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.
Kinase Assay
Cell Assay
Animal Administration
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.
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