PAA5
PAA5 is a methide carbon-centered polynuclear Au(I) cluster. PAA5 can release Au(I) causing Pro-oxidant response and accelerated ferroptosis. PAA5 increases the expression of pH2AX in a time-dependent manner. PAA5 has anticancer activity.
For research use only. We do not sell to patients.
- Formula: C14H8Au5B2F8N2-
- Molecular Weight:1348.66
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
In Vitro
PAA5 (0-4 μM; 24 h) induces ferroptosis and increase of the ferroptosis marker gene prostaglandin-endoperoxide synthase 2 (PTGS2). PAA5 decreases cell viability in EJ cells with IC50 values of 1.0 μM and 2.7 μM for EJ and HUVEC cells, respectively[1].
PAA5 (1.5 μM; 4 h; EJ and HUVEC cells) releases active Au(I) metabolites within cells and increases GSH and ROS level[1].
PAA5 (4 μM; 1, 3 and 6 h, EJ cells) causes significant DNA damage as indicated by the increase of histone H2AX phosphorylation (pH2AX)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HUVEC, EJ cells
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Concentration:0, 0.5, 1, 1.5, 2, and 4 µM
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Incubation Time:24 hours
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Result:Decreased cell viability of EJ cells 57 and 55%, respectively, compare with HUVEC cells.
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Cell Line:EJ cells
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Concentration:4 µM
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Incubation Time:1, 3, and 6 hours
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Result:Increased the expression of pH2AX in a time dependent manner.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:4-6 weeks, 18 g, female BALB/c nude mice[1]
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Dosage:1.5 µM, 100 µL
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Administration:Intravesical delivered into the bladder; 5 times every other day for 8 days
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Result:Exhibited a good antitumor effect with the small average tumor volume of 564 ± 180 mm3 after 22 days and no significant body weight loss.
Chemical Information
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Molecular Weight 1348.66
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Formula C14H8Au5B2F8N2-
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SMILES
[F-][B+3]([F-])([F-])[F-].[F-][B+3]([F-])([F-])[F-].C1(C(C234[Au@@]56[Au@]27[Au]358[Au]46)=[N]([Au]78)C9=C%10C=CC=C9)=C%10C=CC=C1.[2+]
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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.
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)