1. Neuronal Signaling
  2. OGT
  3. Ac4-5SGlcNAc

Ac4-5SGlcNAc is an O-GlcNAc transferase (OGT) inhibitor. Ac4-5SGlcNAc converts intracellularly to UDP-5SGlcNAc, which competes with native UDP-GlcNAc (HY-148596) to block OGT catalytic activity, reduces cellular UDP-GlcNAc pools, and limits global protein O-GlcNAcylation. Ac4-5SGlcNAc reduces OGA levels via feedback, alters lectin signal intensities and glycan-related band masses. Ac4-5SGlcNAc can be used for the research of breast cancer.

For research use only. We do not sell to patients.

Ac4-5SGlcNAc

Ac4-5SGlcNAc Chemical Structure

CAS No. : 67561-97-1

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Description

Ac4-5SGlcNAc is an O-GlcNAc transferase (OGT) inhibitor. Ac4-5SGlcNAc converts intracellularly to UDP-5SGlcNAc, which competes with native UDP-GlcNAc (HY-148596) to block OGT catalytic activity, reduces cellular UDP-GlcNAc pools, and limits global protein O-GlcNAcylation. Ac4-5SGlcNAc reduces OGA levels via feedback, alters lectin signal intensities and glycan-related band masses. Ac4-5SGlcNAc can be used for the research of breast cancer[1][2][3].

IC50 & Target

Glycosyltransferase (OGT)[1]

In Vitro

Ac4-5SGlcNAc (50 μM; 24 h-5 days) potently reduces global O-GlcNAcylation in undifferentiated hESCs, downregulates OGA expression without altering hESC pluripotency or cell viability[1].
Ac4-5SGlcNAc (50 μM; daily from day -2 to day 11 of neural differentiation) reduces global O-GlcNAcylation and cellular UDP-GlcNAc levels in differentiating hESCs, induces compensatory changes in OGT and OGA expression, and does not disrupt core pluripotency or neural progenitor marker expression[1].
Ac4-5SGlcNAc (10-50 μM; daily from day -2 to day 11 of neural differentiation, 48 h prior to neural induction initiation) accelerates neuronal differentiation of H1, H7, and H9 hESCs, inducing premature expression of TUJ1 and MAP2, increasing neurite extension, and increasing the percentage of cells co-expressing these neuronal markers[1].
Ac4-5SGlcNAc (50 μM; daily from day -2 to day 11 of neural differentiation) upregulates neuronal differentiation and forebrain development-related genes in differentiating H1 hESCs, driving transcriptomic changes consistent with accelerated neuronal commitment[1].
Ac4-5SGlcNAc (50 μM; daily from day -2 to day 4 of neural differentiation) causes minor, transient changes to cell surface glycosylation in hESCs, with no detectable differences once neural induction is underway[1].
Ac4-5SGlcNAc (50 μM; 2-24 h) inhibits global O-GlcNAcylation in CHO cells in vitro in a dose-dependent manner, with a maximal effect at 50 μM over 24 h and observable reduction starting at 4 h[2].
Ac4-5SGlcNAc (50 μM; 24 h) modulates established OGT inhibition biomarkers in CHO cells, including a Nup62 mass shift, sOGT accumulation, and reduced OGA levels[2].
Ac4-5SGlcNAc (50 μM; 24 h) inhibits global O-GlcNAcylation in CHO, HEK-293, HeLa, and D283-Med cells[2].
Ac4-5SGlcNAc (50 μM; 24 h) alters specific cell surface glycan structures in CHO cells, as detected by reduced binding of lectins PHA-E, Jacalin, and LCA, while not grossly perturbing glycans recognized by several other tested lectins[2].

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

Western Blot Analysis[1]

Cell Line: undifferentiated human embryonic stem cells (hESCs)
Concentration: 50 μM
Incubation Time: 24 h; 5 days
Result: Abrogated the majority of detectable protein O-GlcNAcylation after 24 h treatment.
Caused a time-dependent decrease in O-GlcNAc levels for up to 3 days, after which levels started to increase following 5 days treatment.
Decreased OGA protein expression over the 5-day period.
Left OCT4 expression (a pluripotency marker) unaffected.
Caused no changes in cell morphology or proliferation.

Western Blot Analysis[1]

Cell Line: hESCs undergoing neural differentiation
Concentration: 50 μM
Incubation Time: daily from day -2 to day 11 of neural differentiation
Result: Maintained consistently lower global O-GlcNAcylation levels than DMSO-treated controls while preserving the oscillation pattern characteristic of neural differentiation.
Decreased OGA protein expression and increased OGT protein expression (compensatory changes).
Left OCT4 and PAX6 expression unchanged relative to controls.
Reduced UDP-GlcNAc levels significantly across all days of differentiation compared to DMSO-treated cells.

Immunofluorescence[1]

Cell Line: H1, H7, H9 hESCs undergoing neural differentiation
Concentration: 10 μM; 50 μM
Incubation Time: daily from day -2 to day 11 of neural differentiation
Result: Accelerated TUJ1 expression compared to controls after 50 μM treatment for 48 h before neural induction.
Caused premature TUJ1 expression as early as day 8 and greater neurite extension via immunofluorescence when 50 μM was added daily from day -2 to day 11.
Enabled detection of TUJ1 and MAP2 co-expression in H1, H7, and H9 hESC lines by day 11.
Caused a 10-fold difference in TUJ1/MAP2 co-expression between treated and DMSO-treated cells by day 6; by day 11, 3% of treated cells co-expressed both markers, compared to 1% of control cells.
Induced similar accelerated neuronal marker expression with 10 μM treatment.

Western Blot Analysis[2]

Cell Line: Chinese hamster ovary (CHO) cells
Concentration: 50 μM
Incubation Time: 24 h
Result: Caused Nup62 to shift to a lower molecular weight, consistent with loss of O-GlcNAc residues.
Resulted in accumulation of the short isoform of OGT (sOGT) while full-length ncOGT levels remained unchanged.
Decreased levels of OGA (O-GlcNAcase).

Western Blot Analysis[2]

Cell Line: Chinese hamster ovary (CHO) cells, HEK-293 cells, HeLa cells, D283-Med cells
Concentration: 50 μM
Incubation Time: 24 h
Result: Reduced global O-GlcNAc levels in all four tested mammalian cell lines.
Molecular Weight

405.42

Formula

C16H23NO9S

CAS No.
SMILES

CC(O[C@H]1[C@@H]([C@H](S[C@@H]([C@@H]1NC(C)=O)OC(C)=O)COC(C)=O)OC(C)=O)=O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

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

Purity & Documentation
References
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Ac4-5SGlcNAc
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