2. Metabolic Enzyme/Protease GPCR/G Protein Stem Cell/Wnt JAK/STAT Signaling Vitamin D Related/Nuclear Receptor Cell Cycle/DNA Damage Anti-infection
  3. Endogenous Metabolite Prostaglandin Receptor STAT PPAR Fungal Drug Metabolite
  4. 15-keto-Prostaglandin E2

15-keto-Prostaglandin E2  (Synonyms: 15-keto-PGE2)

Cat. No.: HY-113205 Purity: 99.0%
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15-keto-Prostaglandin E2 (15-keto-PGE2) is an endogenous PGE2 metabolite. 15-keto-Prostaglandin E2 inhibits STAT3 activation by binding to the Cys259 residue of STAT3. 15-keto-Prostaglandin E2 binds to and stabilizes EP2 and EP4 receptors. 15-keto-Prostaglandin E2 inhibits the growth and progression of breast cancer cells. 15-keto-Prostaglandin E2 activates PPAR-γ and promotes fungal growth. 15-keto-Prostaglandin E2 disrupts glomerular vascularization during zebrafish development and reduces the surface area of the glomerular filtration barrier.

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15-keto-Prostaglandin E2

15-keto-Prostaglandin E2 Chemical Structure

CAS No. : 26441-05-4

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Based on 1 publication(s) in Google Scholar

Other Forms of 15-keto-Prostaglandin E2:

15-keto-Prostaglandin E2 Related Antibodies

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Description

15-keto-Prostaglandin E2 (15-keto-PGE2) is an endogenous PGE2 metabolite. 15-keto-Prostaglandin E2 inhibits STAT3 activation by binding to the Cys259 residue of STAT3. 15-keto-Prostaglandin E2 binds to and stabilizes EP2 and EP4 receptors. 15-keto-Prostaglandin E2 inhibits the growth and progression of breast cancer cells. 15-keto-Prostaglandin E2 activates PPAR-γ and promotes fungal growth. 15-keto-Prostaglandin E2 disrupts glomerular vascularization during zebrafish development and reduces the surface area of the glomerular filtration barrier[1][2][3].

IC50 & Target[1]

PPARγ

 

EP2

 

EP4

 

STAT3

 

Human Endogenous Metabolite

 

In Vitro

15-keto-PGE2 (1 μM; 20 min) binds to and stabilizes HiBiT-tagged hEP2 receptors on the cytoplasmic membrane of MMY28 yeast[1].
15-keto-PGE2 (10-20 μM; 24 h) dose-dependently inhibits the clonogenic capacity of MDA-MB-231 cells[3].

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

15-keto-Prostaglandin E2 Related Antibodies
In Vivo

15-keto-Prostaglandin E2 (500 μM; immersion) impairs pronephric development and glomerular filtration barrier formation in zebrafish via the EP2/EP4 receptor signaling pathway, resulting in pronephric abnormalities combined with yolk sac edema in embryos, late insertion defects in glomeruli, and a significant reduction in glomerular surface area[1].
15-keto-Prostaglandin E2 (10 μM; immersion) significantly increases the fungal load of Cryptococcus neoformans Δplb1-GFP in zebrafish larvae, reaching 1.56 times that of the control group[2].
15-keto-Prostaglandin E2 (70-140 μg/kg; subcutaneous injection; administered daily for 4 consecutive weeks) dose-dependently inhibits the growth of MDA-MB-231 breast cancer xenografts in BALB/c nude mice[3].

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

Animal Model: Tg[wt1b:eGFP] (embryos; early treatment: 6-48 hpf; late treatment: 72-96 hpf)[1]
Dosage: 500 μM
Administration: immersion; continuous
Result: Caused mild yolk edema, with 80% of embryos showing affected pronephros structure plus yolk edema.
Resulted in 20% of glomeruli exhibiting impaired podocyte intercalation and failed glomerular cleft formation at 48 hpf (early treatment).
Induced podocyte clustering at the embryo midline and impaired podocyte intercalation around glomerular capillaries, affecting ~83% of glomeruli (late treatment).
Reduced glomerular surface area significantly in treated embryos compared to controls, while glomerular volume showed a non-significant numerical decrease (late treatment).
Reversed all morphological defects, restoring glomerular surface area to control levels when combined with EP2/EP4 receptor antagonists.
Animal Model: BALB/c (nu/nu) athymic nude mice (female, 7 weeks old)[3]
Dosage: 70 μg/kg; 140 μg/kg
Administration: s.c.; daily; 4 weeks
Result: Retarded tumor growth significantly in both treatment groups, with average tumor volume reduced in a dose-dependent manner.
Markedly decreased STAT3 phosphorylation (P-STAT3Y705) in tumor tissue at 140 μg/kg, as measured by Western blot and immunohistochemical analysis.
Caused no body weight loss or signs of toxicity.
Showed decreased tumor density in treated mice compared to controls via H&E staining.
Molecular Weight

350.45

Formula

C20H30O5
CAS No.
Appearance

Solid

Color

White to light yellow

SMILES

CCCCCC(/C=C/[C@@H]1[C@H](C(C[C@H]1O)=O)C/C=C\CCCC(O)=O)=O
Structure Classification
Initial Source

Gracilaria verrucosa (Huds.) Papenf.
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

-20°C, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

Purity & Documentation

Purity: 99.0%

SDS (557 KB)

COA (254 KB)

Handling Instructions (2659 KB)
References
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15-keto-Prostaglandin E2 Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

15-keto-Prostaglandin E226441-05-415-keto-PGE2Endogenous MetaboliteProstaglandin ReceptorSTATPPARFungalDrug MetabolitePeroxisome proliferator-activated receptorsPPAR-γmammary epithelial cellsCryptococcus neoformansEP2 receptorszebrafish embryosSTAT3BALB/c nude miceMDA-MB-231 cellsEP4 receptorsyeast modelsInhibitorinhibitorinhibit

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