PST3.1a 

PST3.1a is an orally active and brain-penetrant N-acetylglucosamine glycosyltransferase (MGAT5) inhibitor with a human IC₅₀ of 2 µM. PST3.1a inhibits TGFβR and FAK signaling pathway activity. PST3.1a alters β1,6-GlcNAc N-glycans and microtubule/microfilament integrity, increases OLIG2 expression, and inhibits proliferation, migration, invasiveness, and clonogenic capacities of glioblastoma initiating cells. PST3.1a reduces invasive and proliferative capacity of glioblastoma initiating cells in orthotopic graft models, increases overall survival of orthotopic graft model mice. PST3.1a blunts MGAT5 overexpression, decreases renal fibrosis via collagen 1, collagen 4, and galectin 3 downregulation in a rat chronic kidney disease model. PST3.1a can be used for the research of glioblastoma multiforme and chronic kidney disease^[1][2].

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.

PST3.1a (15 mg/kg; p.o.; twice daily; 10 consecutive days) reduces glioblastoma cell invasion and tumoral cell density in orthotopic Gli4 xenografts by 80% in striatal regions^[1].
PST3.1a (25 mg/kg; p.o.; twice daily; two cycles of 30 days separated by 19 days) significantly improves median survival of Gli4 orthotopic xenograft mice to 108 days^[1].
PST3.1a (0.2 mg/mL in drinking water; p.o.; daily; 4 weeks) significantly decreases renal expression of collagen 1 and collagen 4, blunts galectin 3 overexpression, and reduces markers of MGAT5 activity in a rat model of chronic kidney disease induced by 5/6^th subtotal nephrectomy^[2].

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

544.57

C₃₂H₃₃O₆P

1096144-06-7

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• [1]. Hassani Z, et al. Phostine PST3. 1a targets MGAT5 and inhibits glioblastoma-initiating cell invasiveness and proliferation[J]. Molecular Cancer Research, 2017, 15(10): 1376-1387.  [Content Brief]

  [2]. Muyor K, et al. MO072: PST3. 1A, An Inhibitor of MGAT5 Decreases Renal Fibrosis in a Rat Model of Chronic Kidney Disease[J]. Nephrology Dialysis Transplantation, 2022, 37(Supplement_3): gfac063. 024.