1. Metabolic Enzyme/Protease
    Cell Cycle/DNA Damage
    Immunology/Inflammation
    NF-κB
    Apoptosis
    Anti-infection
  2. Endogenous Metabolite
    CDK
    Reactive Oxygen Species
    Apoptosis
    Enterovirus
    Bacterial
  3. Lacto-N-fucopentaose I

Lacto-N-fucopentaose I (Synonyms: LNFP I)

Cat. No.: HY-W019806
Handling Instructions

Lacto-N-fucopentaose I (LNFPI) is a human milk oligosaccharide (HMO), possessing antiviral and antibacterial activity. Lacto-N-fucopentaose I can reduce capsid protein VP1 to block virus adsorption, promote CDK2 and reduce cyclin E to recover cell cycle S phase block. Lacto-N-fucopentaose I inhibits ROS production and apoptosis in virus-infected cells. Lacto-N-fucopentaose I can also regulate intestinal microbiota to affect immune system development.

For research use only. We do not sell to patients.

Lacto-N-fucopentaose I Chemical Structure

Lacto-N-fucopentaose I Chemical Structure

CAS No. : 7578-25-8

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Description

Lacto-N-fucopentaose I (LNFPI) is a human milk oligosaccharide (HMO), possessing antiviral and antibacterial activity. Lacto-N-fucopentaose I can reduce capsid protein VP1 to block virus adsorption, promote CDK2 and reduce cyclin E to recover cell cycle S phase block. Lacto-N-fucopentaose I inhibits ROS production and apoptosis in virus-infected cells. Lacto-N-fucopentaose I can also regulate intestinal microbiota to affect immune system development[1].

IC50 & Target

Human Endogenous Metabolite

 

CDK2/cyclinE

 

In Vitro

Lacto-N-fucopentaose I (25-3200 μg/mL;48 h) exhibits certain cytotoxicity at 3200 μg/mL but no toxic reaction below 1600 μg/mL[1].
Lacto-N-fucopentaose I (25-1600 μg/mL; 14-18 h) can protect EV71-infected RD cells from death[1].
Lacto-N-fucopentaose I (100-400 μg/mL; 16 h) decreases markedly mRNA levels of VP1 and ROS production in EV71-infected RD cells at 400 μg/mL; leads to the recovery of EV71-induced S phase arrest in RD cells[1].
Lacto-N-fucopentaose I (100 and 200 μg/mL; 3 days) inhibits cell apoptosis in Caenorhabditis elegans; significantly decreases the levels of Egl-1, Ced-3 and Ced-4[1].
Lacto-N-fucopentaose I can reduce the abundance of Sphingobacterium, Stenotrophomonas and Achromobacter; can increase the abundance of Micromonospora, Vibrio, Acidibacter, Gaiella, Devosia, Steroidobacter, Variibacter, Dactylosporangium, RB41, Pir4_lineage, Pirellula, Haliangium, Roseiflexus, Pedomicrobium, and Bradyrhizobium.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

Cell Line: RD cells
Concentration: 25, 50, 100, 200, 400, 800, 1600 and 3200 μg/mL
Incubation Time: 48 h
Result: Exhibited certain cytotoxicity at 3200 μg/mL but no toxic reaction below 1600 μg/mL.

RT-PCR[1]

Cell Line: RD cells (infected with EV71)
Concentration: 100, 200 and 400 μg/mL
Incubation Time: 16 h
Result: Decreased markedly mRNA levels of VP1 only at 400 μg/mL.

Apoptosis Analysis[1]

Cell Line: RD cells (infected with EV71)
Concentration: 100, 200 and 400 μg/mL
Incubation Time: 16 h
Result: Decreased the rate of cells in early apoptosis to 10.9% ± 1.26% at 400 μg/mL, while the untreated EV71 group was 27.7% ± 2.13%.
Significantly inhibited the activity of caspase-3, caspase-8 and caspase-9.
Recovered the decreased mRNA expression of PAPR, NF-κB and Bcl-2 and properly regulated Bad and Fas into their normal levels.

Cell Cycle Analysis[1]

Cell Line: RD cells (infected with EV71)
Concentration: 100, 200 and 400 μg/mL
Incubation Time: 12 h
Result: Rescued EV71-induced S phase arrest, which promoted the transition of the G1 phase to the S phase.
Molecular Weight

853.77

Formula

C32H55NO25

CAS No.
SMILES
Structure Classification
Source

human milk

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Lacto-N-fucopentaose I
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