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heme precursor

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By Targets:	Apoptosis (3) Autophagy (3) Endogenous Metabolite (6) Isotope-Labeled Compounds (1) Mitophagy (3) Reactive Oxygen Species (ROS) (2)
By Research Areas:	Cancer (3) Cardiovascular Disease (1) Inflammation/Immunology (1) Metabolic Disease (7) Neurological Disease (2)

8

Inhibitors & Agonists

4

Natural
Products

3

Isotope-Labeled Compounds

Targets Recommended: Heme Oxygenase (HO)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

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 .

Succinyl-Coenzyme A sodium 3 Publications Verification Succinyl-CoA sodium	Endogenous Metabolite	Neurological Disease Metabolic Disease
Succinyl CoA (Succinyl-coenzyme A) sodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA sodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA sodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA sodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .

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 .

Succinyl CoA Succinyl-coenzyme A; S-(Hydrogen succinyl)coenzyme A	Endogenous Metabolite	Metabolic Disease
Succinyl CoA (Succinyl-coenzyme A) is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .

5-Aminolevulinic acid-15N hydrochloride 5-ALA-15N hydrochloride; δ-Aminolevulinic acid-15N hydrochloride; 5-Amino-4-oxopentanoic acid-15N hydrochloride	Isotope-Labeled Compounds Autophagy Mitophagy Endogenous Metabolite Apoptosis	Metabolic Disease Cancer
5-Aminolevulinic acid- ¹⁵N (hydrochloride) is the ¹⁵N-labeled 5-Aminolevulinic acid (hydrochloride). 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles.

5-Aminolevulinic acid-13C-1 hydrochloride 5-ALA-13C-1 hydrochloride; δ-Aminolevulinic acid-13C-1 hydrochloride; 5-Amino-4-oxopentanoic acid-13C-1 hydrochloride	Apoptosis Autophagy Mitophagy Endogenous Metabolite	Metabolic Disease
5-Aminolevulinic acid- ¹³C-1 (5-ALA- ¹³C-1) hydrochloride is the ¹³C labeled 5-Aminolevulinic acid hydrochloride . 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles .

5-Aminolevulinic acid-13C hydrochloride 5-ALA-13C hydrochloride; δ-Aminolevulinic acid-13C hydrochloride; 5-Amino-4-oxopentanoic acid-13C hydrochloride	Apoptosis Autophagy Mitophagy Endogenous Metabolite	Metabolic Disease
5-Aminolevulinic acid- ¹³C (hydrochloride) is the ¹³C labeled 5-Aminolevulinic acid hydrochloride . 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles .

Succinyl CoA disodium Succinyl-coenzyme A disodium; S-(Hydrogen succinyl)coenzyme A disodium	Endogenous Metabolite	Metabolic Disease
Succinyl CoA (Succinyl-coenzyme A) disodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA disodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA disodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA disodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl-Coenzyme A sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .

Cat. No.	Product Name	Category	Target	Chemical Structure

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 .

Succinyl-Coenzyme A sodium 3 Publications Verification Succinyl-CoA sodium	Structural Classification Natural Products Neurological Disease Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
Succinyl CoA (Succinyl-coenzyme A) sodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA sodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA sodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA sodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .

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 .

Succinyl CoA Succinyl-coenzyme A; S-(Hydrogen succinyl)coenzyme A	Human Gut Microbiota Metabolites Microorganisms Endogenous metabolite Source Classification	Endogenous Metabolite
Succinyl CoA (Succinyl-coenzyme A) is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .

Cat. No.	Product Name	Chemical Structure

5-Aminolevulinic acid-15N hydrochloride
5-Aminolevulinic acid- ¹⁵N (hydrochloride) is the ¹⁵N-labeled 5-Aminolevulinic acid (hydrochloride). 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles.

5-Aminolevulinic acid-13C-1 hydrochloride
5-Aminolevulinic acid- ¹³C-1 (5-ALA- ¹³C-1) hydrochloride is the ¹³C labeled 5-Aminolevulinic acid hydrochloride . 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles .

5-Aminolevulinic acid-13C hydrochloride
5-Aminolevulinic acid- ¹³C (hydrochloride) is the ¹³C labeled 5-Aminolevulinic acid hydrochloride . 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) is an intermediate in heme biosynthesis in the body and the universal precursor of tetrapyrroles .

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