SNX-2112

SNX-2112
Cat. No. : CS-0481 CAS No. : 908112-43-6
M. Wt. : 464.4807
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  • Data Sheet

  • Introduction

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  • COA & Spectra

Name: SNX-2112; 
Cat. No. : CS-0481
CAS No. : 908112-43-6
Formula: C23H27F3N4O3
M. Wt. : 464.4807
Solubility: 10 mM in DMSO

Activity:

SNX-2112 is a potent synthetic heat shock protein 90 (HSP90) inhibitor with an IC50 of 0.92 μM for K562 cells. IC50 Value: 0.92 μM for K562 cells Target: HSP90 in vitro: SNX-2112 competitively binds to the N-terminal adenosine triphosphate binding site of Hsp90. SNX-2112 induces apoptosis via caspase-8, -9, -3, and poly (ADPribose) polymerase cleavage. SNX-2112 inhibits cytokine-inducedAkt and extracellular signal-related kinase (ERK) activation and also overcomes the growth advantages conferred by interleukin-6, insulin-like growth factor-1, and bone marrow stromal cells. SNX-2112 inhibits tube formation by human umbilical vein endothelial cells via abrogation of eNOS/Akt pathway and markedly inhibits osteoclast formation via down-regulation of ERK/c-fos and PU.1. Cell lines (eight cell lines from osteosarcoma, neuroblastoma, hepatoblastoma, and ymphoma) studied demonstrates sensitivity to SNX-2112 with IC50 values ranging from 10-100 nM. A higher dose (70 nM) exhibits a more prolonged inhibition and larger sub-G1 accumulation. Observed levels of Akt1 and C-Raf are markedly reduced over time along with an increase in PARP cleavage. A recent research indicates NX-2112 induces autophagy in a time- and dose-dependent manner via Akt/mTOR/p70S6K inhibition. SNX-2112 induces significant apoptosis and utophagy in human melanoma A-375 cells, and may be an effective targeted therapy agent. in vivo: SNX-2112, delivered by its prodrug SNX-5422, inhibits MM cell growth and prolongs survival in a xenograft murine model and blockade of Hsp90 by SNX-2112 not only inhibits MM cell growth but also acts in the bone marrow microenvironment to block angiogenesis and osteoclastogenesis.

Protocol:

Cell assay [1] Cells were seeded in 100 mm dishes at a density of 5 × 105 cells per dish. Forty-eight hours later, the cells were treated with drug or vehicle (dimethyl sulfoxide) for 24h. Both adherent and floating cells were harvested and stained with ethidium bromide. Quantitation of the cell cycle distribution was performed by flow cytometric analysis.

References:

Xiang YF, Qian CW, Xing GW, Hao J, Xia M, Wang YF.Anti-herpes simplex virus efficacies of 2-aminobenzamide derivatives as novel HSP90 inhibitors.Bioorg Med Chem Lett. 2012 Jul 15;22(14):4703-6. Epub 2012 May 26.

Liu KS, Ding WC, Wang SX, Liu Z, Xing GW, Wang Y, Wang YF.The heat shock protein 90 inhibitor SNX-2112 inhibits B16 melanoma cell growth in vitro and in vivo.Oncol Rep. 2012 Jun;27(6):1904-10. doi: 10.3892/or.2012.1738. Epub 2012 Mar 22.

Liu KS, Liu H, Qi JH, Liu QY, Liu Z, Xia M, Xing GW, Wang SX, Wang YF.SNX-2112, an Hsp90 inhibitor, induces apoptosis and autophagy via degradation of Hsp90 client proteins in human melanoma A-375 cells.Cancer Lett. 2012 May 28;318(2):180-8.

Thomas Bachleitner-Hofmann et al. Antitumor Activity of SNX-2112, a Synthetic Heat Shock Protein-90 Inhibitor, in MET-Amplified Tumor Cells with or without Resistance to Selective MET Inhibition Clin Cancer Res January 1, 2011 17; 122

Rajan A, Kelly RJ, Trepel JB, Kim YS, Alarcon SV, Kummar S, Gutierrez M, Crandon S, Zein WM, Jain L, Mannargudi B, Figg WD, Houk BE, Shnaidman M, Brega N, Giaccone G.A phase I study of PF-04929113 (SNX-5422), an orally bioavailable heat shock protein 90 inhibitor, in patients with refractory solid tumor malignancies and lymphomas.Clin Cancer Res. 2011 Nov 1;17(21):6831-9. Epub 2011 Sep 9.

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