D3215 Lyso-Cu(II)
Lyso-Cu (II) is a lysosome-targeted divalent copper ion probe. Lyso-Cu (II) is applicable to the research of Wilson's disease, Menkes disease and Alzheimer's disease.
Fluorescent Dye  
Alzheimer's Disease  
/
HY-B0300S Penicillamine-d3
Penicillamine-d3 is the deuterium labeled Penicillamine. Penicillamine (D-(-)-Penicillamine) is the most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.
Drug Metabolite   Cuproptosis   Isotope-Labeled Compounds  
Inflammation or Immune System Disease  
/
HY-D2969 CYDA
CYDA is a colorimetric probe based on cyanine dyes, which enables highly sensitive and selective detection of Cu²⁺. CYDA can be used for urine copper detection in Wilson's disease.
Fluorescent Dye  
Mineral Metabolism  
/
HY-P11358 IRW
IRW is an orally active tripeptide produced from egg white with angiotensin converting enzyme (ACE) inhibitory properties. IRW can prevent high-fat diet (HFD)-induced Non-alcoholic fatty liver disease (NAFLD) by modulating hepatic lipid metabolism and increasing mitochondrial content. IRW decreases hepatic triglyceride content and lipid droplet size. IRW increases the hepatic mitochondrial complexes and citrate synthase activity, phosphorylation of 5’-AMP-activated protein kinase and microsomal triglyceride transfer protein abundance. IRW increases phosphorylated acetyl CoA carboxylase and mitochondrial complexes, IRW can be used for the research of inflammation.
Angiotensin-converting Enzyme (ACE)   Acetyl-CoA Carboxylase   Mitochondrial Metabolism  
Inflammation or Immune System Disease  
/
HY-B1637S Ditiocarb-d10 sodium
Ditiocarb-d10 sodium (Sodium diethyldithiocarbamate-d10) is the deuterium labeled Ditiocarb sodium (HY-B1637). Ditiocarb sodium (Sodium diethyldithiocarbamate) is an orally active copper reagent. Ditiocarb sodium exhibits activities such as antioxidation, chelation, anti-tumor effects, immunomodulation, and anti-HIV properties. Ditiocarb sodium can be used in the research of tumors, inflammatory, and immune-related diseases.
Isotope-Labeled Compounds   HIV   Biochemical Assay Reagents  
Cancer   Infection   Inflammation or Immune System Disease  
/
HY-34740S1 Ethylmalonic acid-d5
Ethylmalonic acid-d5 is the deuterium labeled Ethylmalonic acid (HY-34740). Ethylmalonic acid is a short-chain organic dicarboxylic acid. Ethylmalonic acid synergistically induces mitochondrial permeability transition (MP) with Ca2+, inhibits Mi-CK, and disrupts mitochondrial energy metabolism. Ethylmalonic acid can be used in the research of SCADD, EE and other genetic metabolic diseases characterized by EMA accumulation.
Mitochondrial Metabolism   Isotope-Labeled Compounds  
Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
/
HY-D3207 DHUCu-1
DHUCu-1 is a lysosome-targeted NIR divalent copper ion probe with high water solubility. DHUCu-1 serves as a tool for investigating the physiological functions of Cu2+ and related diseases, such as Menke syndrome, Wilson's disease, and Alzheimer's disease.
Fluorescent Dye  
Alzheimer's Disease  
/
HY-12040S Elesclomol-d2
Elesclomol-d2 (STA-4783-d2) is a deuterium labeled Elesclomol (HY-12040). 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.
Isotope-Labeled Compounds   Reactive Oxygen Species (ROS)   Apoptosis   Cuproptosis  
/
HY-D3282 CCF1
CCF1 is a carbon-rhodol-based turn-on fluorescent copper sensor with high selectivity for Cu+ over other biologically relevant metal ions. CCF1 detects changes in labile copper pools in living cells upon copper supplementation and/or depletion. CCF1 identifies elevations in labile copper pools in Atp7a-/- fibroblast cell models. CCF1 can be used for the research of Menkes disease.
Fluorescent Dye  
Metabolic or Endocrine Disease  
/
HY-P0245 Speract
Speract, a sea urchin egg peptide that regulates sperm motility, also stimulates sperm mitochondrial metabolism.
Mitochondrial Metabolism  
Metabolic or Endocrine Disease  
/
HY-B0300R Penicillamine (Standard)
Penicillamine (Standard) is the analytical standard of Penicillamine. This product is intended for research and analytical applications. Penicillamine (D-(-)-Penicillamine) is a penicillin metabolic degradation product, can be used as a heavy metal chelator. Penicillamine increases free copper and increases oxidative stress. Penicillamine has effect of seizures through nitric oxide/NMDA pathways. Penicillamine is a potential immune modulator. Penicillamine can be used for the research of Wilson disease, rheumatoid arthritis, and cystinuria.
Reference Standards   Cuproptosis   Drug Metabolite  
Cancer   Inflammation or Immune System Disease  
/
HY-N14780 Pochonin D
Pochonin D ((+)-Pochonin D) is an inhibitor of heat shock protein 90 (Hsp90) with antiviral and anti-inflammatory activities. Pochonin D inhibits Hsp90, affects the homeostasis, folding and assembly processes of viral proteins, and reduces the replication capacity of viruses. Pochonin D is a copper ion carrier that can induce cuproptosis in triple-negative breast cancer cells by targeting PRDX1. Pochonin D reduces the infiltration of inflammatory cells, decreases the secretion of inflammatory cytokines such as TNF-α and IL-1β, and alleviates inflammatory responses. Pochonin D is a promising candidate for research on human rhinovirus (HRV) infection and cancer.

Source: Humicola sp. FO-2942

HSP   Interleukin Related   TNF Receptor   Enterovirus   Cuproptosis  
Cancer   Inflammation or Immune System Disease   Parasitic Infection  
/
HY-145965 Ferroportin-IN-1
Ferroportin-IN-1 is a ferroportin inhibitor extracted from patent WO2020123850A1 compound 23. Ferroportin-IN-1 can be used for the research of diseases caused by a lack of hepcidin or iron metabolism disorders.
Ferroportin  
Metabolic or Endocrine Disease  
/
HY-W101299 N-Acetyl-D-allo-isoleucine
N-Acetyl-D-allo-isoleucine is an amino acid derivative. N-Acetyl-D-allo-isoleucine is promising for research of amino acid metabolism, such as abnormal isoleucine metabolism.
Amino Acid Derivatives  
Metabolic or Endocrine Disease  
/
HY-119976R Boscalid (Standard)
Boscalid (Standard) is the analytical standard of Boscalid. This product is intended for research and analytical applications. Boscalid is a succinate dehydrogenase (SDHI) inhibitor with antifungal activity. Boscalid binds to the ubiquinone-binding site of fungal mitochondrial complex II, blocks ATP production and aerobic respiration, exhibits good control efficacy against a variety of plant fungal diseases including gray mold, sclerotinia rot and powdery mildew, and is widely used for disease control in agriculture. Boscalid induces apoptosis, altered lipid metabolism, mitochondrial dysfunction, respiratory impairment, oxidative stress, ROS accumulation and neurodevelopmental disorders in zebrafish. Boscalid reduces foraging ability, shortens median death time and causes chronic toxicity in exposed honeybees. Boscalid also possesses genotoxicity, cytotoxicity, elevated mitochondrial superoxide levels and early-stage apoptosis.
Reference Standards   Apoptosis   Fungal   Mitochondrial Metabolism   Succinate Dehydrogenase  
Infection  
/
HY-B0158S5 Cytidine-13C9,15N3
Cytidine-13C9,15N3 is the 13C and 15N labeled Cytidine. Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function.
Nucleoside Antimetabolite/Analog   Endogenous Metabolite  
Neurological, Eye or Ear Disease  
/
HY-P991881 KY1070
KY1070 is a fully human anti-BMP6 antibody with a Kd of 0.00014 μM against the human BMP6. It exhibits high specificity for BMP6, showing no cross-reactivity with other members of the BMP family, and effectively inhibits BMP6-induced BMP receptor heterodimerization and hepcidin expression. KY1070 modulates Ferroportin expression on erythroid progenitor cells and accelerates erythropoiesis. In rodent anemia models, KY1070 reduces the required dose of erythropoietin (EPO) when used in combination with EPO and enhances the responsiveness of mice with chronic kidney disease (CKD)-associated anemia to EPO treatment. KY1070 is applicable for research on anemia of chronic disease .

Species: Human

TGF-β Receptor   Hepcidin   Ferroportin  
Blood Disease  
/
HY-B0658A Zinc acetate dihydrate, ACS, 98%
Zinc acetate dihydrate, ACS, 98% (Zinc (II) acetate dihydrate, ACS, 98%) acts as a metal chelator and an intestinal metallothionein inducer. Zinc acetate dihydrate, ACS, 98% induces intestinal metallothionein synthesis and shortens the course of the common cold. Zinc acetate dihydrate, ACS, 98% is applicable to the research of copper metabolism disorder-related diseases, the common cold and Wilson's disease, as well as protein experiments.
Biochemical Assay Reagents  
/
HY-119976S Boscalid-d4
Boscalid-d4 is the deuterium labeled Boscalid. Boscalid is a succinate dehydrogenase (SDHI) inhibitor with antifungal activity. Boscalid binds to the ubiquinone-binding site of fungal mitochondrial complex II, blocks ATP production and aerobic respiration, exhibits good control efficacy against a variety of plant fungal diseases including gray mold, sclerotinia rot and powdery mildew, and is widely used for disease control in agriculture. Boscalid induces apoptosis, altered lipid metabolism, mitochondrial dysfunction, respiratory impairment, oxidative stress, ROS accumulation and neurodevelopmental disorders in zebrafish. Boscalid reduces foraging ability, shortens median death time and causes chronic toxicity in exposed honeybees. Boscalid also possesses genotoxicity, cytotoxicity, elevated mitochondrial superoxide levels and early-stage apoptosis.
Isotope-Labeled Compounds   Apoptosis   Fungal   Mitochondrial Metabolism   Succinate Dehydrogenase  
/
HY-107980 DS28120313
DS28120313 (compound 32) is an orally hepcidin production inhibitor with an IC50 of 0.093 μM.
Ferroportin  
Inflammation or Immune System Disease  
/
HY-142026 Vitisin A
Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC50 values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases.
Caspase   ERK   NF-κB   Influenza Virus   PAK   LDLR   PPAR   PCSK9   Androgen Receptor   Keap1-Nrf2   Monoamine Oxidase   Cholinesterase (ChE)   IKK   Wnt   β-catenin   Reactive Oxygen Species (ROS)   Apoptosis   Cuproptosis  
Cancer   Infection   Metabolic or Endocrine Disease   Neurodegenerative Disease   Antioxidant Agent  
/
HY-B0158S Cytidine-d2
Cytidine-d2 is the deuterium labeled Cytidine. Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function.
Nucleoside Antimetabolite/Analog   Endogenous Metabolite  
Neurological, Eye or Ear Disease  
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HY-B0158S6 Cytidine-15N3
Cytidine-15N3 is the 15N labeled Cytidine. Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function.
Nucleoside Antimetabolite/Analog   Endogenous Metabolite  
Neurological, Eye or Ear Disease  
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HY-P4613 Fmoc-D-allo-Thr-OH
Fmoc-D-allo-Thr-OH is a derivative of D-allothreonine (HY-W001959), which is commonly used as a building block in solid-phase peptide synthesis (SPPS).
Drug Derivative   Drug Intermediate  
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HY-162386 UM4118
UM4118 is a potent copper-selective non-genotoxic copper ionophore that induces cuproptosis in acute myeloid leukemia cells. UM4118 exhibits stronger activity against SF3B1G12C mutant acute myeloid leukemia cells. UM4118 transports extracellular copper into cells, elevates intracellular and mitochondrial copper levels, and triggers lipoylated DLAT aggregation, proteotoxic stress, iron-sulfur cluster protein depletion, reduced lipoylated protein levels, and maximal mitochondrial respiratory damage. UM4118 cytotoxicity can be enhanced by supplementation with extracellular copper, abolished by copper chelation, and shows synthetic lethal effects in the absence of iron-sulfur cluster biosynthesis/transport genes. UM4118 can be used for the study of acute myeloid leukemia.
Cuproptosis   Mitochondrial Metabolism  
Leukemia/Lymphoma/Myeloma  
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HY-B0158S7 Cytidine-13C9
Cytidine-13C9 (Cytosine β-D-riboside-13C9) is 13C labeled Cytidine (HY-B0158). Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function.
Nucleoside Antimetabolite/Analog   Endogenous Metabolite   Isotope-Labeled Compounds  
Neurological, Eye or Ear Disease  
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HY-147379 Hepcidin antagonist-1
Hepcidin antagonist-1 (example 104) is a potent hepcidin (hepcidine) antagonist with an IC50<50 μM. Hepcidin antagonist-1 can be used for researching iron metabolism disorders, such as anemias.
Ferroportin  
Metabolic or Endocrine Disease   Blood Disease  
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HY-34740S Ethylmalonic acid-d3
Ethylmalonic acid-d3 is the deuterium labeled Ethylmalonic acid (HY-34740). Ethylmalonic acid is a short-chain organic dicarboxylic acid. Ethylmalonic acid synergistically induces mitochondrial permeability transition (MP) with Ca2+, inhibits Mi-CK, and disrupts mitochondrial energy metabolism. Ethylmalonic acid can be used in the research of SCADD, EE and other genetic metabolic diseases characterized by EMA accumulation.
Mitochondrial Metabolism   Isotope-Labeled Compounds  
Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
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HY-B2082 Fursultiamine
Fursultiamine is a vitamin B1 derivative, has anti-nociceptive and antineoplastic activity. Fursultiamine can be used for vitamin B1?deficiency, osteoarthritis (OA) and cancer research.
VEGFR   Ferroportin   NF-κB   Mitochondrial Metabolism  
Lung Cancer   Breast Cancer   Colorectal Cancer   Prostate Cancer   Liver Cancer   Leukemia/Lymphoma/Myeloma   Pancreatic Cancer   Ovarian Cancer   Depression   Pain   Digestive System Inflammation   Obesity   Lung Fibrosis  
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HY-B2153 Tetraethylenepentamine pentahydrochloride
Tetraethylenepentamine pentahydrochloride is an orally active copper chelator and copper mobilizer. Tetraethylenepentamine pentahydrochloride exhibits growth inhibitory and hypolipidemic properties. Tetraethylenepentamine pentahydrochloride significantly increases urinary copper excretion and reduces renal copper accumulation in copper overload models, but does not significantly alter hepatic copper levels. Tetraethylenepentamine pentahydrochloride exerts growth inhibitory effects on Candida albicans and Fluconazole (HY-B0101)-resistant strains, and can be widely used in studies related to Wilson's disease and Candida infections.
Cuproptosis   Bacterial  
Candida Infection  
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HY-P10409 SHLP2
SHLP2 (Small humanin-like peptide 2) is a small molecule peptide encoded by mitochondrial DNA, belonging to mitochondria derived peptide. SHLP2 has the activity of regulating apoptosis and inhibits cell death. SHLP2 binds to mitochondrial complex 1. SHLP2 improves mitochondrial metabolism by increasing respiration and biogenesis, reducing ROS, and decreasing mtDNA oxidation. SHLP2 also regulated energy homeostasis through the activation of hypothalamic neurons. SHLP2 can be used in the study of diseases related to mitochondrial dysfunction and anti-aging diseases, such as age-related macular degeneration and Parkinson’s disease.
Apoptosis   Reactive Oxygen Species (ROS)  
Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
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HY-B0762S Acetyl-L-carnitine-d3 hydrochloride
Acetyl-L-carnitine-d3 (O-Acetyl-L-carnitine-d3) hydrochloride is the deuterium labeled Acetyl-L-carnitine hydrochloride (HY-B0762). Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression.
Isotope-Labeled Compounds   Apoptosis   Caspase  
Neurological, Eye or Ear Disease  
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HY-B0762S1 Acetyl-L-carnitine-d3-1 hydrochloride
Acetyl-L-carnitine-d3-1 (O-Acetyl-L-carnitine-d3-1) hydrochloride is the deuterium labeled Acetyl-L-carnitine hydrochloride (HY-B0762). Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression.
Isotope-Labeled Compounds   Apoptosis   Caspase  
Neurological, Eye or Ear Disease  
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HY-16739 Emeramide
Emeramide is a thiol-redox antioxidant and heavy metal chelator.
Cuproptosis   Reactive Oxygen Species (ROS)  
Cancer   Inflammation or Immune System Disease  
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HY-P3267A Apo-Bovine Transferrin
Apo-Bovine Transferrin refers to iron free Transferrin (HY-P3267), serves as Transferrin receptor ligand and mediates iron release from endothelial cells. Apo-Transferrin can directly bind to hephaestin, which can convert Fe2+ to Fe3+. Apo-Transferrin mediates iron efflux most likely in cooperation with ferroportin 1. Apo-Bovine Transferrin can be used in neuroretinal research.
Ferroportin   Transferrin Receptor  
Neurological, Eye or Ear Disease  
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HY-W012382 N-Acetyl-L-tyrosine
N-Acetyl-L-tyrosine is an orally active endogenous mitochondrial stress response regulator that can permeate the cell membrane by passive diffusion. N-Acetyl-L-tyrosine induces low-level reactive oxygen species (ROS) generation by transiently perturbing mitochondrial membrane potential, triggering reverse signaling to activate FoxO and Keap1 pathways. As a result, N-Acetyl-L-tyrosine enhances the expression of antioxidant enzyme genes, exerting anti-stress and cytoprotective effects. N-Acetyl-L-tyrosine can improve heat stress tolerance, inhibit tumor growth, and regulate energy metabolism. N-Acetyl-L-tyrosine can be used in the research of aging, metabolic diseases (such as diabetes), and cancer.
Endogenous Metabolite  
Colorectal Cancer   Glucose Metabolism  
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HY-126358 Acetylcarnitine
Acetylcarnitine is a CNS-penetrant endogenous metabolite. Acetylcarnitine shuttling links mitochondrial metabolism to histone acetylation and lipogenesis. Acetylcarnitine attenuates oxidative stress and neuroinflammation. Acetylcarnitine can be used for fatigue-associated diseases research. Acetylcarnitine can be used as a candidate diagnostic and prognostic biomarker of hepatocellular carcinoma.
Endogenous Metabolite   Mitochondrial Metabolism  
Cancer   Neurological, Eye or Ear Disease   Metabolic or Endocrine Disease  
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HY-B0240R Disulfiram (Standard)
Disulfiram (Standard) is the analytical standard of Disulfiram. This product is intended for research and analytical applications. 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 + Cu2+ increases intracellular ROS levels triggering apoptosis of ovarian cancer stem cells.
Reference Standards   Aldehyde Dehydrogenase (ALDH)   Interleukin Related   Pyroptosis   Apoptosis   Cuproptosis  
Cancer   Metabolic or Endocrine Disease  
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HY-P10272 Rusfertide
Rusfertide is a peptide mimetic of natural hepcidin, which targets and degrades ferroportin, reduces serum iron and transferrin-saturation, and thus regulates the production of red blood cells. Rusfertide ameliorates the polycythemia vera, β-thalassemia and hereditary hemochromatosis.
Ferroportin  
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HY-P75316 CUTC Protein, Human (His)
CUTC proteins potentially regulate copper homeostasis by binding Cu(1+) of each subunit, suggesting a role in the control of cellular copper levels. As a homotetramer, the tetrameric arrangement of CUTC suggests cooperative behavior in managing copper ions. CUTC Protein, Human (His) is the recombinant human-derived CUTC protein, expressed by E. coli , with N-His labeled tag.

Species: Human; Source: E. coli

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HY-P82284 ATP7B Antibody (YA2029)
ATP7B Antibody (YA2029) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to ATP7B.

Host: Rabbit; Reactivity: Human

Monoclonal Antibodies Recombinant Antibodies Flow Cytometry Antibodies Primary Antibodies

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HY-P811101 ATP7B Antibody
ATP7B Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to ATP7B.

Host: Rabbit; Reactivity: Human, Mouse

Polyclonal Antibodies Primary Antibodies

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Keywords

copper metabolism | copper homeostasis | Wilson disease | ATP7B | ATP7A | copper deficiency | cuproptosis | mitochondrial metabolism | metalloproteostasis | copper chelation