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Results for "

glutamine+metabolism

" in MedChemExpress (MCE) Product Catalog:

標的別:	Akt (3) Aminotransferases (Transaminases) (1) AMPK (3) Apoptosis (8) Autophagy (3) Bacterial (1) Cholinesterase (ChE) (1) COX (3) Glutaminase (5) Interleukin Related (3) Lipase (1) MMP (3) mTOR (3) NF-κB (3) p38 MAPK (3) PI3K (3) PKC (3) Reactive Oxygen Species (ROS) (6) Reference Standards (1) STAT (3) Xanthine Oxidase (1)
研究分野別:	Cancer (10) Infection (1) Inflammation/Immunology (4) Metabolic Disease (1) Neurological Disease (3)

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スクリーニングライブラリ

天然物

製品番号	製品名	Target	研究分野	構造式

HY-N0327

Lobetyolin 4 Publications Verification	Apoptosis Xanthine Oxidase	Metabolic Disease
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.

HY-N0735

Phellodendrine chloride 2 Publications Verification	Autophagy Apoptosis AMPK mTOR STAT Interleukin Related PKC p38 MAPK NF-κB COX Reactive Oxygen Species (ROS) PI3K Akt MMP	Neurological Disease Inflammation/Immunology Cancer
Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and *glutamine* metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .

HY-N0427

Phellodendrine	Akt NF-κB AMPK mTOR PKC STAT Interleukin Related p38 MAPK COX Reactive Oxygen Species (ROS) Apoptosis Autophagy PI3K MMP	Neurological Disease Inflammation/Immunology Cancer
Phellodendrine is an orally active plant alkaloid. Phellodendrine inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and *glutamine* metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .

HY-N6237

Aspulvinone O	Aminotransferases (Transaminases) Apoptosis	Cancer
Aspulvinone O is a selective inhibitor of glutamate oxaloacetate aminotransferase GOT1. Aspulvinone O inhibits glutamine metabolism and reduces NADPH production, thereby inducing oxidative stress and apoptosis in pancreatic ductal adenocarcinoma (PDAC) cells. Aspulvinone O inhibits PDAC cell proliferation in vitro and tumor growth in xenograft models .

HY-152207

LWG-301	Glutaminase Apoptosis	Cancer
LWG-301 is an allosteric inhibitor of Glutaminase 1 (GLS1) with an IC₅₀ value of 7 nM. LWG-301 significantly block glutamine metabolism, increases intracellular ROS, thus induces apoptosis. LWG-301 exhibits moderate antitumor effects in HCT116 xenograft model .

HY-146617

GLS1 Inhibitor-4	Glutaminase Apoptosis	Cancer
GLS1 Inhibitor-4 (compound 41e) is a potent GLS1 inhibitor with an IC₅₀ of 11.86 nM. GLS1 Inhibitor-4 shows antiproliferative activity, good metabolic stability, robust GLS1 binding affinity. GLS1 Inhibitor-4 blocks the glutamine metabolism and induce the production of ROS. GLS1 Inhibitor-4 induces apoptosis and shows antitumor activity .

HY-N0735R

Phellodendrine chloride (Standard)	Reference Standards Autophagy mTOR AMPK Apoptosis STAT Interleukin Related PKC p38 MAPK NF-κB COX Reactive Oxygen Species (ROS) PI3K Akt MMP	Neurological Disease Inflammation/Immunology Cancer
Phellodendrine chloride (Standard) is the analytical standard of Phellodendrine chloride (HY-N0735). Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and *glutamine* metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway.

HY-149602

Glutaminase C-IN-2	Glutaminase Reactive Oxygen Species (ROS)	Cancer
Glutaminase C-IN-2 (compound 11) is glutaminase C (GAC) allosteric inhibitor with an IC₅₀ of 10.64 nM. Glutaminase C-IN-2 regulates the cellular metabolite, thereby increasing reactive oxygen species (ROS) by blocking glutamine metabolism. Glutaminase C-IN-2 has anticancer effects .

HY-158378

Trivalent hydroxyarsinothricn R-AST-OH	Glutaminase	Cancer
Trivalent hydroxyarsinothricn (R-AST-OH) is a covalent and irreversible kidney-type glutaminase (KGA) inhibitor. Trivalent hydroxyarsinothricn binds to the glutamine binding site and forms a covalent bond with an active site cysteine residue. Trivalent hydroxyarsinothricn selectively kills triple-negative breast cancer (TNBC) cells and is not cytotoxic to the control cell line. KGA is the enzyme that controls glutamine metabolism and is correlated with tumor malignancy .

HY-180241

Glutaminase C-IN-3	Glutaminase Reactive Oxygen Species (ROS)	Cancer
Glutaminase C-IN-3 is a potent allosteric inhibitor of Glutaminase C (GAC) with an EC₅₀ of 116 nM. Glutaminase C-IN-3 regulates cellular metabolites and increases reactive oxygen species (ROS) production by blocking glutamine metabolism. Glutaminase C-IN-3 exhibits strong antitumor activity in an A549 xenograft mouse model. Glutaminase C-IN-3 can be used for the research of non-small cell lung cancer (NSCLC) .

HY-N14093

Aspulvinone H	Cholinesterase (ChE) Lipase Reactive Oxygen Species (ROS) Apoptosis Bacterial	Infection Inflammation/Immunology Cancer
Aspulvinone H is an orally active inhibitor of AChE, pancreatic lipase, glutamic-oxaloacetic transaminase 1, and α-glucosidase, with IC₅₀ values of 25.95 μM, 47.06 μM, 5.91/6.91 μM, and 4.6 μM, respectively. It has a K_a of 2.14 μM against GOT1 and a K_i of 6.58 μM against α-glucosidase. Aspulvinone H inhibits cancer cell proliferation, interferes with glutamine metabolism, elevates ROS levels, and induces cell apoptosis and S-phase arrest. Aspulvinone H exhibits antibacterial activity against Staphylococcus aureus. Aspulvinone H inhibits the growth of pancreatic ductal adenocarcinoma xenografts. Aspulvinone H reduces postprandial blood glucose in mice. Aspulvinone H can be used in research related to pancreatic ductal adenocarcinoma, diabetes, and Staphylococcus aureus infection .

製品番号	製品名

HY-L064

Glutamine Metabolism Compound Library	1,690 compounds
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 1,690 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.

Glutamine Metabolism Compound Library

1,690 compounds

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 1,690 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.

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-L133

Cuproptosis Compound Library	403 compounds
Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis". The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis. Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism. Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis. MCE supplies a unique collection of 403 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.

Cuproptosis Compound Library

403 compounds

Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis".

The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis.

Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism.

Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis.

MCE supplies a unique collection of 403 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.

製品番号	製品名	Category	Target	構造式

HY-N0327

Lobetyolin 4 Publications Verification	天然物 Classification of Application Fields Campanulaceae Codonopsis pilosula (Franch.) Nannf. Metabolic Disease Plants Disease Research Fields Source Classification	Apoptosis Xanthine Oxidase
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.

HY-N0735

Phellodendrine chloride 2 Publications Verification	Alkaloids Phellodendron amurense Rupr. Classification of Application Fields Rutaceae Phenols Polyphenols Plants Isoquinoline Alkaloids Disease Research Fields Source Classification Cancer	Autophagy Apoptosis AMPK mTOR STAT Interleukin Related PKC p38 MAPK NF-κB COX Reactive Oxygen Species (ROS) PI3K Akt MMP
Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and *glutamine* metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .

HY-N0427

Phellodendrine	Alkaloids Phellodendron amurense Rupr. Classification of Application Fields Rutaceae Phenols Polyphenols Quinoline Alkaloids Plants Inflammation/Immunology Disease Research Fields Source Classification	Akt NF-κB AMPK mTOR PKC STAT Interleukin Related p38 MAPK COX Reactive Oxygen Species (ROS) Apoptosis Autophagy PI3K MMP
Phellodendrine is an orally active plant alkaloid. Phellodendrine inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and *glutamine* metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .

HY-N6237

Aspulvinone O	Infection Structural Classification Microorganisms Classification of Application Fields Phenols Polyphenols Disease Research Fields Source Classification	Aminotransferases (Transaminases) Apoptosis
Aspulvinone O is a selective inhibitor of glutamate oxaloacetate aminotransferase GOT1. Aspulvinone O inhibits glutamine metabolism and reduces NADPH production, thereby inducing oxidative stress and apoptosis in pancreatic ductal adenocarcinoma (PDAC) cells. Aspulvinone O inhibits PDAC cell proliferation in vitro and tumor growth in xenograft models .

HY-N0735R

Phellodendrine chloride (Standard)	Alkaloids Structural Classification Phellodendron amurense Rupr. Rutaceae Phenols Polyphenols Plants Isoquinoline Alkaloids Source Classification	Reference Standards Autophagy mTOR AMPK Apoptosis STAT Interleukin Related PKC p38 MAPK NF-κB COX Reactive Oxygen Species (ROS) PI3K Akt MMP
Phellodendrine chloride (Standard) is the analytical standard of Phellodendrine chloride (HY-N0735). Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and *glutamine* metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway.

HY-N14093

Aspulvinone H	Structural Classification Microorganisms Phenols Polyphenols Source Classification	Cholinesterase (ChE) Lipase Reactive Oxygen Species (ROS) Apoptosis Bacterial
Aspulvinone H is an orally active inhibitor of AChE, pancreatic lipase, glutamic-oxaloacetic transaminase 1, and α-glucosidase, with IC₅₀ values of 25.95 μM, 47.06 μM, 5.91/6.91 μM, and 4.6 μM, respectively. It has a K_a of 2.14 μM against GOT1 and a K_i of 6.58 μM against α-glucosidase. Aspulvinone H inhibits cancer cell proliferation, interferes with glutamine metabolism, elevates ROS levels, and induces cell apoptosis and S-phase arrest. Aspulvinone H exhibits antibacterial activity against Staphylococcus aureus. Aspulvinone H inhibits the growth of pancreatic ductal adenocarcinoma xenografts. Aspulvinone H reduces postprandial blood glucose in mice. Aspulvinone H can be used in research related to pancreatic ductal adenocarcinoma, diabetes, and Staphylococcus aureus infection .

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