1. Anti-infection PI3K/Akt/mTOR NF-κB Apoptosis MAPK/ERK Pathway Stem Cell/Wnt Immunology/Inflammation
  2. Bacterial mTOR Akt PI3K NF-κB Caspase JNK ERK COX NO Synthase Apoptosis
  3. Licoflavanone

Licoflavanone (3′-Prenylnaringenin) is a flavanone with antioxidant, anti-inflammatory and anticancer activities. Licoflavanone can be isolated from the leaf extract of Glycyrrhiza glabra. Licoflavanone downregulates the mTOR/PI3K/AKT signaling pathway to inhibit the proliferation, migration and invasion of cancer cells, while activates Bax, Bad and multiple caspase enzymes to induce apoptosis. Its anti-inflammatory effect is manifested by reducing the nuclear translocation of NF-κB, decreasing the phosphorylation levels of p38, JNK and ERK1/2, thereby inhibiting the expression of nitric oxide, proinflammatory cytokines, COX-2 and iNOS. Licoflavanone is used in studies on nasopharyngeal carcinoma and related mechanisms.

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

Licoflavanone

Licoflavanone Chemical Structure

CAS No. : 119240-82-3

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Description

Licoflavanone (3′-Prenylnaringenin) is a flavanone with antioxidant, anti-inflammatory and anticancer activities. Licoflavanone can be isolated from the leaf extract of Glycyrrhiza glabra. Licoflavanone downregulates the mTOR/PI3K/AKT signaling pathway to inhibit the proliferation, migration and invasion of cancer cells, while activates Bax, Bad and multiple caspase enzymes to induce apoptosis. Its anti-inflammatory effect is manifested by reducing the nuclear translocation of NF-κB, decreasing the phosphorylation levels of p38, JNK and ERK1/2, thereby inhibiting the expression of nitric oxide, proinflammatory cytokines, COX-2 and iNOS. Licoflavanone is used in studies on nasopharyngeal carcinoma and related mechanisms[1][2].

IC50 & Target

iNOS

 

COX-2

 

In Vitro

Licoflavanone (12.5-100 μM; 24 h) reduces the viability of human nasopharyngeal carcinoma HK1 cells in a concentration-dependent manner[1].
Licoflavanone (12.5-100 μM; 72 h) induces destructive morphological changes and apoptosis in human nasopharyngeal HK1 cancer cells following 72 h of treatment at concentrations of 12.5, 25, and 100 μM[1].
Licoflavanone (12.5-100 μM; 24 h) regulates the expression of apoptosis-related proteins, upregulates pro-apoptotic proteins and downregulates anti-apoptotic proteins in human nasopharyngeal HK1 cancer cells following 24 h of treatment at concentrations of 12.5, 25 and 100 μM[1].
Licoflavanone (12.5-100 μM; 24 h) inhibits the mTOR/PI3K/AKT pathway in human nasopharyngeal carcinoma HK1 cells in a concentration-dependent manner by downregulating the expression of phosphorylated mTOR, PI3K and AKT (treatment concentrations: 12.5, 25 and 100 μM, treatment duration: 24 h)[1].
Licoflavanone (12.5-100 μM; 24 h) inhibits the migration and invasion of human nasopharyngeal HK1 cancer cells in a concentration-dependent manner[1].
Licoflavanone inhibits NO production in LPS-stimulated RAW 264.7 mouse macrophages with an IC50 of 37.68 μM, and suppresses the phosphorylation and activation of p38, JNK and ERK1/2 MAPKs[2].

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

Cell Viability Assay[1]

Cell Line: human nasopharyngeal HK1 carcinoma cells
Concentration: 12.5-100 μM
Incubation Time: 24 h
Result: Reduced cell viability in a concentration-dependent manner, with viability dropping to almost 10% at the highest concentration tested.
Showed statistically significant effects in triplicate experiments.

Apoptosis Analysis[1]

Cell Line: human nasopharyngeal HK1 carcinoma cells
Concentration: 12.5, 25, 100 μM
Incubation Time: 24 h
Result: Induced pro-apoptotic changes including membrane damage, chromatin condensation, nuclear disintegration, formation of apoptotic bodies, and loss of normal cell morphology, while control cells showed normal structure and intact nuclear membranes.

Western Blot Analysis[1]

Cell Line: human nasopharyngeal HK1 carcinoma cells
Concentration: 12.5-100 μM
Incubation Time: 24 h
Result: Significantly up-regulated protein expression of pro-apoptotic caspase-3, caspase-8, caspase-9, cleaved caspase-3, Bax, and Bad.
Markedly down-regulated protein expression of anti-apoptotic Bcl-2, XIAP, and Bcl-2-xL.\nMarkedly and concentration-dependently down-regulated the expression levels of phosphorylated mTOR, PI3K, and AKT.
Maintained almost constant protein expression levels of non-phosphorylated mTOR, PI3K, and AKT.
Showed statistically significant effects in triplicate experiments.

Real Time qPCR[2]

Cell Line: RAW 264.7 murine macrophages
Concentration: IC50 concentration
Incubation Time: 6 h
Result: Significantly decreased mRNA levels of inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6) (p < 0.001 for all targets).
Molecular Weight

340.37

Formula

C20H20O5

CAS No.
SMILES

O=C1C[C@@H](C2=CC=C(O)C(C/C=C(C)\C)=C2)OC3=CC(O)=CC(O)=C13

Structure Classification
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Room temperature in continental US; may vary elsewhere.

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

Purity & Documentation
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Licoflavanone
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