| Predicate |
Object |
| assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_d21cbff64022f95c237c0bd3ec8656ca |
| classificationCPCAdditional |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K2319-10 |
| classificationCPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-705
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K38-08
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K9-0019
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K9-0073
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P11-00
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K47-645 |
| classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K7-04
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K9-14
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K14-705
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-49
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-17
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-08 |
| filingDate |
2019-11-21-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_281e6e167a62bbe0a0d1701f74ba1805 |
| publicationDate |
2020-05-28-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber |
WO-2020106922-A1 |
| titleOfInvention |
Peptide therapeutics for acute and chronic airway and alveolar diseases |
| abstract |
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease encompassing chronic bronchitis, emphysema and remodeling of small airways that can be treated by the caveolin-1 peptide CSP7 (SEQ ID NO:1). Chronic tobacco smoke exposure (TSE)-induced lung injury includes increased alveolar and airway inflammation, type II alveolar epithelial cells (A2Cs) senescence and apoptosis, and mucus hypersecretion by AECs. Interleukin 17A-mediated induction of plasminogen activator inhibitor-1 (PAI-1) expression through caveolin-1 led to TSE-induced lung injury, which was abrogated by CSP7 treatment which abolished A2Cs senescence and apoptosis, and AECs mucus hypersecretion in TSE wild type (WT) mice. Ex vivo CSP7 treatment of lung tissue of COPD patients decreased A2C apoptosis and AEC mucus hypersecretion. Lung injury induced by PAI-1 expression in COPD lung tissue and WT mice (20 weeks TSE), with A2Cs senescence and apoptosis, and AEC mucus hypersecretion was abolished by CSP7. |
| isCitedBy |
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2022119776-A1
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11787838-B2
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/EP-3937966-A4 |
| priorityDate |
2018-11-21-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type |
http://data.epo.org/linked-data/def/patent/Publication |