Limocitrin
Based on 1 Customer Validation
Limocitrin is a flavonol glycoside. Limocitrin inhibits AKT phosphorylation and JNK phosphorylation, upregulates p38 phosphorylation, and inhibits ERK1/2 phosphorylation, thereby blocking MAPK signaling. Limocitrin induces Apoptosis through the mitochondrial pathway, death receptor-mediated signaling, Caspase activation, and G2/M cell cycle arrest. Limocitrin possesses anti-inflammatory and anticancer properties. Limocitrin can be used for research on oral squamous cell carcinoma and chronic myeloid leukemia.
For research use only. We do not sell to patients.
- Purity : 99.58%
- CAS No.: 489-33-8
- Formula: C17H14O8
- Molecular Weight:346.29
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Storage:
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
IC50 & Target
[1]|
ERK1 |
ERK2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| Monocyte | IC50 |
67 μM
Compound: Limocitrin
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Inhibition of TNFalpha expression in LPS-stimulated human monocytes treated 30 mins before LPS challenge measured after 14 hrs by ELISA
Inhibition of TNFalpha expression in LPS-stimulated human monocytes treated 30 mins before LPS challenge measured after 14 hrs by ELISA
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[PMID: 10096854] |
In Vitro
Limocitrin (0-40 µM; 24-72 h) significantly inhibits the viability of SCC-9 and SCC-47 oral cancer cells in a concentration- and time-dependent manner, with SCC-9 cells exhibiting higher sensitivity[1].
Limocitrin (0-40 µM; 24 h) exerts a strong antiproliferative effect on SCC-9 and SCC-47 oral cancer cells by reducing colony formation[1].
Limocitrin (5-20 μM; 72 h) enhances the cytotoxicity of KHYG-1 cells against K562 cells[2].
Limocitrin (24 h) induces apoptosis in oral cancer cells through the mitochondrial pathway, manifested by a decrease in mitochondrial membrane potential[1].
Limocitrin (0-40 µM; 24 h) induces apoptosis in SCC-9 and SCC-47 oral cancer cells by modulating the expression of Bcl-2 family proteins and death receptor-related proteins[1].
Limocitrin (0-40 µM; 24 h) induces G2/M phase arrest in SCC-9 and SCC-47 oral cancer cells by downregulating cyclin E1, E2, CDK2, CDK4, and CDK6, and upregulating p21[1].
Limocitrin (24 h) inhibits the AKT/ERK/JNK signaling pathways and activates p38 in SCC-9 and SCC-47 oral cancer cells[1].
Limocitrin (5-20 μM; 24 h) increases the protein expression of cytolytic effector molecules perforin, granzyme A and B, and granulysin in KHYG-1 cells[2].
Limocitrin (5-20 μM; 24 h) dose-dependently increases CREB phosphorylation and histone H3 acetylation in KHYG-1 cells[2].
Limocitrin (5-20 μM; 24 h) dose-dependently increases mitochondrial membrane depolarization in K562 cells co-cultured with KHYG-1 cells[2].
Limocitrin (5-20 μM) increases apoptosis of K562 cells co-cultured with KHYG-1 cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SCC-9 and SCC-47
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Concentration:0, 10, 20, 40 µM
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Incubation Time:24, 48, and 72 h
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Result:Inhibited the viability of SCC-9 and SCC-47 cells in a concentration-dependent and time-dependent manner.
Found the effective dose to inhibit SCC-9 to be 40 µM at 48 h and 72 h treatment.
Inhibited only 40% of SCC-47 cell viability at 40 µM until 72 h treatment.
Showed a better cell inhibitory effect on SCC-9 cells than SCC-47 cells.
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Cell Line:SCC-47 and SCC-9
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Concentration:0, 10, 20, 40 µM
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Incubation Time:24 h
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Result:Dramatically reduced the number of colonies in SCC-9 and SCC-47 oral cancer cells in a concentration-dependent manner.
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Cell Line:SCC-9 and SCC-47
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Concentration:0, 10, 20, 40 µM
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Incubation Time:24 h
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Result:Increased the expression of pro-apoptotic proteins Bax and Bak and decreased the expression of anti-apoptotic proteins Bcl-xL and Bcl-2.
Increased the expression of Fas, DcR2, DcR3, and DR5 compared with the control group.
Slightly increased Fas and DR5 expression in both cancer cell lines.
Greatly increased DcR3 in SCC-9 cells.
Significantly increased DcR2 expression more than DcR3 expression in SCC-47 cells.\nDecreased Cyclin E1 and E2 expression and increased p21 expression in a dose-dependent manner.
Potently downregulated CDK2, CDK4, and CDK6 expression levels.\nResulted in dose-dependent inhibition of XIAP, cIAP-1, and pHSP-27 protein expression in SCC-9 and SCC-47 cells.
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Cell Line:SCC-9 and SCC-47
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Concentration:0, 10, 20, 40 µM
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Incubation Time:24 h
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Result:Significantly enhanced the apoptosis rates of SCC-9 and SCC-47 cells.
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Cell Line:KHYG-1
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Concentration:5-20 μM
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Incubation Time:24 h
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Result:Significantly increased the protein expressions of perforin, granzymes A and B, and granulysin.\nSignificantly and dose-dependently elevated the expression of phosphorylated CREB.
Significantly increased the expression of acetyl-histone H3.
Chemical Information
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CAS No. 489-33-8
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Appearance Solid
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Molecular Weight 346.29
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Formula C17H14O8
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SMILES
O=C1C(O)=C(OC2=C(C(O)=CC(O)=C12)OC)C3=CC(OC)=C(C=C3)O
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Limocitrin Related Classifications
HY-119539 Related Classifications
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