CeY-B1
CeY-B1 is a ceramide analog. CeY-B1 inhibits the proliferation, migration and invasion of cervical cancer cells, induces apoptosis and cell cycle arrest. CeY-B1 upregulates ASK1, promotes the phosphorylation of JNK, downregulates Bcl‑2, and inhibits the PI3K/AKT pathway. CeY-B1 suppresses tumor growth in cervical cancer xenograft mouse models. CeY-B1 can be used for relevant research on cervical cancer.
For research use only. We do not sell to patients.
- CAS No.: 2376783-79-6
- Formula: C21H44N2O4
- Molecular Weight:388.59
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| SiHa | IC50 |
25 μM
|
Inhibition of cell viability against human SiHa cervical cancer cells assessed by CCK-8 assay after 48 h of incubation.
Inhibition of cell viability against human SiHa cervical cancer cells assessed by CCK-8 assay after 48 h of incubation.
|
41904495 |
| HeLa | IC50 |
5.25 μM
|
Inhibition of cell viability against human HeLa cervical cancer cells assessed by CCK-8 assay after 48 h of incubation.
Inhibition of cell viability against human HeLa cervical cancer cells assessed by CCK-8 assay after 48 h of incubation.
|
41904495 |
In Vitro
CeY-B1 (0-160 µM; 48 h) inhibits the viability of SiHa cervical cancer cells with an IC50 of approximately 25 µM; it also inhibits the viability of HeLa cervical cancer cells with an IC50 of 5.25 µM[1].
CeY-B1 (10-20 µM; 48 h) inhibits the proliferation, migration and invasion of SiHa and HeLa cells[1].
CeY-B1 (5-20 µM; 48 h) induces apoptosis in SiHa and HeLa cells, and this effect is partially mediated by the JNK pathway[1].
CeY-B1 (20 µM) upregulates the mRNA expression of ASK1 and JNK in SiHa cervical cancer cells, and downregulates the mRNA expression of Bcl-2 and cytochrome C, suggesting that the ASK1-JNK axis is activated while anti-apoptotic signals are inhibited[1].
CeY-B1 (10-20 µM) activates the JNK/c-Jun pathway, downregulates Bcl-2, and inhibits the PI3K/AKT pathway in SiHa cervical cancer cells; it activates the JNK/c-Jun pathway and inhibits the PI3K/AKT pathway in HeLa cervical cancer cells, thereby promoting cell apoptosis[1].
CeY-B1 (10-20 µM; 48 h) induces S-phase cell cycle arrest in SiHa cervical cancer cells and G2/M-phase cell cycle arrest in HeLa cervical cancer cells[1].
CeY-B1 (25.6 µM; 48 h) alters lipid metabolism in SiHa cells, specifically by inducing the accumulation of pro-apoptotic ceramides and activating the sphingolipid signaling pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SiHa cervical cancer cells, HeLa cervical cancer cells
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Concentration:20 µM (SiHa cells); 10 µM (HeLa cells)
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Incubation Time:48 h
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Result:Significantly reduced colony formation ability of SiHa and HeLa cells.
Indicated inhibition of cervical cancer cell proliferation.
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Cell Line:SiHa cervical cancer cells, HeLa cervical cancer cells
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Concentration:20 µM (SiHa cells); 10 µM (HeLa cells)
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Incubation Time:24 h
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Result:Significantly reduced cell migration distance compared to control in both SiHa and HeLa cells.
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Cell Line:SiHa cervical cancer cells, HeLa cervical cancer cells
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Concentration:20 µM (SiHa cells); 10 µM (HeLa cells)
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Incubation Time:48 h
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Result:Significantly reduced the number of migrated SiHa and HeLa cells compared to control.
Significantly reduced the number of invaded SiHa cells compared to control.
Resulted in migrated cell number in the control group being approximately twice that in the CeY-B1 group.
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Cell Line:SiHa cervical cancer cells, HeLa cervical cancer cells
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Concentration:20 µM (SiHa cells); 10 µM (HeLa cells)
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Incubation Time:48 h
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Result:Significantly increased the apoptosis rate of SiHa and HeLa cells.
Had its induced apoptosis in both cell lines significantly reduced by treatment with JNK inhibitor.
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Cell Line:SiHa cervical cancer cells, HeLa cervical cancer cells
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Concentration:5, 10, 20 µM
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Incubation Time:48 h
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Result:Increased the apoptosis rate of SiHa and HeLa cells significantly with higher concentrations, as measured by the percentage of Hoechst-positive cells.
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Cell Line:SiHa cervical cancer cells, HeLa cervical cancer cells
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Concentration:20 µM (SiHa cells); 10 µM (HeLa cells)
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Incubation Time:48 h
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Result:Led to a significant increase in the proportion of SiHa cells in the S phase (S-phase arrest).
Caused significant accumulation of HeLa cells in the G2/M phase (G2/M-phase arrest).
In Vivo
CeY-B1 (0.02-2 g/kg; p.o.; single dose) show no acute toxicity in C57BL/6J female mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude mice[1]
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Dosage:10 mg/kg
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Administration:i.p.; twice weekly; 3 weeks
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Result:Significantly reduced tumor volume and tumor weight compared to control.
Showed increased tumor necrosis, reduced tumor cell density, and reduced nuclear atypia in treated tumors via H&E staining.
Significantly reduced expression of proliferation marker Ki-67 and angiogenesis marker CD31 in treated tumors via immunohistochemical staining.
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Animal Model:C57BL/6J female mice[1]
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Dosage:0.02 g/kg; 0.2 g/kg; 2 g/kg
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Administration:p.o.; single dose
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Result:Showed no significant difference in mouse body weight compared to control.
Showed no significant difference in organ coefficients of liver, kidney, lung, and heart compared to control.
Showed no significant difference in gross morphology or tissue structure of liver, kidney, lung, and heart compared to control.
Showed no significant difference in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared to control.
Chemical Information
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CAS No. 2376783-79-6
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Molecular Weight 388.59
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Formula C21H44N2O4
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SMILES
CCNC(N[C@H](CO)[C@@H](O)[C@@H](O)CCCCCCCCCCCCCC)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)