Cas No.: | 1071098-42-4 |
Chemical Name: | AZA1 |
Synonyms: | AZA1;AZA-1;AZA 1 |
SMILES: | CC(N1)=CC2=C1C=CC(NC3=NC(NC4=CC5=C(NC(C)=C5)C=C4)=NC=C3)=C2 |
Formula: | C22H20N6 |
M.Wt: | 368.43 |
Purity: | >98% |
Sotrage: | Powder-20°C3 years4°C2 yearsIn solvent-80°C6 months-20°C1 month |
Description: | AZA1 is a potent dual inhibitor of Rac1 and Cdc42. AZA1 induces prostate cancer cells apoptosis and inhibits prostate cancer cells proliferation, migration and invasion[1][2]. |
In Vivo: | AZA1 (Rac1/Cdc42-IN-1) (100 μg; i.p.; daily for 2 weeks) is potent in suppressing human 22Rv1 xenograft growth in mice and improving survival[1]. Animal Model: 5 week-old athymic nu/nu (nude) mice (bearing 22Rv1 prostate cancer cell xenografts)[1] Dosage: 100 μg in 100 µl 30% DMSO Administration: I.p.; daily for 2 weeks Result: The suppressive effect of AZA1 on tumor growth was significant. |
In Vitro: | AZA1 (Rac1/Cdc42-IN-1) (2-10 μM; 72 hours) blocks the proliferation of human prostate cancer cells 22Rv1 prostate cancer cells[1]. AZA1 (2-10 μM; 24 hours) reduces phosphorylation of PAK1, AKT and BAD in EGF-stimulated 22Rv1 prostate cancer cells[1]. AZA1 (10 μM; 24 hours) blocks Rac1 and Cdc42-dependent cell cycle events in 22Rv1 prostate cancer cells[1]. AZA1 blocks Rac1 and Cdc42-dependent migration of 22Rv1, DU 145 and PC-3 prostate cancer cells[1]. AZA1 affects cell motility and actin rearrangement in prostate cancer cells by suppressing Rac1 and Cdc42 activity via PAK1/2 phosphorylation[1]. Cell Proliferation Assay[1] Cell Line: 22Rv1 prostate cancer cells Concentration: 2, 5, 10 μM Incubation Time: 72 hours Result: Suppressed 22Rv1 prostate cancer cell proliferation in both unstimulated and EGF-stimulated cancer cells in a dose-dependent manner. Western Blot Analysis[1] Cell Line: 22Rv1 prostate cancer cells (EGF-stimulated) Concentration: 2, 5, 10 μM Incubation Time: 24 hours Result: Reduced phosphorylation of PAK1, AKT and BAD in EGF-stimulated 22Rv1 prostate cancer cells. |
References: | [1]. Zins K, et al. A Rac1/Cdc42 GTPase-specific small molecule inhibitor suppresses growth of primary human prostate cancer xenografts and prolongs survival in mice. PLoS One. 2013;8(9):e74924. Published 2013 Sep 11. [2]. Suzuki O, et al. Sialylation and glycosylation modulate cell adhesion and invasion to extracellular matrix in human malignant lymphoma: Dependency on integrin and the Rho GTPase family. Int J Oncol. 2015;47(6):2091‐2099. |