http://rdf.ncbi.nlm.nih.gov/pubchem/patent/CN-109833321-A

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assignee http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_008c9107ff464e201e724ad32b7630cc
classificationIPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P35-00
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-616
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-44
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-196
filingDate 2017-11-28-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_3059e696380c352fc124336aa628bcc0
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_cd7adc3961b66f442010346a2bcb3f77
publicationDate 2019-06-04-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber CN-109833321-A
titleOfInvention It is a kind of to reverse liver cancer cells to the pharmaceutical composition of sorafenib drug resistance
abstract Pharmaceutical composition of the invention is related to inhibitor Aspirin, Flufenamic acid of the key enzyme AKR1C3 on a kind of prostaglandin synthesis access, and collaboration Sorafenib can reverse liver cancer cells to the drug resistance of sorafenib in low concentration.The method specifically used is the sorafenib collective effect of AKR1C3 inhibitor Aspirin, Flufenamic acid and low concentration in the drug resistant HepG2 hepatoma cell strain of sorafenib, the growth of the drug resistant HepG2 cell of sorafenib can significantly be inhibited, thus to overcome sorafenib drug resistance to provide effective method.
isCitedBy http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2021110085-A1
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/CN-114917214-A
priorityDate 2017-11-28-04:00^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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