SZ0232
Based on 1 Customer Validation
SZ0232 is a selective mPGES-2 inhibitor. SZ0232 binds to the active site of mPGES-2 via hydrogen bonds and π-π stacking, reduces the production of prostaglandin E2 (PGE2) and blocks the PGE2-EP3 pathway. SZ0232 regulates Ferroptosis by activating the heme-dependent p53/SLC7A11/GPX4 axis, inhibits lipid peroxidation, and protects renal tubules. SZ0232 enhances glucose-stimulated insulin secretion, inhibits β-cell senescence, and improves glucose homeostasis. SZ0232 reduces renal lipid accumulation, alleviates fibrosis, and ameliorates renal dysfunction in diabetic mice. SZ0232 inhibits renal cyst growth in polycystic kidney disease models. SZ0232 exhibits an insulinotropic effect that strengthens with the increase of animal age. SZ0232 can be used in studies related to type 2 diabetes, acute kidney injury, diabetic kidney disease, and autosomal dominant polycystic kidney disease.
For research use only. We do not sell to patients.
- Purity : 98.89%
- CAS No.: 924851-91-2
- Formula: C24H30N4O7S
- Molecular Weight:518.58
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[2]|
GPX4 |
In Vitro
SZ0232 (10-9 to 10-3; 10 min pre-incubation, 100 s assay incubation) potently inhibits mPGES-2 enzymatic activity via specific binding to the enzyme's active site, and reduces PGE2 production in cell-free biochemical assays[1].
SZ0232 (0.01-100 μM) shows no significant cytotoxicity in MIN6 mouse pancreatic islet β cells[1].
SZ0232 inhibits β-cell senescence induced by mPGES-2 overexpression in INS-1 rat pancreatic islet β-cells[1].
SZ0232 upregulates the expression of ferroptosis protective markers GPX4 and SLC7A11 in renal tubular epithelial cells HK-2[2].
SZ0232 (40-160 μM; 8 days) inhibits Forskolin (HY-15371)-induced cyst growth in MDCK cells in a dose-dependent manner, with the maximum reduction in cyst diameter observed at the concentration of 160 μM[4].
SZ0232 (0.1-1000 μM) shows no effect on the viability of normal MDCK cells[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
SZ0232 (1 mg/kg; i.p.; once daily for 7 consecutive days) protects male C57BL/6 J mice against cisplatin-induced acute kidney injury (AKI), alleviating renal dysfunction, tubular injury, lipid peroxidation and cell death without altering PGE2 levels[2].
SZ0232 (1 mg/kg; i.p.; once daily; for 7 consecutive days) protects male C57BL/6 J mice against ischemia/reperfusion-induced acute kidney injury (AKI), and alleviates renal dysfunction, renal tubular injury, lipid peroxidation and cell death[2].
SZ0232 (0.5 mg/kg; i.p.; once every two days; for 8 weeks) inhibits mPGES-2, improves renal lipid metabolism, alleviates renal function injury, podocyte injury and tubulointerstitial fibrosis, thereby blocking the progression of diabetic kidney disease (DKD)[3].
SZ0232 (2 mg/kg/day; subcutaneous injection; daily, for 7 consecutive days) significantly reduces the kidney weight/body weight ratio, renal cyst index, and proliferation level of renal epithelial cells in ADPKD mouse models[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BKS-db/db (male, 8-week-old, mixed C57BKS and C57BL/6J background, type 2 diabetes genetic model)[1]
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Dosage:0.5 mg/kg
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Administration:i.p.; daily; 8 weeks
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Result:Improved glucose tolerance relative to vehicle control, as shown by lower blood glucose levels at 15, 30, 60, 90, and 120 minutes during IPGTT, and a reduced area under the curve (AUC) for glucose (P=0.0414).
Increased relative expression of β-cell identity markers MafA (P=0.0125), Pdx1 (P=0.0445), Glut2 (P=0.0130), and NR4A1 (P=0.0368) in islets.
Significantly reduced relative expression of senescence markers p16 (P=0.0206), IGF1R (P=0.0311), and β-galactosidase (β-Gal) (P=0.0306) in islets.
Caused no significant changes in body weight, serum liver/kidney function indices, or histomorphology of liver, kidney, muscle, or white fat relative to control group.
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Animal Model:C57BL/6 J (8-week-old male, cisplatin-induced AKI)[2]
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Dosage:1 mg/kg
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Administration:i.p.; daily; 7 days
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Result:Significantly reduced serum creatinine (SCr) levels (P=0.0451).
Significantly reduced blood urea nitrogen (BUN) levels (P=0.0007).
Reduced the tubular injury score (P<0.0001).
Increased renal glutathione (GSH) levels (P=0.0070).
Decreased renal malondialdehyde (MDA) levels (P=0.0005).
Reduced the percentage of TUNEL-positive renal cells (P=0.0001).
Did not alter renal prostaglandin E2 (PGE2) levels.
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Animal Model:C57BL/6 J (8-week-old male, ischemia/reperfusion-induced AKI)[2]
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Dosage:1 mg/kg
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Administration:i.p.; daily; 7 days
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Result:Significantly reduced SCr levels (P=0.0498).
Significantly reduced BUN levels (P=0.0224).
Reduced the tubular injury score (P=0.0156).
Increased renal GSH levels (P=0.0185).
Decreased renal MDA levels (P=0.0015).
Reduced the percentage of TUNEL-positive renal cells (P=0.0013).
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Animal Model:db/db (leptin-receptor-deficient, 8-week-old)[3]
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Dosage:0.5 mg/kg
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Administration:i.p.; once every two days; 8 weeks
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Result:Reduced urinary albumin-to-creatinine ratio and serum blood urea nitrogen levels.
Reduced tubular injury and glomerulosclerosis.
Decreased collagen deposition and tubulointerstitial fibrosis.
Reduced renal lipid accumulation.
Increased glomerular expression of podocyte markers WT-1, nephrin, and synaptopodin.
Reduced tubular expression of the injury marker KIM-1.
Decreased renal expression of ADRP and FABP5.
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Animal Model:C57BL/6 J mice (postnatal day 4 pups; Ksp-Cre; Pkd1flox/flox ADPKD model)[4]
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Dosage:2 mg/kg/day
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Administration:s.c.; daily; 7 consecutive days
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Result:Reduced kidney weight-to-body weight ratio significantly compared with vehicle controls.
Reduced renal cyst index significantly compared with vehicle controls.
Decreased positive cell rates of proliferation markers PCNA and Ki67 significantly compared with vehicle controls.
Lowered PCNA protein expression relative to vehicle controls.
Chemical Information
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CAS No. 924851-91-2
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Appearance Solid
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Molecular Weight 518.58
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Formula C24H30N4O7S
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Color White to off-white
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SMILES
O=C(NCCOC1=CC=C(C=C1OCCNC(C)=O)NS(=O)(C2=CC=C(C=C2)N3CCCC3=O)=O)C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (192.83 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- 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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (4.82 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
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.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (4.82 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%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
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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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
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3T3-L1 preadipocyte-to-adipocyte differentiation
3T3-L1 preadipocytes are induced to differentiate after growth arrest using adipogenic media containing insulin, dexamethasone, and IBMX; differentiation is assessed by lipid-droplet accumulation, triglyceride increase, Oil Red O staining, and adipocyte-marker induction such as PPARγ and C/EBPα.
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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.
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Nephrotoxicity Study
This protocol assesses nephrotoxicity by combining functional kidney injury readouts, urinary/tissue injury biomarkers, and renal histopathology. Serum creatinine and BUN reflect impaired kidney function, while KIM-1, NGAL, clusterin, osteopontin, IL-18, cystatin C, nephrin, Oat5, urinary protein, glucose, and alkaline phosphatase have been used to detect tubular injury in cisplatin-, gentamicin-, and acetaminophen-induced nephrotoxicity models.
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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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
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Human Islet Cell Culture
The method of preserving islets in vitro, with purified reduced immunogenicity. The steps are islet isolation, islet cell purification, in vitro determination of islet function and islet cell culture.
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Senescence-associated β-galactosidase staining
Senescence-associated β-galactosidase staining detects β-galactosidase activity that is histochemically visible at pH 6. 0 in senescent cells, where X-gal cleavage produces an insoluble blue precipitate observable by bright-field microscopy. This activity reflects increased lysosomal β-galactosidase/lysosomal mass rather than a senescence-essential enzyme, because GLB1 depletion or genetic lysosomal β-galactosidase deficiency can abolish SA-β-gal staining while cells still undergo senescence. SA-β-gal was originally reported in senescent but not presenescent fibroblasts and keratinocytes, absent from quiescent fibroblasts and terminally differentiated keratinocytes, and increased with donor age in human skin samples. Because SA-β-gal can also appear in some non-senescent or tissue-specific contexts, interpretation should be paired with experimental controls and, when possible, independent senescence markers.
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Lipid Droplets: Oil Red O/Sudan Dye Lipid Staining
Lipid droplets are intracellular organelles with a neutral-lipid core that stores triacylglycerols and sterol esters, and Oil Red O or Sudan dyes detect these hydrophobic lipid deposits by partitioning into retained lipids in fresh or frozen specimens. Oil Red O stains neutral triglycerides and lipids in frozen tissue sections or air-dried cytologic preparations, while Sudan Black B has also been used as a histochemical fat stain for lipid-rich tissue structures.
Purity & Documentation
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Data Sheet (285 KB)
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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)
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Handling Instructions (2659 KB)
References
[1]. Zhong D, et al. mPGES-2 blockade antagonizes β-cell senescence to ameliorate diabetes by acting on NR4A1. Nat Metab. 2022;4(2):269-283. [Content Brief]
[2]. Zhong D, et al. Targeting mPGES-2 to protect against acute kidney injury via inhibition of ferroptosis dependent on p53. Cell Death Dis. 2023;14(10):710. Published 2023 Oct 31. [Content Brief]
[3]. Zhong D, et al. Genetic or pharmacologic blockade of mPGES-2 attenuates renal lipotoxicity and diabetic kidney disease by targeting Rev-Erbα/FABP5 signaling. Cell Rep. 2024;43(4):114075. [Content Brief]
[4]. Zhong DD, et al. Inhibiting mPGES-2 impedes renal cyst growth in mice with polycystic kidney disease. Acta Pharmacol Sin. 2026;47(3):689-700. [Content Brief]
Complete Stock Solution Preparation Table
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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 1.9283 mL | 9.6417 mL | 19.2834 mL | 48.2086 mL |
| 5 mM | 0.3857 mL | 1.9283 mL | 3.8567 mL | 9.6417 mL | |
| 10 mM | 0.1928 mL | 0.9642 mL | 1.9283 mL | 4.8209 mL | |
| 15 mM | 0.1286 mL | 0.6428 mL | 1.2856 mL | 3.2139 mL | |
| 20 mM | 0.0964 mL | 0.4821 mL | 0.9642 mL | 2.4104 mL | |
| 25 mM | 0.0771 mL | 0.3857 mL | 0.7713 mL | 1.9283 mL | |
| 30 mM | 0.0643 mL | 0.3214 mL | 0.6428 mL | 1.6070 mL | |
| 40 mM | 0.0482 mL | 0.2410 mL | 0.4821 mL | 1.2052 mL | |
| 50 mM | 0.0386 mL | 0.1928 mL | 0.3857 mL | 0.9642 mL | |
| 60 mM | 0.0321 mL | 0.1607 mL | 0.3214 mL | 0.8035 mL | |
| 80 mM | 0.0241 mL | 0.1205 mL | 0.2410 mL | 0.6026 mL | |
| 100 mM | 0.0193 mL | 0.0964 mL | 0.1928 mL | 0.4821 mL |
SZ0232 Related Classifications
HY-179041 Related Classifications
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Keywords
- SZ0232
- 924851-91-2
- SZ 0232
- SZ-0232
- PGE synthase
- Prostaglandin Receptor
- MDM-2/p53
- Amino acid Transporter
- Glutathione Peroxidase
- Ferroptosis
- p53/SLC7A11/GPX4 axis
- ferroptosis
- COX-2
- renal tubular cells
- type 2 diabetes mellitus
- mPGES-1
- prostaglandin E2
- PGE2-EP3 pathway
- microsomal prostaglandin E synthase-2
- β-cell
- Inhibitor
- inhibitor
- inhibit