ulinastatin

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Ligands
ulinastatin (Human)

GtoPdb Ligand ID: 10359

Synonyms: Miraclid® | Ulinase® | Urinastatin®

ulinastatin is an approved drug (Japan, China)

Compound class: Endogenous peptide in human, mouse or rat

Comment: Ulinastatin is considered to be a metabolite of inter-α-trypsin inhibitor (ITI) that is one of the cleavage products from the AMBP precursor protein [3]. Compared to full length ITI, ulinastatin lacks the carboxyterminal RFSN amino acids. Functionally ulinastatin is a protease inhibitor, that plays an important role in physiological and pathological processes, and has notable anti-inflammatory activity [1-2,6]. It can be purified from healthy human urine or produced using recombinant technology.

Species: Human

Immunopharmacology Comments
Ulinastatin is a urinary proteinase inhibitor that is produced from the inter-α-trypsin inhibitor (ITI) protein via proteolytic degradation by neutrophil elastase during inflammation [5]. Its production is upregulated by pro-inflammatory cytokines (e.g. IL-6, IL-8, IL-1β and TNFα) and it acts to downregulate production of proinflammatory mediators including MMPs, CXC chemokines, cytokines, iNOS and suppress activation of MAP kinases and NF-κB and neutrophil accumulation and activity. Ulinastatin has also been shown to modulate the Treg cell population in rodent models of acute inflammation [1,4]. Its main physiological role appears to be to alleviate the inflammatory response and associated tissue/organ damage.

Immunopharmacology Comments

Ulinastatin is a urinary proteinase inhibitor that is produced from the inter-α-trypsin inhibitor (ITI) protein via proteolytic degradation by neutrophil elastase during inflammation [5]. Its production is upregulated by pro-inflammatory cytokines (e.g. IL-6, IL-8, IL-1β and TNFα) and it acts to downregulate production of proinflammatory mediators including MMPs, CXC chemokines, cytokines, iNOS and suppress activation of MAP kinases and NF-κB and neutrophil accumulation and activity. Ulinastatin has also been shown to modulate the Treg cell population in rodent models of acute inflammation [1,4]. Its main physiological role appears to be to alleviate the inflammatory response and associated tissue/organ damage.