Avicin G
Avicin G is a sphingomyelinase inhibitor and plasma membrane disruptor. Avicin G inhibits the enzymatic activities of neutral sphingomyelinases (SMPD2/3) and acid sphingomyelinase (SMPD1), elevates intracellular sphingomyelin levels, and alters the distribution of sphingomyelin. Avicin G interferes with the lateral segregation of GTP- and GDP-bound H-Ras, inhibits the signal output of oncogenic K-Ras and H-Ras, reduces the phosphorylation of ERK and Akt, increases lysosomal pH, and inhibits the endocytic recycling of epidermal growth factor receptor. Avicin G can be used in research related to pancreatic ductal adenocarcinoma and non-small cell lung cancer.
For research use only. We do not sell to patients.
- CAS No.: 197787-17-0
- Formula: C98H155NO45
- Molecular Weight:2067.26
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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- References
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Biological Activity
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Cell Line
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Type | Value | Description | References |
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| Jurkat | IC50 |
0.22 μg/mL
Compound: 2, avicin G
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Cytotoxicity against human Jurkat cells after 72 hrs by MTT assay
Cytotoxicity against human Jurkat cells after 72 hrs by MTT assay
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[PMID: 12828461] |
Avicin G (50-500 nM; 48 h) mislocalizes mGFP-K-RasG12V from the plasma membrane to endomembranes in MDCK cells with an IC50 of 73.8 nM after 48 h of treatment[1].
Avicin G (500 nM; 48 h) translocates mGFP-K-RasG12V from the plasma membrane to multiple endomembrane compartments including early endosomes, late endosomes, lysosomes, mitochondria, Golgi, and ER in MDCK cells, and increases the number and size of LAMP1-positive vesicles[1].
Avicin G (5-500 nM; 48 h) inhibits oncogenic Ras signal output by reducing phosphorylated ERK and Akt levels in MDCK cells expressing mGFP-K-RasG12V or mGFP-H-RasG12V, and increases mGFP-K-RasG12V expression levels[1].
Avicin G (1.25 μM; 4 days) inhibits the growth of KRAS-addicted human PDAC and NSCLC cell lines[1].
Avicin G (500 nM; 48 h) disrupts mGFP-K-RasG12V plasma membrane nanoclustering and the lateral segregation of GTP- and GDP-bound mGFP-H-RasG12V in BHK cells, contributing to reduced oncogenic Ras signal output[1].
Avicin G (5-1000 nM; 48 h) inhibits neutral sphingomyelinase activity with greater potency than acid sphingomyelinase activity in MDCK cells expressing mGFP-K-RasG12V, with significant inhibition of neutral SMase at ≥5 nM and acid SMase at ≥500 nM after 48 h of treatment[1].
Avicin G (5-1000 nM; 48 h) disrupts subcellular localization of SMPD1-GFP and SMPD2-GFP in MDCK cells, reduces SMPD1-GFP expression at ≥500 nM, increases SMPD2-GFP expression at ≥10 nM, and does not affect SMPD3-GFP expression or localization[1].
Avicin G (10-1000 nM; 48 h) increases lysosomal pH in a dose-dependent manner in WT MDCK cells, significantly elevating pH from 3.7 to 5.7 after 48 h of treatment with high concentrations[1].
Avicin G (100 nM; 48 h) inhibits endocytic recycling of EGFR-mGFP in CHO cells, causing accumulation of EGFR-mGFP in the perinuclear region instead of return to the plasma membrane[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MDCK cells stably expressing mGFP-K-RasG12V or mGFP-H-RasG12V
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Concentration:5 nM, 10 nM, 100 nM, 500 nM
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Incubation Time:48 h
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Result:Significantly reduced ppERK and pAkt levels in both K-RasG12V and H-RasG12V cells, with greater effects observed in K-RasG12V cells.
Significantly increased the expression level of mGFP-K-RasG12V, but not mGFP-H-RasG12V.
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Cell Line:Human pancreatic ductal adenocarcinoma (PDAC) and non-small cell lung cancer (NSCLC) cells
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Concentration:1.25 μM
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Incubation Time:4 days, with daily media replacement
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Result:Significantly inhibited the growth of all tested K-Ras-addicted PDAC cell lines (AsPC-1, Panc10.05, MiaPaCa-2, HPAF-II, PANC-1) and K-Ras-addicted NSCLC cell lines (H358, H441).
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Cell Line:MDCK cells stably expressing SMPD1-GFP, SMPD2-GFP, or SMPD3-GFP
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Concentration:5 nM, 10 nM, 100 nM, 500 nM, 1000 nM
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Incubation Time:48 h
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Result:Disrupted the lysosomal localization of SMPD1-GFP and accumulated SMPD2-GFP in vesicular structures, but did not alter the PM localization of SMPD3-GFP.
Significantly reduced SMPD1-GFP expression at ≥500 nM.
Significantly increased SMPD2-GFP expression at ≥10 nM.
Did not change SMPD3-GFP expression.
Chemical Information
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CAS No. 197787-17-0
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Molecular Weight 2067.26
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Formula C98H155NO45
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SMILES
C=C[C@@](O)(C)CC/C=C(C)/C(O[C@@H]([C@H](O)[C@H]1O)[C@@H](C)O[C@H]1O[C@@](C)(C=C)CC/C=C(CO)/C(O[C@H]2C[C@]3(C(O[C@H]4[C@H](O[C@@H]5O[C@@H](C)[C@H](O[C@H]6[C@H](O)[C@@H](O)[C@H](CO)O6)[C@@H](O[C@H]7[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O7)[C@H]5O)[C@@H](O)[C@H](O)[C@@H](CO)O4)=O)[C@H](O)C[C@@]8(C)[C@]9(C)CC[C@@]%10([H])C(C)(C)[C@@H](O[C@H]%11[C@@H]([C@@H](O)[C@H](O)[C@@H](CO[C@@H]%12O[C@H](C)[C@H](O)[C@H](O)[C@H]%12O[C@@H]%13OC[C@@H](O)[C@H](O)[C@H]%13O)O%11)NC(C)=O)CC[C@]%10(C)[C@@]9([H])CC=C8[C@]3([H])CC2(C)C)=O)=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
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)
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