δ-aminolevulinic acid

5-Aminolevulinic acid is an intermediate in heme synthesis which is the first compound in the porphyrin synthesis pathway.It is a photosensitizing agent, an antineoplastic agent and a prodrug.It can also be used (in the form of the hydrochloride salt)in combination with blue light illumination for the treatment of minimally to moderately thick actinic keratosis of the face or scalp.

5-Aminolevulinic acid hydrochloride (5-ALA) is an intermediate in heme biosynthesis and a universal precursor of tetrapyrroles.

Methyl Aminolevulinate Hydrochloride (5-Aminolevulinic acid methyl ester) is commonly used in photosentizer reagents for photodynamic therapy to treat conditions such as Acne vulgaris and hypertrophic scarring.

Hexaminolevulinate hydrochloride (P-1206) has approved for cystoscopic detection of papillary bladder cancer and it also is a fluorescent agent.

5-Aminolevulinic acid-d2 (hydrochloride) is the deuterated form of 5-Aminolevulinic acid (hydrochloride). 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) serves as an intermediate in the biosynthesis of heme in the body and acts as a precursor to tetrapyrroles.

5-Aminolevulinic acid-13C-1 (5-ALA-13C-1) hydrochloride is the 13C-labeled form of 5-Aminolevulinic acid hydrochloride. 5-Aminolevulinic acid hydrochloride (5-ALA hydrochloride) serves as an intermediate in the biosynthesis of heme within the body and acts as a precursor to tetrapyrroles.

Hemin (Hemin chloride) is a chlorinated iron-containing porphyrin, a heme oxygenase (HO)-1 inducer. Hemin has therapeutic activity in porphyrias by reducing heme deficiency in patients, thereby inhibiting δ-aminolevulinic acid synthetase activity through biochemical feedback.

Heme arginine (or heme arginine) is a compound of heme and arginine used to treat acute porphyria by reducing the excessive production of δ-aminolevulinic acid, which causes acute symptoms during the onset of acute porphyria.

Givosiran (ALN-AS1) is a small interfering RNA compound that selectively targets hepatic aminolevulinate synthase 1 (ALAS1) mRNA, leading to efficient downregulation of ALAS1 expression and consequent inhibition of neurotoxic δ-aminolevulinic acid and porphobilinogen accumulation. Givosiran provides a mechanism-driven research tool with significant relevance for studying metabolic dysregulation and therapeutic intervention strategies in acute intermittent porphyria.

Thioacetamide-S-oxide, a metabolite of Thiocetamide, functions as a δ-aminolevulinic acid (ALA) synthetase inhibitor [1].

4,6-Dioxoheptanoic acid (Standard) is an endogenous metabolite, a metabolic by-product of tyrosine catabolism, that inhibits α-aminolevulinic acid (ALA) dehydratase in the hemoglobin biosynthesis pathway; it is a specific marker for Type I Tyrosinemia and can be used in the diagnosis of this disease. 4,6-Dioxoheptanoic acid (Standard) can be used for quantitative analysis and study of metabolic pathways.

Hemin (Standard) is the standard substance of Hemin, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Hemin (Hemin chloride) is a chlorinated iron-containing porphyrin, a heme oxygenase (HO)-1 inducer. Hemin has therapeutic activity in porphyrias by reducing heme deficiency in patients, thereby inhibiting δ-aminolevulinic acid synthetase activity through biochemical feedback.