PST3.1a

PST3.1a selectively inhibits purified recombinant human MGAT5 with an IC₅₀ of 2 µM, without affecting recombinant human MGAT3 activity^[1].
PST3.1a (5 µM; 10 days) reduces levels of multibranched β1,6-GlcNAc N-glycans in proliferative Gli4NS, confirming in-cellulo MGAT5 inhibition^[1].
PST3.1a (2 µM; 10 days) reduces β1,6-GlcNAc branching and sialylation of N-glycans in proliferative Gli4NS, without affecting core fucosylation or O-glycosylation^[1].
PST3.1a (5 µM; 48 h) does not reduce PHA-L binding in proliferative Gli4NS or GliTNS alone, but enhances the reduction in PHA-L binding caused by siMGAT5-mediated MGAT5 knockdown in these cells^[1].
PST3.1a (2 µM; 48 h) increases MGAT5 expression in proliferative Gli4NS at 48 hours (which returns to control levels by 5 days) and upregulates OLIG2 expression without altering SMAD2 phosphorylation^[1].
PST3.1a (1-10 µM; 10 days) increases the number of small neurospheres in proliferative Gli4NS and GliTNS by disrupting cell and neurosphere interactions, with effects enhanced in siMGAT5-transfected cells^[1].
PST3.1a (2 µM; 48 h) impairs the clonogenic capacity of proliferative Gli4NS, with no additional effect from continuous treatment during colony formation^[1].
PST3.1a (0.03-1 µM; 72 h) reduces β1,6-GlcNAc branching in differentiated Gli4DC and GliTDC^[1].
PST3.1a (2 µM; 48 h) downregulates MGAT5 expression, inhibits SMAD2 phosphorylation, and inhibits FAK phosphorylation in differentiated Gli4DC^[1].
PST3.1a (24 h) inhibits migration of differentiated Gli4DC, Gli7DC, GliTDC, and SNB75 cells on fibronectin, vitronectin, and laminin with IC₅₀ values between 1 and 30 nM^[1].
PST3.1a (48-72 h) inhibits proliferation of differentiated Gli4DC, Gli7DC, GliTDC, and SNB75 cells with IC₅₀ values between 1.7 and 2.6 µM^[1].
PST3.1a (24 h) inhibits invasion of differentiated Gli4DC, GliTDC, Gli7DC, and SNB75 cells through Matrigel, with IC₅₀ values of 7 nM (Gli4DC) and 2.5 nM (GliTDC)^[1].
PST3.1a (2 µM; 48 h) impairs migration of differentiated Gli4 cells, reduces long-distance migration from neurospheres, and disrupts the actin cytoskeleton^[1].
PST3.1a (1-10 µM; 48 h)-induced cytotoxicity is reduced by E-cadherin overexpression in Gli4DC and enhanced by E-cadherin knockout in PANC-1 cells^[1].

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