N-Acetyl-D-mannosamine

N-Acetyl-D-mannosamine (ManNAc) is an oral active sialic acid precursor that can prevent hypertension by increasing sialylation of IgG, making it a promising candidate for cardiovascular disease research. Additionally, N-Acetyl-D-mannosamine can activate hypocretin (HCRT) gene expression in orexin neurons and improve neurodegeneration caused by aging, offering potential avenues for research in neurological disorders[1][2][3][4][5].

Product Specifications

CAS Number

[3615-17-6]

Product Name Alternative

N-Acetylmannosamine; ManNAc

UNSPSC

12352211

Hazard Statement

H302, H315, H319, H335

Target

Endogenous Metabolite

Type

Reference compound

Related Pathways

Metabolic Enzyme/Protease

Applications

Neuroscience-Neuromodulation

Field of Research

Neurological Disease; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/n-acetyl-d-mannosamine.html

Purity

99.99

Solubility

H2O : 116.67 mg/mL (ultrasonic)

Smiles

OC[C@@H](O)[C@@H](O)[C@H](O)[C@@H](C=O)NC(C)=O

Molecular Formula

C8H15NO6

Molecular Weight

221.21

Precautions

H302, H315, H319, H335

References & Citations

[1]Revilla-Nuin B, et al. Transport of N-acetyl-D-mannosamine and N-acetyl-D-glucosamine in Escherichia coli K1: effect on capsular polysialic acid production. FEBS Lett. 2002 Jan 30;511 (1-3) :97-101.|[2]Hayakawa K, et al. Reactivation of hyperglycemia-induced hypocretin (HCRT) gene silencing by N-acetyl-d-mannosamine in the orexin neurons derived from human iPS cells. Epigenetics. 2017 Sep;12 (9) :764-778.|[3]Peng J, et al. Supplementation With the Sialic Acid Precursor N-Acetyl-D-Mannosamine Breaks the Link Between Obesity and Hypertension. Circulation. 2019 Dec 10;140 (24) :2005-2018.|[4]Niethamer TK, et al. Oral monosaccharide therapies to reverse renal and muscle hyposialylation in a mouse model of GNE myopathy. Mol Genet Metab. 2012 Dec;107 (4) :748-55.|[5]Taniguchi S, et al. Chronic administration of N-acetyl-D-mannosamine improves age-associated impairment of long-term potentiation in the senescence-accelerated mouse. Neurosci Lett. 2015 Jun 26;598:41-6.