Name | (2S)-1-[(2S)-1-[(2S)-1-[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-1-[2-[[1-[2-[[2-[(2-amino-5-guanidino-pentanoyl)amino]-5-guanidino-pentanoyl]amino]-5-guanidino-pentanoyl]pyrrolidine-2-carbonyl]amino]-5-guanidino-pentanoyl]pyrrolidine-2-carbonyl]pyrrolidine-2-carbonyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methyl-pentanoyl]pyrrolidine-2-carbonyl]amino]-5-guanidino-pentanoyl]pyrrolidine-2-carbonyl]amino]-5-guanidino-pentanoyl]pyrrolidine-2-carbonyl]pyrrolidine-2-carbonyl]-N-[(1S)-1-benzyl-2-[[(1S)-1-benzyl-2-[(2S)-2-[(2S)-2-[[(1S)-1-[[(1S)-1-[(2S)-2-[(2S)-2-[[(1S)-1-[[(1S,2S)-1-[(2S)-2-[(2S)-2-[[2-[[(1S)-1-benzyl-2-[(2S)-2-[(2S)-2-[[(1S)-1-[[(1S)-1-benzyl-2-[(2S)-2-[2-[[(1S)-1-[[(1S)-1-benzyl-2-(2-carbamoylpyrrolidin-1-yl)-2-oxo-ethyl]carbamoyl]-4-guanidino-butyl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-2-oxo-ethyl]carbamoyl]-4-guanidino-butyl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-2-oxo-ethyl]amino]-2-oxo-ethyl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidine-1-carbonyl]-2-methyl-butyl]carbamoyl]-4-guanidino-butyl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidine-1-carbonyl]-3-methyl-butyl]carbamoyl]-4-guanidino-butyl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-2-oxo-ethyl]amino]-2-oxo-ethyl]pyrrolidine-2-carboxamide |
---|
Description | PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice[1][2]. |
---|---|
Related Catalog | |
In Vitro | PR-39, shown to selectively affect proteasomemediated protein degradation in vivo, alters the shape of the 20S and 26S cylinder and affects the binding of 19S caps in a reversible manner. PR-39 specifically blocks degradation of IκBα and HIF-1α by the proteasome[1]. PR-39 (100 nM) blocks TNF-α-induced (1 ng/mL; for 20 minutes) activation of VCAM-1 (2 hours) and ICAM-1 (8 hours) expression in human umbilical vein endothelial cells (HUVEC)[2]. PR-39 (10 μM) does not affect the ability to proliferate of ECV304 cell. PR39 is able to inhibit IκBα degradation without significantly affecting overall protein degradation in cells[2]. |
In Vivo | PR-39 (10 mg/kg, intravenously; 1 hour before Caerulein of 50μg/kg, ip) blocks IκBα degradation and NF-κB-dependent transcription in the mouse pancreas after induction of acute pancreatitis[2]. PR-39 (1 μg/kg/day; 7-day intraperitoneal infusion) demonstrates significantly small infarct in C57BL/6 mice[2]. |
References |
Molecular Formula | C229H345N70O40 |
---|---|
Molecular Weight | 4720.627 |
Hazard Codes | Xi |
---|