Predicate |
Object |
assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_ed3c2f63a5b1c705b1b389a6f1f1f7c8 http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_e3b4f2ef8f062dcde3a2b7cd81748472 http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_df02dc2eab1779ebc7dfb5accf94318b http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_43a72884e25aaecffebe0942132d704f |
classificationCPCAdditional |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2500-04 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K16-40 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2800-325 |
classificationCPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-7088 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-713 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q1-37 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K16-40 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K45-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K39-395 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P9-00 |
classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P9-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K16-40 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-713 |
filingDate |
2020-07-31-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_8957a700b0849d0e16d6649d9dd56576 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_0b47095d860b02526c719a680f91b6ee http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_3183747480c7789aa503f7aba60a8c56 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_ad99d31470133a13fc996d7dccbb57bf |
publicationDate |
2022-09-01-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber |
US-2022275105-A1 |
titleOfInvention |
Neutralizing granzyme b for providing cardioprotection in a subject who experienced a myocardial infarction |
abstract |
A method for providing cardioprotection in a subject who experienced a myocardial infarction, including administering a therapeutically effective amount of a Granzyme B inhibitor. Following acute MI in mice, CD8+ T lymphocytes are quickly recruited and activated in ischemic heart tissue, and release Granzyme B, leading to cardiomyocyte apoptosis and deterioration of myocardial function. Antibody-mediated depletion of CD8+ T lymphocytes decreases Granzyme B content and apoptotic within the myocardium and inflammatory response. mAb mediated-CD8 depletion limits myocardial injury and improves heart function. These effects are recapitulated in mice with CD8+ T cell selective Granzyme B deficiency in mice. Granzyme B is produced by other cell types (e.g., NK cells). Global Granzyme B deletion (GzmB-/- mice) decreases apoptotic within the myocardium, reduces local pro-inflammatory signature and ultimately limits infarct size after MI. Elevated circulating levels of Granzyme B in patients with acute MI predict increased risk of death after 1 year. |
priorityDate |
2019-08-02-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type |
http://data.epo.org/linked-data/def/patent/Publication |