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1949720-50-6

" in MedChemExpress (MCE) Product Catalog:

標的別:	Apoptosis (1) Endogenous Metabolite (4)
研究分野別:	Endocrinology (1) Inflammation/Immunology (1) Metabolic Disease (3) Neurological Disease (1)

阻害剤およびアゴニスト

生化学アッセイ試薬

天然物

製品番号	製品名	Target	研究分野	構造式

HY-F0001A

NADH disodium hydrate Disodium NADH hydrate	Endogenous Metabolite	Metabolic Disease
NADH disodium salt (Disodium NADH) hydrate is an orally active reduced coenzyme. NADH disodium salt hydrate is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. NADH disodium salt hydrate plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

HY-F0001

NADH disodium salt 5+ Cited Publications Disodium NADH	Endogenous Metabolite	Metabolic Disease
NADH disodium salt (Disodium NADH) is an orally active reduced coenzyme. NADH disodium salt is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. NADH disodium salt plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

HY-113355

NADH	Endogenous Metabolite Apoptosis	Neurological Disease Inflammation/Immunology Endocrinology
NADH is an orally active dehydrogenase coenzyme that acts as a crucial electron carrier in cellular respiration and participates in ATP production. NADH promotes metabolism, supports brain function, and counteracts oxidative stress by transferring electrons to the electron transport chain. As a signaling molecule, NADH regulates multiple biological processes, including anti-apoptosis, synaptic plasticity, gene expression, and calcium homeostasis. Redox imbalance of NADH/NAD⁺ is one of the key pathological mechanisms of various diseases, such as diabetic nephropathy, neurodegenerative diseases, and ischemia-reperfusion injury.

HY-W250154

β-Nicotinamide adenine dinucleotide reduced dipotassium	Endogenous Metabolite	Metabolic Disease
β-Nicotinamide adenine dinucleotide reduced dipotassium is an orally active reduced coenzyme. β-Nicotinamide adenine dinucleotide reduced dipotassium is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. β-Nicotinamide adenine dinucleotide reduced dipotassium plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

製品番号	製品名	Type

HY-W250154

β-Nicotinamide adenine dinucleotide reduced dipotassium	生化学アッセイ試薬
β-Nicotinamide adenine dinucleotide reduced dipotassium is an orally active reduced coenzyme. β-Nicotinamide adenine dinucleotide reduced dipotassium is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. β-Nicotinamide adenine dinucleotide reduced dipotassium plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

β-Nicotinamide adenine dinucleotide reduced dipotassium

生化学アッセイ試薬

β-Nicotinamide adenine dinucleotide reduced dipotassium is an orally active reduced coenzyme. β-Nicotinamide adenine dinucleotide reduced dipotassium is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. β-Nicotinamide adenine dinucleotide reduced dipotassium plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

製品番号	製品名	Category	Target	構造式

HY-F0001

NADH disodium salt 5+ Cited Publications Disodium NADH	天然物 Classification of Application Fields Other Diseases Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
NADH disodium salt (Disodium NADH) is an orally active reduced coenzyme. NADH disodium salt is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. NADH disodium salt plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

HY-113355

NADH	Human Gut Microbiota Metabolites Microorganisms Endogenous metabolite Source Classification	Endogenous Metabolite Apoptosis
NADH is an orally active dehydrogenase coenzyme that acts as a crucial electron carrier in cellular respiration and participates in ATP production. NADH promotes metabolism, supports brain function, and counteracts oxidative stress by transferring electrons to the electron transport chain. As a signaling molecule, NADH regulates multiple biological processes, including anti-apoptosis, synaptic plasticity, gene expression, and calcium homeostasis. Redox imbalance of NADH/NAD⁺ is one of the key pathological mechanisms of various diseases, such as diabetic nephropathy, neurodegenerative diseases, and ischemia-reperfusion injury.

HY-W250154

β-Nicotinamide adenine dinucleotide reduced dipotassium	天然物 Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
β-Nicotinamide adenine dinucleotide reduced dipotassium is an orally active reduced coenzyme. β-Nicotinamide adenine dinucleotide reduced dipotassium is a donor of ADP-ribose units in ADP-ribosylaton reactions and a precursor of cyclic ADP-ribose. β-Nicotinamide adenine dinucleotide reduced dipotassium plays a role as a regenerative electron donor in cellular energy metabolism, including glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle .

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BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.

BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

MedchemExpress Validation 03

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred

MedchemExpress Validation 04

MedchemExpress Validation

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