WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#: 408099
Description: RA-9 is a cell permeable and potent inhibitor of the ubiquitin-proteasome system (UPS). RA-9 Inhibits Proteasome-Associated DUBs and Ovarian Cancer in Vitro and in Vivo via Exacerbating Unfolded Protein Responses. Treatment with RA-9 selectively induces onset of apoptosis in ovarian cancer cell lines and primary cultures derived from donors. Loss of cell viability following RA-9 exposure is associated with an unfolded protein response as mechanism to compensate for unsustainable levels of proteotoxic stress. In vivo treatment with RA-9 retards tumor growth, increases overall survival, and was well tolerated by the host.
MedKoo Cat#: 408099
Name: RA-9 UPS inhibitor
Chemical Formula: C19H15N3O5
Exact Mass: 365.1012
Molecular Weight: 365.345
Elemental Analysis: C, 62.46; H, 4.14; N, 11.50; O, 21.90
Synonym: RA-9; RA 9; RA9; RA-9 UPS inhibitor
IUPAC/Chemical Name: (3E,5E)-3,5-Bis[(4-nitrophenyl)methylene]-4-piperidinone
InChi Key: YUYPWAMLWZVHAE-KAVGSWPWSA-N
InChi Code: InChI=1S/C19H15N3O5/c23-19-15(9-13-1-5-17(6-2-13)21(24)25)11-20-12-16(19)10-14-3-7-18(8-4-14)22(26)27/h1-10,20H,11-12H2/b15-9+,16-10+
SMILES Code: O=C1/C(CNC/C1=C\C2=CC=C([N+]([O-])=O)C=C2)=C/C3=CC=C([N+]([O-])=O)C=C3
Ovarian cancer is the deadliest of the gynecologic malignancies. Carcinogenic progression is accompanied by upregulation of ubiquitin-dependent protein degradation machinery as a mechanism to compensate with elevated endogenous proteotoxic stress. Recent studies support the notion that deubiquitinating enzymes (DUB) are essential factors in proteolytic degradation and that their aberrant activity is linked to cancer progression and chemoresistance. Thus, DUBs are an attractive therapeutic target for ovarian cancer.
1. Coughlin K, Anchoori R, Iizuka Y, et al. Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian cancer in vitro and in vivo via exacerbating unfolded protein responses. Clin Cancer Res. 2014;20(12):3174‐3186. doi:10.1158/1078-0432.CCR-13-2658