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Drug-Target Interaction

Drug

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PubChem ID:466151
Structure:
Synonyms:
(3S)-N-hydroxy-2,2-dimethyl-4-(4-pyridin-4-yloxyphenyl)sulfonylthiomorphol
192329-42-3
3-Thiomorpholinecarboxamide, N-hydroxy-2,2-dimethyl-4-[[4-(4-pyridinyloxy)phenyl]sulfonyl]-, (3S)-
AC1LAD25
AG 3340
AG-3340
AG-3354
AG-3362
AG3340
AIDS-045699
AIDS045699
AKOS000280753
CHEBI:220195
CHEMBL75094
D03797
Prinomastat
Prinomastat (USAN/INN)

Target

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Uniprot ID:Q9Y354_HUMAN
Synonyms:
Matrix metalloproteinase 9
EC-Numbers:3.4.24.35
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

11726397
Ventilator-induced lung injury upregulates and activates gelatinases and EMMPRIN: attenuation by the synthetic matrix metalloproteinase inhibitor, Prinomastat (AG3340).. H D Foda; E E Rollo; M Drews; C Conner; K Appelt; D R Shalinsky; S Zucker (2001) American journal of respiratory cell and molecular biology display abstract
Mechanical ventilation has become an indispensable therapeutic modality for patients with respiratory failure. However, a serious potential complication of MV is the newly recognized ventilator-induced acute lung injury. There is strong evidence suggesting that matrix metalloproteinases (MMPs) play an important role in the development of acute lung injury. Another factor to be considered is extracellular matrix metalloproteinase inducer (EMMPRIN). EMMPRIN is responsible for inducing fibroblasts to produce/secrete MMPs. In this report we sought to determine: (1) the role played by MMPs and EMMPRIN in the development of ventilator-induced lung injury (VILI) in an in vivo rat model of high volume ventilation; and (2) whether the synthetic MMP inhibitor Prinomastat (AG3340) could prevent this type of lung injury. We have demonstrated that high volume ventilation caused acute lung injury. This was accompanied by an upregulation of gelatinase A, gelatinase B, MT1-MMP, and EMMPRIN mRNA demonstrated by in situ hybridization. Pretreatment with the MMP inhibitor Prinomastat attenuated the lung injury caused by high volume ventilation. Our results suggest that MMPs play an important role in the development of VILI in rat lungs and that the MMP-inhibitor Prinomastat is effective in attenuating this type of lung injury.