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D-Pantothenic Acid (sodium salt) Sale

(Synonyms: D-泛酸钠; Sodium pantothenate; Vitamin B5 sodium) 目录号 : GC43566

A precursor in the biosynthesis of coenzyme A

D-Pantothenic Acid (sodium salt) Chemical Structure

Cas No.:867-81-2

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25g
¥741.00
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50g
¥1,404.00
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100g
¥2,704.00
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250g
¥5,044.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

Pantothenic acid (vitamin B5) is a precursor in the biosynthesis of coenzyme A , which is an essential cofactor functioning as an acyl group carrier and carbonyl-activating group for the citric acid cycle and fatty acid metabolism. Two enantiomers of pantothenic acid exist, D- or L-form. D-Pantothenic acid (sodium salt) is a sodium salt form of the biologically active enantiomer of vitamin B5 and is used in the synthesis of coenzyme A. The L-form of pantothenic acid is biologically inactive and has been shown to act as an antagonist of D-pantothenic acid.

Chemical Properties

Cas No. 867-81-2 SDF
别名 D-泛酸钠; Sodium pantothenate; Vitamin B5 sodium
Canonical SMILES OC(CCNC([C@H](O)C(C)(C)C[O-])=O)=O.[Na+]
分子式 C9H16NO5•Na 分子量 241.2
溶解度 PBS (pH 7.2): 10 mg/ml 储存条件 Store at 2-8°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 4.1459 mL 20.7297 mL 41.4594 mL
5 mM 0.8292 mL 4.1459 mL 8.2919 mL
10 mM 0.4146 mL 2.073 mL 4.1459 mL
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Research Update

Simultaneous determination of some water-soluble vitamins and preservatives in multivitamin syrup by validated stability-indicating high-performance liquid chromatography method

J Chromatogr A 2008 Aug 22;1202(2):155-62.PMID:18644604DOI:10.1016/j.chroma.2008.06.039.

HPLC stability-indicating method has been developed for the simultaneous determination of some water-soluble vitamins (ascorbic acid, thiamine hydrochloride, riboflavin-5'-phosphate sodium, pyridoxine hydrochloride, nicotinamide, D(+)-panthenol) and two preservatives (methylparaben and sodium benzoate) in multivitamin syrup preparation. Water-soluble vitamins, preservatives and their degradants were separated on Zorbax SB-Aq (C(18)) (250 mm x 4.6 mm, 5 microm) column at an ambient temperature. Combined isocratic and gradient elution was performed with a mobile phase consisting of 0.0125 M hexane-1-sulfonic acid sodium salt in 0.1% (m/v) o-phosphoric acid, pH 2.4-2.5 (solvent A) and acetonitrile (solvent B) at the flow-rate 1 ml min(-1). Starting with solvent A an isocratic elution was performed for 15 min, then the composition was changed to 85% of A and 15% of B during the next 20 min and it was constant for 5 min, then the composition was changed to 70% of A and 30% of B during next 15 min and it was constant for 5 min and finally was changed to 100% of A as at the beginning of the elution. Detection was performed with diode array detector at 210, 230 and 254 nm. Multivitamin syrup preparation was subjected to stress testing (forced degradation) in order to demonstrate that degradants from the vitamins, preservatives and/or product excipients do not interfere with the quantification of vitamins and preservatives. Typical validation characteristics: selectivity, accuracy, precision, linearity, range, limit of quantification and limit of detection were evaluated for vitamins and preservatives.

[Proteinization and biotransformation of pantothenic acid in the liver during the activation of lipogenesis]

Vopr Pitan 1986 Nov-Dec;(6):50-4.PMID:3825021doi

White female rats received a balanced synthetic ration (control) or a ration devoid of pantothenic acid (PAA) during 3 weeks. After 36-hour fasting adaptive hyperlipogenesis was induced by feeding the animals with a high-carbohydrate ration, then [114-C]-PAA (sodium salt, 182 nmol/kg) was administered with intervals of 3, 6, 24 hours up to 1 hour before decapitation. Radioactivity of the rats' boiled liver extracts depended on the hyperlipogenesis stage, its level rose progressively, in the control and reached the maximum in PAA-deficient animals by hour 6 after the feeding resumption. The PAA-deficient animals possessed a high PAA-accumulating capacity of the liver and cytosole of the liver including non-covalent radionuclide binding by protein complexes. CoA-synthesizing capacity of the liver in the control animals, evaluated by the biotransformation of the labeled vitamin with CoA precursors of CoA, was intensified with the lipogenesis activation; in vitamin-deficiency CoA biosynthesis was accelerated more than two-fold as compared to the control at the initial and extended periods of hyperlipogenesis (3.6 h). The differences in proteinization and biotransformation of PAA in the liver of control and PAA-deficient animals disappeared by 25 h of adaptive hyperlipogenesis.