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3-Hydroxypropionic Acid (sodium salt) Sale

(Synonyms: Sodium β-hydroxypropionate) 目录号 : GC42292

A building block in the synthesis of a variety of compounds

3-Hydroxypropionic Acid (sodium salt) Chemical Structure

Cas No.:6487-38-3

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100mg
¥599.00
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250mg
¥1,422.00
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500mg
¥2,707.00
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1g
¥4,797.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

3-Hydroxypropionic acid is a building block in the synthesis of a variety of compounds with industrial applications, including acrylic acid, acrylamide, and 1,3-propanediol. Accumulation of 3-hydroxypropionic acid is also used as a biomarker of defects in propionic acid and branched-chain amino acid catabolism in patients with methylmalonic acidemia or propionic acidemia.

Chemical Properties

Cas No. 6487-38-3 SDF
别名 Sodium β-hydroxypropionate
Canonical SMILES [O-]C(CCO)=O.[Na+]
分子式 C3H5O3•Na 分子量 112.1
溶解度 PBS (pH 7.2): 10 mg/ml 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 8.9206 mL 44.603 mL 89.2061 mL
5 mM 1.7841 mL 8.9206 mL 17.8412 mL
10 mM 0.8921 mL 4.4603 mL 8.9206 mL
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Research Update

Anaplerotic therapy in propionic acidemia

Mol Genet Metab 2017 Sep;122(1-2):51-59.PMID:28712602DOI:PMC5612888

Background: Propionic acidemia is a rare metabolic disorder caused by a deficiency of propionyl- CoA carboxylase, the enzyme converting propionyl-CoA to methylmalonyl-CoA that subsequently enters the citric acid cycle as succinyl-CoA. Patients with propionic acidemia cannot metabolize propionic acid, which combines with oxaloacetate to form methylcitric acid. This, with the defective supply of succinyl-CoA, may lead to a deficiency in citric acid cycle intermediates. Purpose: The objective of this study was to determine whether supplements with glutamine (400mg/kg per day), citrate (7.5mEq/kg per day), or ornithine α-ketoglutarate (400mg/kg per day) (anaplerotic agents that could fill up the citric acid cycle) would affect plasma levels of glutamine and ammonia, the urinary excretion of Krebs cycle intermediates, and the clinical outcome in 3 patients with propionic acidemia. Methods: Each supplement was administered daily for four weeks with a two week washout period between supplements. The supplement that produced the most favorable changes was supplemented for 30 weeks following the initial study period and then for a 2 year extension. Results: The urinary excretion of the Krebs cycle intermediates, α-ketoglutarate, succinate, and fumarate increased significantly compared to baseline during citrate supplementation, but not with the other two supplements. For this reason, citrate supplements were continued in the second part of the study. The urinary excretion of methylcitric acid and 3-Hydroxypropionic Acid did not change with any intervention. No significant changes in ammonia or glutamine levels were observed with any supplement. However, supplementation with any anaplerotic agents normalized the physiological buffering of ammonia by glutamate, with plasma glutamate and alanine levels significantly increasing, rather than decreasing with increasing ammonia levels. No significant side effects were observed with any therapy and safety labs (blood counts, chemistry and thyroid profile) remained unchanged. Motor and cognitive development was severely delayed before the trial and did not change significantly with therapy. Hospitalizations per year did not change during the trial period, but decreased significantly (p<0.05) in the 2years following the study (when citrate was continued) compared to the 2years before and during the study. Conclusions: These results indicate that citrate entered the Krebs cycle providing successful anaplerotic therapy by increasing levels of the downstream intermediates of the Krebs cycle: α-ketoglutarate, succinate and fumarate. Citrate supplements were safe and might have contributed to reduce hospitalizations in patients with propionic acidemia.