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Results for "

aerobic metabolism

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Mitochondrial Metabolism (6) Antibiotic (1) Apoptosis (5) Bacterial (4) Endogenous Metabolite (3) Environmental Pollutants (2) Fungal (3) Hexokinase (2) Isotope-Labeled Compounds (1) Lactate Dehydrogenase (1) Oxidative Phosphorylation (4) Parasite (2) Reactive Oxygen Species (ROS) (5) Reference Standards (3) Succinate Dehydrogenase (3)
By Research Areas:	Cancer (9) Cardiovascular Disease (1) Infection (4) Inflammation/Immunology (3) Metabolic Disease (7) Neurological Disease (1)

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: Mitochondrial Metabolism

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-N0305

5-Aminolevulinic acid hydrochloride Maximum Cited Publications 20 Publications Verification 5-ALA hydrochloride; δ-Aminolevulinic acid hydrochloride; 5-Amino-4-oxopentanoic acid hydrochloride	Reactive Oxygen Species (ROS)	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
5-Aminolevulinic acid (5-ALA; δ-Aminolevulinic acid; 5-Amino-4-oxopentanoic acid) hydrochloride is an orally active heme precursor. 5-Aminolevulinic acid hydrochloride promotes aerobic energy metabolism and increases ATP levels by enhancing the activity of cytochrome c oxidase. 5-Aminolevulinic acid hydrochloride enhances LPS-induced proinflammatory cytokine production and gene activation, and restores the phagocytic activity and ROS generation capacity of neutrophils. 5-Aminolevulinic acid hydrochloride selectively accumulates protoporphyrin IX in tumor cells; as a photosensitizer and radiosensitizer, it induces ROS burst upon light or X-ray irradiation to inhibit tumor growth. 5-Aminolevulinic acid hydrochloride can be applied to the research of septic shock, melanoma, and cancer radiotherapy .

HY-B0486

Lonidamine 15+ Cited Publications AF-1890; Diclondazolic Acid; DICA	Hexokinase Mitochondrial Metabolism Apoptosis Parasite	Inflammation/Immunology Cancer
Lonidamine (AF-1890) is a hexokinase and mitochondrial pyruvate carrier inhibitor (K_i: 2.5 μM). Lonidamine also inhibits aerobic glycolysis in cancer cells. Lonidamine can be used in the research of mitochondrial metabolism and inflammation, such as pulmonary fibrosis .

HY-N10574

Queuine 1 Publications Verification	Bacterial	Metabolic Disease Cancer
Queuine is a selective substrate for tRNA guanine transglycosylase (TGT) and can be incorporated into eukaryotic tRNA. Queuine promotes tRNA modification, affecting mitochondrial function and Warburg metabolic phenotype. If Queuine is deficient, aerobic glycolysis can be enhanced, oxidative phosphorylation can be inhibited, and Warburg metabolism can be promoted, accompanied by increased ammonia and lactate production and increased lactate dehydrogenase activity. Queuine can be used for autoimmune diseases (such as experimental models of multiple sclerosis) and cancer metabolic regulation, and its deficiency is associated with low tRNA modification in tumor cells .

HY-119976

Boscalid 1 Publications Verification	Environmental Pollutants Apoptosis Fungal Mitochondrial Metabolism Succinate Dehydrogenase	Infection
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 .

HY-W000450

5-Aminolevulinic acid Maximum Cited Publications 20 Publications Verification 5-ALA; δ-Aminolevulinic acid; 5-Amino-4-oxopentanoic acid	Reactive Oxygen Species (ROS)	Cardiovascular Disease Cancer
5-Aminolevulinic acid (5-ALA; δ-Aminolevulinic acid; 5-Amino-4-oxopentanoic acid) is an orally active heme precursor. 5-Aminolevulinic acid promotes aerobic energy metabolism and increases ATP levels by enhancing the activity of cytochrome c oxidase. 5-Aminolevulinic acid enhances LPS-induced proinflammatory cytokine production and gene activation, and restores the phagocytic activity and ROS generation capacity of neutrophils. 5-Aminolevulinic acid selectively accumulates protoporphyrin IX in tumor cells; as a photosensitizer and radiosensitizer, it induces ROS burst upon light or X-ray irradiation to inhibit tumor growth. 5-Aminolevulinic acid can be applied to the research of septic shock, melanoma, and cancer radiotherapy .

HY-P2832

Acyl coenzyme A synthetase ACS	Endogenous Metabolite	Metabolic Disease Cancer
Acyl coenzyme A synthetase (ACS), namely acetyl coenzyme A synthetase, is often used in biochemical research. Acyl coenzyme A synthetase can catalyze the activation of fatty acids by coenzyme A through a two-step thioesterification reaction to produce acyl coenzyme A, and then participate in a variety of anabolic and catabolic lipid metabolism pathways, and participate in the TCA cycle in aerobic respiration .

HY-W561907

IMipenem and cilastatin sodium	Antibiotic Bacterial	Infection
IMipenem and cilastatin sodium is a broad-spectrum Carbapenem Antibiotic combination. Imipenem (HY-B1369A) is a Carbapenem antibiotic. IMipenem demonstrates excellent activity against gram-positive and gram-negative aerobic and anaerobic organisms. Cilastatin (HY-A0166) is a renal Dehydropeptidase inhibitor that inhibits the metabolism of Imipenem by renal brush-border enzymes, thus increasing imipenem concentrations in urine .

HY-B0831

Buprofezin 2 Publications Verification	Environmental Pollutants Reactive Oxygen Species (ROS) Oxidative Phosphorylation	Others
Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .

HY-P2733

Glycerol-3-phosphate oxidase, E. coli 2 Publications Verification GPO	Endogenous Metabolite Bacterial	Infection Metabolic Disease
Glycerol-3-phosphate oxidase, E. coli (GPO) is a key intermediate in glycerol metabolism. Glycerol-3-phosphate oxidase, E. coli is the skeleton of phospholipids in membrane lipids, and also a substrate in the respiratory chain. Glycerol-3-phosphate oxidase, E. coli produces electrons through oxidation. Glycerol-3-phosphate oxidase, E. coli is an enzyme with important functions in the field of biochemistry, and is widely used in medical testing and scientific research .

HY-B0486R

Lonidamine (Standard) AF-1890 (Standard); Diclondazolic Acid (Standard); DICA (Standard)	Reference Standards Hexokinase Mitochondrial Metabolism Apoptosis Parasite	Inflammation/Immunology Cancer
Lonidamine (Standard) is the analytical standard of Lonidamine. This product is intended for research and analytical applications. Lonidamine (AF-1890) is a hexokinase and mitochondrial pyruvate carrier inhibitor (K_i: 2.5 μM). Lonidamine also inhibits aerobic glycolysis in cancer cells. Lonidamine can be used in the research of mitochondrial metabolism and inflammation, such as pulmonary fibrosis .

HY-N10574A

Queuine dihydrochloride 1 Publications Verification	Others	Metabolic Disease Cancer
Queuine dihydrochloride is a selective substrate for tRNA guanine transglycosylase (TGT) and can be incorporated into eukaryotic tRNA. Queuine dihydrochloride promotes tRNA modification, affecting mitochondrial function and Warburg metabolic phenotype. If Queuine dihydrochloride is deficient, aerobic glycolysis can be enhanced, oxidative phosphorylation can be inhibited, and Warburg metabolism can be promoted, accompanied by increased ammonia and lactate production and increased lactate dehydrogenase activity. Queuine dihydrochloride can be used for autoimmune diseases (such as experimental models of multiple sclerosis) and cancer metabolic regulation, and its deficiency is associated with low tRNA modification in tumor cells .

HY-119669

Furylfuramide	Bacterial	Others
Furylfuramide is a food preservative that exhibits mutagenic activity. Furylfuramide can be degraded through the aerobic metabolism by liver microsomes .

HY-W023323

(S)-β-Aminoisobutyric acid hydrochloride 1 Publications Verification	Endogenous Metabolite	Metabolic Disease
(S)-β-Aminoisobutyric acid hydrochloride is a cytoprotective agent, which is a non-proteinogenic amino acid enantiomer derived from valine metabolism in skeletal muscle mitochondria. The plasma level of (S)-β-Aminoisobutyric acid hydrochloride increases significantly after acute aerobic exercise (and is not affected by the AGXT2 rs37369 genotype), and it is secreted by mouse extensor digitorum longus and soleus muscles in ex vivo contraction assays. (S)-β-Aminoisobutyric acid hydrochloride specifically protects osteocytes from oxidative stress-induced cell death .

HY-B0831S

Buprofezin-d6	Oxidative Phosphorylation Reactive Oxygen Species (ROS)	Metabolic Disease
Buprofezin-d₆ is the deuterium labeled Buprofezin. Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .

HY-145306

DX3-234	Oxidative Phosphorylation Mitochondrial Metabolism	Cancer
DX3-234 is an oxidative phosphorylation (OXPHOS) inhibitor. DX3-234 shows significant tumor suppression in the Pan02 syngeneic model of pancreatic cancer .

HY-B0831R

Buprofezin (Standard)	Oxidative Phosphorylation Reference Standards Reactive Oxygen Species (ROS)	Others
Buprofezin (Standard) is the analytical standard of Buprofezin. This product is intended for research and analytical applications. Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .

HY-119976S

Boscalid-d4	Isotope-Labeled Compounds Apoptosis Fungal Mitochondrial Metabolism Succinate Dehydrogenase	Others
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 .

HY-119976R

Boscalid (Standard)	Reference Standards Apoptosis Fungal Mitochondrial Metabolism Succinate Dehydrogenase	Infection
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 .

HY-183858

NCATS-SM1440	Lactate Dehydrogenase	Cancer
NCATS-SM1440 is a glycolysis inhibitor and metabolic regulator that targets LDHA and LDHB (IC₅₀=0.06 μM and 0.03 μM, respectively). Upon binding to LDHA, NCATS-SM1440 blocks the glycolysis pathway and reduces lactate production. NCATS-SM1440 drives the shift of pyruvate metabolism toward mitochondrial metabolism, effectively disrupting the dependence of cancer cells on aerobic glycolysis. NCATS-SM1440 can be widely used in research related to cancer, Ewing's sarcoma, and other related conditions .

Cat. No.	Product Name

HY-L083

Anti-Cancer Metabolism Compound Library	3,552 compounds
Mutations in oncogenes and tumor suppressor genes can modify multiple signaling pathways and in turn cell metabolism, which facilitates tumorigenesis. The paramount hallmark of tumor metabolism is “aerobic glycolysis” or the Warburg effect, coined by Otto Warburg in 1926, in which cancer cells produce most of energy from glycolysis pathway regardless of whether in aerobic or anaerobic condition. Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside. The increased uptake of glucose is facilitated by the overexpression of several isoforms of membrane glucose transporters (GLUTs). Likewise, the metabolic pathways of glutamine, amino acid and fat metabolism are also altered. Recent trends in anti-cancer drug discovery suggests that targeting the altered metabolic pathways of cancer cells result in energy crisis inside the cancer cells and can selectively inhibit cancer cell proliferation by delaying or suppressing tumor growth. MCE provides a unique collection of 3,552 compounds which cover various tumor metabolism-related signaling pathways. These compounds can be used for anti-cancer metabolism targets identification, validation as well anti-cancer drug discovery.

Anti-Cancer Metabolism Compound Library

3,552 compounds

Mutations in oncogenes and tumor suppressor genes can modify multiple signaling pathways and in turn cell metabolism, which facilitates tumorigenesis. The paramount hallmark of tumor metabolism is “aerobic glycolysis” or the Warburg effect, coined by Otto Warburg in 1926, in which cancer cells produce most of energy from glycolysis pathway regardless of whether in aerobic or anaerobic condition. Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside. The increased uptake of glucose is facilitated by the overexpression of several isoforms of membrane glucose transporters (GLUTs). Likewise, the metabolic pathways of glutamine, amino acid and fat metabolism are also altered. Recent trends in anti-cancer drug discovery suggests that targeting the altered metabolic pathways of cancer cells result in energy crisis inside the cancer cells and can selectively inhibit cancer cell proliferation by delaying or suppressing tumor growth.

MCE provides a unique collection of 3,552 compounds which cover various tumor metabolism-related signaling pathways. These compounds can be used for anti-cancer metabolism targets identification, validation as well anti-cancer drug discovery.

HY-L252

Carbohydrate Metabolite Compound Library	0 compounds
Carbohydrate metabolism serves as a central hub for energy supply and biosynthesis in living organisms and plays a critical role in the onset and progression of various diseases. In recent years, studies have shown that tumor cells reprogram their energy metabolism through aerobic glycolysis (the Warburg effect) to support rapid proliferation. Immune cells also rely on specific carbohydrate metabolic pathways to regulate their activation and differentiation states, while disorders such as diabetes and metabolic syndrome arise directly from dysregulation of carbohydrate metabolism. In addition, enzymes and key metabolic nodes involved in carbohydrate metabolism have become important targets for drug discovery, and therapeutic strategies targeting glycolysis, the pentose phosphate pathway, and energy metabolism are continuously advancing the treatment of cancer and metabolic diseases. Therefore, systematic analysis of carbohydrate metabolic networks and their associated metabolites is of great significance for elucidating disease mechanisms and developing novel therapeutic approaches. The MCE Carbohydrate Metabolism Metabolite Library is constructed based on classical carbohydrate metabolic pathways and contains 0 metabolites. It systematically integrates key metabolic networks, including glycolysis, the pentose phosphate pathway, the tricarboxylic acid (TCA) cycle, monosaccharide metabolism, and sugar acid interconversions. The library comprehensively covers core metabolic nodes from glucose uptake and utilization to energy production and biosynthesis, while also incorporating important upstream and downstream intermediates. It enables accurate representation of intracellular metabolic flux dynamics and is well suited for applications such as metabolic flux analysis, target validation, and mechanistic studies. Furthermore, it provides robust support for multi-omics integration and the development of precision intervention strategies.

Carbohydrate Metabolite Compound Library

0 compounds

Carbohydrate metabolism serves as a central hub for energy supply and biosynthesis in living organisms and plays a critical role in the onset and progression of various diseases. In recent years, studies have shown that tumor cells reprogram their energy metabolism through aerobic glycolysis (the Warburg effect) to support rapid proliferation. Immune cells also rely on specific carbohydrate metabolic pathways to regulate their activation and differentiation states, while disorders such as diabetes and metabolic syndrome arise directly from dysregulation of carbohydrate metabolism. In addition, enzymes and key metabolic nodes involved in carbohydrate metabolism have become important targets for drug discovery, and therapeutic strategies targeting glycolysis, the pentose phosphate pathway, and energy metabolism are continuously advancing the treatment of cancer and metabolic diseases. Therefore, systematic analysis of carbohydrate metabolic networks and their associated metabolites is of great significance for elucidating disease mechanisms and developing novel therapeutic approaches.

The MCE Carbohydrate Metabolism Metabolite Library is constructed based on classical carbohydrate metabolic pathways and contains 0 metabolites. It systematically integrates key metabolic networks, including glycolysis, the pentose phosphate pathway, the tricarboxylic acid (TCA) cycle, monosaccharide metabolism, and sugar acid interconversions. The library comprehensively covers core metabolic nodes from glucose uptake and utilization to energy production and biosynthesis, while also incorporating important upstream and downstream intermediates. It enables accurate representation of intracellular metabolic flux dynamics and is well suited for applications such as metabolic flux analysis, target validation, and mechanistic studies. Furthermore, it provides robust support for multi-omics integration and the development of precision intervention strategies.

HY-L058

Glycolysis Compound Library	1,258 compounds
Glycolysis is a series of metabolic processes by which one molecule of glucose is catabolized to two molecules of pyruvate with a net gain of two ATP. Glycolysis takes place in 10 steps and catalyzed by a series of enzyme, such as hexokinase, Glucose-6-phosphate isomerase, Phosphofructokinase, etc. Glycolysis is used by all cells in the body for energy generation. Most cancer cells exhibit increased glycolysis and use this metabolic pathway for generation of ATP as a main source of their energy supply. This phenomenon is known as the Warburg effect and is considered as one of the most fundamental metabolic alterations during malignant transformation. Because increased aerobic glycolysis is commonly seen in a wide spectrum of human cancers, development of novel glycolytic inhibitors as a new class of anticancer agents is likely to have broad therapeutic applications. MCE provides a unique collection of 1,258 glycolysis compounds that mainly target hexokinase, glucokinase, enolase, pyruvate kinase, PDHK, etc. MCE Glycolysis Compound Library is a useful tool for glucose metabolism research and anti-cancer drug discovery.

Glycolysis Compound Library

1,258 compounds

Glycolysis is a series of metabolic processes by which one molecule of glucose is catabolized to two molecules of pyruvate with a net gain of two ATP. Glycolysis takes place in 10 steps and catalyzed by a series of enzyme, such as hexokinase, Glucose-6-phosphate isomerase, Phosphofructokinase, etc. Glycolysis is used by all cells in the body for energy generation.

Most cancer cells exhibit increased glycolysis and use this metabolic pathway for generation of ATP as a main source of their energy supply. This phenomenon is known as the Warburg effect and is considered as one of the most fundamental metabolic alterations during malignant transformation. Because increased aerobic glycolysis is commonly seen in a wide spectrum of human cancers, development of novel glycolytic inhibitors as a new class of anticancer agents is likely to have broad therapeutic applications.

MCE provides a unique collection of 1,258 glycolysis compounds that mainly target hexokinase, glucokinase, enolase, pyruvate kinase, PDHK, etc. MCE Glycolysis Compound Library is a useful tool for glucose metabolism research and anti-cancer drug discovery.

Cat. No.	Product Name	Type

HY-119976

Boscalid 1 Publications Verification	Biochemical Assay Reagents
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 .

Boscalid

1 Publications Verification

Biochemical Assay Reagents

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 .

HY-119976R

Boscalid (Standard)	Biochemical Assay Reagents
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 .

Boscalid (Standard)

Biochemical Assay Reagents

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 .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N0305

5-Aminolevulinic acid hydrochloride Maximum Cited Publications 20 Publications Verification 5-ALA hydrochloride; δ-Aminolevulinic acid hydrochloride; 5-Amino-4-oxopentanoic acid hydrochloride	Structural Classification Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Disease Research Fields Cancer	Reactive Oxygen Species (ROS)
5-Aminolevulinic acid (5-ALA; δ-Aminolevulinic acid; 5-Amino-4-oxopentanoic acid) hydrochloride is an orally active heme precursor. 5-Aminolevulinic acid hydrochloride promotes aerobic energy metabolism and increases ATP levels by enhancing the activity of cytochrome c oxidase. 5-Aminolevulinic acid hydrochloride enhances LPS-induced proinflammatory cytokine production and gene activation, and restores the phagocytic activity and ROS generation capacity of neutrophils. 5-Aminolevulinic acid hydrochloride selectively accumulates protoporphyrin IX in tumor cells; as a photosensitizer and radiosensitizer, it induces ROS burst upon light or X-ray irradiation to inhibit tumor growth. 5-Aminolevulinic acid hydrochloride can be applied to the research of septic shock, melanoma, and cancer radiotherapy .

HY-N10574

Queuine 1 Publications Verification	Alkaloids Microorganisms Pyrrole Alkaloids Source Classification	Bacterial
Queuine is a selective substrate for tRNA guanine transglycosylase (TGT) and can be incorporated into eukaryotic tRNA. Queuine promotes tRNA modification, affecting mitochondrial function and Warburg metabolic phenotype. If Queuine is deficient, aerobic glycolysis can be enhanced, oxidative phosphorylation can be inhibited, and Warburg metabolism can be promoted, accompanied by increased ammonia and lactate production and increased lactate dehydrogenase activity. Queuine can be used for autoimmune diseases (such as experimental models of multiple sclerosis) and cancer metabolic regulation, and its deficiency is associated with low tRNA modification in tumor cells .

HY-W000450

5-Aminolevulinic acid Maximum Cited Publications 20 Publications Verification 5-ALA; δ-Aminolevulinic acid; 5-Amino-4-oxopentanoic acid	Cardiovascular Disease Structural Classification Classification of Application Fields Amino acids Endogenous metabolite Human Gut Microbiota Metabolites Immune System Disorder Microorganisms Ketones, Aldehydes, Acids Disease markers Disease Research Fields Source Classification Cancer	Reactive Oxygen Species (ROS)
5-Aminolevulinic acid (5-ALA; δ-Aminolevulinic acid; 5-Amino-4-oxopentanoic acid) is an orally active heme precursor. 5-Aminolevulinic acid promotes aerobic energy metabolism and increases ATP levels by enhancing the activity of cytochrome c oxidase. 5-Aminolevulinic acid enhances LPS-induced proinflammatory cytokine production and gene activation, and restores the phagocytic activity and ROS generation capacity of neutrophils. 5-Aminolevulinic acid selectively accumulates protoporphyrin IX in tumor cells; as a photosensitizer and radiosensitizer, it induces ROS burst upon light or X-ray irradiation to inhibit tumor growth. 5-Aminolevulinic acid can be applied to the research of septic shock, melanoma, and cancer radiotherapy .

HY-N10574A

Queuine dihydrochloride 1 Publications Verification	Alkaloids Microorganisms Pyrrole Alkaloids Source Classification	Others
Queuine dihydrochloride is a selective substrate for tRNA guanine transglycosylase (TGT) and can be incorporated into eukaryotic tRNA. Queuine dihydrochloride promotes tRNA modification, affecting mitochondrial function and Warburg metabolic phenotype. If Queuine dihydrochloride is deficient, aerobic glycolysis can be enhanced, oxidative phosphorylation can be inhibited, and Warburg metabolism can be promoted, accompanied by increased ammonia and lactate production and increased lactate dehydrogenase activity. Queuine dihydrochloride can be used for autoimmune diseases (such as experimental models of multiple sclerosis) and cancer metabolic regulation, and its deficiency is associated with low tRNA modification in tumor cells .

Cat. No.	Product Name	Chemical Structure

HY-B0831S

Buprofezin-d6
Buprofezin-d₆ is the deuterium labeled Buprofezin. Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .

Buprofezin-d6

Buprofezin-d₆ is the deuterium labeled Buprofezin. Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .

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 .

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 .

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aerobic metabolism

Inhibitors & Agonists

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