H-ARG-ARG-ARG-PRO-ARG-PRO-PRO-TYR-LEU-PRO-ARG-PRO-ARG-PRO-PRO-PRO-PHE-PHE-PRO-PRO-ARG-LEU-PRO-PRO-ARG-ILE-PRO-PRO-GLY-PHE-PRO-PRO-ARG-PHE-PRO-PRO-ARG-PHE-PRO-NH2

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.
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).
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.

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.
PR-39 (1 μg/kg/day; 7-day intraperitoneal infusion) demonstrates significantly small infarct in C57BL/6 mice.