(Rac)-AAA
Based on 1 publication(s) in Google Scholar
(Rac)-AAA is a regulator and inhibitor targeting GPR75. By blocking the 20-HETE-induced downregulation of GPR75 expression, (Rac)-AAA effectively inhibits the activation of key downstream signaling pathways including EGFR, AKT, NF-κB and FAK. (Rac)-AAA reverses 20-HETE-mediated epithelial-mesenchymal transition, which is specifically characterized by downregulating vimentin (vimentin), upregulating E-Cadherin, as well as reducing MMP-2 activity and cancer cell migration ability. (Rac)-AAA also abolishes the 20-HETE-induced upregulation of HIC-5 expression and anchorage-independent growth, and modulates the subcellular localization of PKC-α and phosphorylated AKT. (Rac)-AAA is investigated in androgen-independent prostate cancer (castration-resistant prostate cancer).
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- CAS. Nr.: 3055022-23-3
- Formel: C24H39NNa2O6
- Molecular Weight:483.55
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Speicherung:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biologische Aktivität
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MMP-2 |
(Rac)-AAA (5-10 μM; 12 h) reverses the 20-HETE-induced reduction in GPR75 expression, and increases baseline GPR75 expression in PC-3 human prostate cancer cells[1].
(Rac)-AAA (5-10 μM; 2 h) reduces 20-HETE-induced phosphorylation of EGFR, AKT, and NF-κB, and increases baseline p38 phosphorylation in PC-3 human prostate cancer cells[1].
(Rac)-AAA (5-10 μM; 24 h) reverses 20-HETE-induced epithelial-mesenchymal transition by restoring E-cadherin expression and reducing or abrogating vimentin expression in PC-3 human prostate cancer cells[1].
(Rac)-AAA (5-10 μM; 24 h) reduces or abrogates 20-HETE-induced MMP-2 activity in conditioned medium from PC-3 human prostate cancer cells[1].
(Rac)-AAA (5 μM; 21 days) abrogates the increase in anchorage-independent colony formation induced by 5,14-HEDGE in PC-3 human prostate cancer cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:PC-3 human prostate cancer cells
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Concentration:5 μM (co-incubated with 20-HETE); 10 μM (co-incubated with 20-HETE); 10 μM (incubated alone)
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Incubation Time:2 h (all conditions)
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Result:Decreased 20-HETE-induced EGFR phosphorylation by 44% (5 μM) and 68% (10 μM) relative to 20-HETE alone.
Decreased 20-HETE-induced AKT phosphorylation by 40% (5 μM) and 58% (10 μM) relative to 20-HETE alone.
Decreased 20-HETE-induced NF-κB phosphorylation by 66% (both 5 μM and 10 μM) relative to 20-HETE alone.
Increased baseline p38 phosphorylation by 248% relative to control.
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Cell Line:PC-3 human prostate cancer cells
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Concentration:5 μM (co-incubated with 20-HETE); 10 μM (co-incubated with 20-HETE)
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Incubation Time:24 h (all conditions)
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Result:Reversed the 20-HETE-induced 40% downregulation of E-cadherin.
Reduced the 20-HETE-induced 150% upregulation of vimentin by 75% (5 μM) relative to 20-HETE alone, and completely abrogated this upregulation at 10 μM.
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Cell Line:PC-3 human prostate cancer cells
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Concentration:5 μM (co-incubated with 20-HETE)
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Incubation Time:16 h
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Result:Reduced 20-HETE-induced wound closure from 48.9% to 36.0% relative to 20-HETE alone.
Chemical Information
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CAS. Nr. 3055022-23-3
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Appearance Solid
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Molecular Weight 483.55
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Formel C24H39NNa2O6
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Color White to off-white
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SMILES
O=C(C(NC(CCCC/C=C\CCCCCCC/C=C\CCCCO)=O)CC(O[Na])=O)O[Na]
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Data Sheet (273 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)
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Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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