Cat. No.: HY-163121

PST3.1a

Name: PST3.1a
Brand: MedChemExpress
SKU: HY-163121
Price: 540.00 USD
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Based on 1 publication(s) in Google Scholar

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.

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

Purity : 99.51%
CAS No.: 1096144-06-7
Formula: C₃₂H₃₃O₆P
Molecular Weight:544.57

Storage:

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

PST3.1a Chemical Structure

CAS No.: 1096144-06-7

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Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Publications (1)
Solvent & Solubility
- In Vitro
- In Vivo
Protocols (8)
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]

MGAT5

2 μM (IC₅₀)

Collagen I

Collagen IV

Galectin-3

All TGF-β Receptor Isoforms :

All Galectin Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A-431	EC₅₀	14.5 μM Compound: 3.1a, diastereomer	Antiproliferative activity against human A431 cells after 48 hrs by MTT assay Antiproliferative activity against human A431 cells after 48 hrs by MTT assay	[PMID: 22268526]
B16-F10	EC₅₀	4.9 μM Compound: 3.1a, diastereomer	Antiproliferative activity against mouse B16F10 cells after 48 hrs by MTT assay Antiproliferative activity against mouse B16F10 cells after 48 hrs by MTT assay	[PMID: 22268526]
C6	EC₅₀	0.52 μM Compound: 3.1a, diastereomer	Antiproliferative activity against rat C6 cells after 48 hrs by MTT assay Antiproliferative activity against rat C6 cells after 48 hrs by MTT assay	[PMID: 22268526]
Caco-2	EC₅₀	57 μM Compound: 3.1a, diastereomer	Antiproliferative activity against human Caco2 cells after 48 hrs by MTT assay Antiproliferative activity against human Caco2 cells after 48 hrs by MTT assay	[PMID: 22268526]
DU-145	EC₅₀	65 μM Compound: 3.1a, diastereomer	Antiproliferative activity against human DU145 cells after 48 hrs by MTT assay Antiproliferative activity against human DU145 cells after 48 hrs by MTT assay	[PMID: 22268526]
Huh-7	EC₅₀	30 μM Compound: 3.1a, diastereomer	Antiproliferative activity against human HuH7 cells after 48 hrs by MTT assay Antiproliferative activity against human HuH7 cells after 48 hrs by MTT assay	[PMID: 22268526]
MDA-MB-435	EC₅₀	13.9 μM Compound: 3.1a, diastereomer	Antiproliferative activity against human MDA-MB-435 cells after 48 hrs by MTT assay Antiproliferative activity against human MDA-MB-435 cells after 48 hrs by MTT assay	[PMID: 22268526]

In Vitro

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. Further protocols information, click here.

Western Blot Analysis^[1]

View Protocol

Cell Line:

Gli4NS
Concentration:

2 µM
Incubation Time:

48 h
Result:

Increased MGAT5 protein expression and OLIG2 protein expression after 48 hours of treatment.
Left SMAD2 phosphorylation unchanged after 48 hours of treatment.
Restored MGAT5 protein expression to control levels after 5 days of treatment.

Western Blot Analysis^[1]

View Protocol

Cell Line:

Gli4DC
Concentration:

2 µM
Incubation Time:

48 h
Result:

Reduced MGAT5 protein expression.
Inhibited SMAD2 phosphorylation.
Inhibited FAK phosphorylation.
Left MGAT3 protein expression unchanged.

Cell Viability Assay^[1]

View Protocol

Cell Line:

Gli4DC, PANC-1 cells (with E-cadherin manipulation)
Concentration:

1, 3,10 µM
Incubation Time:

48 h
Result:

Reduced sensitivity to PST3.1a-induced cytotoxicity in Gli4DC with E-cadherin overexpression.
Increased sensitivity to PST3.1a-induced cytotoxicity in PANC-1 cells with E-cadherin knockout.

Parmacokinetics

Species	Dose	Route	Brain Concentration
Mice^[1]	27 mg/kg	p.o.	4.6 ng/g

In Vivo

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.

Animal Model:

NMRI-nude with orthotopic Gli4 xenografts (6-week-old female)^[1]
Dosage:

15 mg/kg
Administration:

p.o.; twice daily; 10 consecutive days
Result:

Reduced the overall Gli4-invaded brain surface significantly.
Reduced the number of Gli4 cells in the striatum of both ipsilateral and contralateral hemispheres by 80%.
Lowered tumoral cell densities within invaded cortex, corpus callosum, and striatum regions substantially compared to untreated mice.\nPrevented clinical signs of brain tumor development (prostration, weight loss) at the time control mice exhibited overt symptoms.
Increased the dorso-ventral axis of brains by 28% compared to control mice, reflecting reduced tumor-induced brain compression.

Animal Model:

Sprague-Dawley (6-week-old; chronic kidney disease induced via 5/6^th subtotal nephrectomy)^[2]
Dosage:

0.2 mg/mL
Administration:

p.o.; in drinking water; daily; 4 weeks
Result:

Significantly decreased renal expression of collagen 1 from 2.1% to 1.3%.
Significantly decreased renal expression of collagen 4 from 9.4% to 6.4%.
Showed a non-significant trend toward decrease in collagen 3 expression.
Caused a non-significant reduction in fibrosis (from 8.4% to 6.7%) via Sirius red staining.
Significantly blunted overexpression of galectin 3 from 9.4% to 5.7%.
Blunted overexpression of PHA-L.

Chemical Information

CAS No. 1096144-06-7
Appearance Solid
Molecular Weight 544.57
Formula C₃₂H₃₃O₆P
Color White to off-white
SMILES

O[C@@H]([P@@](O[C@@H]1COCC2=CC=CC=C2)(C3=CC=CC=C3)=O)[C@@H](OCC4=CC=CC=C4)[C@@H]1OCC5=CC=CC=C5
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Publications (1)

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Journal Impact Factor

Cancer Res

Targeting Sialylation Enhances the Therapeutic Efficacy of the Nectin-4-Targeted Antibody-Drug Conjugate Enfortumab Vedotin in Bladder Cancer. [Abstract]

2025 Oct 9. PMID: 41066596

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (183.63 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.8363 mL

9.1816 mL

18.3631 mL

5 mM

0.3673 mL

1.8363 mL

3.6726 mL

10 mM

0.1836 mL

0.9182 mL

1.8363 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: 2.5 mg/mL (4.59 mM); Suspended solution; Need ultrasonic

This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (4.59 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Protocols

All Histomorphology Molecular Biology Cell Biology Animals and Diseases

Fibrosis/Collagen Morphometry
Fibrosis and collagen morphometry is based on the quantitative visualization of fibrillar collagen deposition in tissue sections using histochemical stains such as Sirius Red (Picrosirius Red) or Masson's trichrome, followed by image-based or polarization-enhanced analysis to estimate collagen proportional area as a surrogate of extracellular matrix accumulation during fibrotic remodeling. Sirius Red combined with polarized light microscopy enhances detection of collagen fibers due to birefringence properties, enabling more specific visualization of collagen type I and III fibrils compared to conventional bright-field histology, while whole-section or region-restricted digital morphometry reduces field-selection bias in fibrosis assessment. Alternative quantitative approaches include second harmonic generation (SHG) and two-photon excited fluorescence microscopy, which enable label-free detection of fibrillar collagen and have been validated against histological staining and biochemica
RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
Collagen: Sirius Red Staining
Sirius Red or picrosirius red staining is a histochemical method for visualizing collagen-rich extracellular matrix in tissue sections, and collagen fibers are detected as red-stained structures under bright-field microscopy with enhanced birefringence under polarized light. Picrosirius red is useful for assessing total collagen organization, distribution, and fibrosis burden, but polarized color should not be interpreted as a definitive collagen type I versus type III readout because color is affected by fiber orientation, thickness, and packing.
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
Masson’s Trichrome (collagen/trichrome staining) is a histological technique that differentially stains tissue compartments using sequential acidic dyes to distinguish collagen from muscle and cytoplasmic components based on dye affinity and tissue permeability differences, enabling visualization of fibrosis and connective tissue architecture in histological sections. The classical formulation typically uses Weigert's iron hematoxylin for nuclear staining, Biebrich scarlet-acid fuchsin for cytoplasm and muscle, and aniline blue (or light green variants) for collagen, producing a characteristic blue/green collagen signal contrasted against red cytoplasm and dark nuclei. The staining principle relies on selective displacement of smaller dye molecules by larger anionic dyes in collagen-rich regions under controlled acidified conditions, which enhances collagen-specific dye retention. This property makes the method widely used for fibrosis assessment in organs such as heart, liver, lung, a
Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (290 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[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.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.8363 mL	9.1816 mL	18.3631 mL	45.9078 mL
	5 mM	0.3673 mL	1.8363 mL	3.6726 mL	9.1816 mL
	10 mM	0.1836 mL	0.9182 mL	1.8363 mL	4.5908 mL
	15 mM	0.1224 mL	0.6121 mL	1.2242 mL	3.0605 mL
	20 mM	0.0918 mL	0.4591 mL	0.9182 mL	2.2954 mL
	25 mM	0.0735 mL	0.3673 mL	0.7345 mL	1.8363 mL
	30 mM	0.0612 mL	0.3061 mL	0.6121 mL	1.5303 mL
	40 mM	0.0459 mL	0.2295 mL	0.4591 mL	1.1477 mL
	50 mM	0.0367 mL	0.1836 mL	0.3673 mL	0.9182 mL
	60 mM	0.0306 mL	0.1530 mL	0.3061 mL	0.7651 mL
	80 mM	0.0230 mL	0.1148 mL	0.2295 mL	0.5738 mL
	100 mM	0.0184 mL	0.0918 mL	0.1836 mL	0.4591 mL

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PST3.1a

Publications Citing Use of MedChemExpress (MCE) PST3.1a

All TGF-β Receptor Isoforms

All Galectin Isoforms