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^[1].

Avicin G (50-500 nM; 48 h) mislocalizes mGFP-K-Ras^G12V 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-Ras^G12V 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-Ras^G12V or mGFP-H-Ras^G12V, and increases mGFP-K-Ras^G12V expression levels^[1].
Avicin G (1.25 μM; 4 days with daily media replacement) inhibits the growth of KRAS-addicted human PDAC and NSCLC cell lines^[1].
Avicin G (500 nM; 48 h) disrupts mGFP-K-Ras^G12V plasma membrane nanoclustering and the lateral segregation of GTP- and GDP-bound mGFP-H-Ras^G12V 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-Ras^G12V, 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, with continued presence during subsequent serum starvation and EGF treatment) 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.

2067.26

C₉₈H₁₅₅NO₄₅

197787-17-0

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

Room temperature in continental US; may vary elsewhere.

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

• [1]. Garrido CM, et al. Avicin G is a potent sphingomyelinase inhibitor and blocks oncogenic K- and H-Ras signaling. Sci Rep. 2020 Jun 4;10(1):9120.  [Content Brief]