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http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_48aeabf6526dce1cf810644e397533ce
classificationCPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-343
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K33-24
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K33-243
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filingDate 2015-01-16-04:00^^<http://www.w3.org/2001/XMLSchema#date>
grantDate 2017-09-12-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_fb900d43874757a91df820ea68495009
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_4f90eaadde1ed17018dae2fefbb5ca68
publicationDate 2017-09-12-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-9757350-B2
titleOfInvention Small molecule inhibitors of replication protein A that also act synergistically with cisplatin
abstract Replication protein A (RPA) is a single-strand DNA-binding protein with essential roles in DNA replication, recombination and repair. Small molecule inhibitors (SMIs) with the ability to disrupt RPA binding activity to ssDNA have been identified and assessed using both lung and ovarian cancer cell lines. Lung cancer cell lines demonstrated increased apoptotic cell death following treatment with the SMI MCI13E, with IC50 values of ˜5 μM. The A2780 ovarian cancer cell line and the p53-null lung cancer cell line HI 299 were particularly sensitive to MCI13E treatment with IC 50 values below 3 μM. Sequential treatment with MCI13E and cisplatin resulted in synergism, suggesting that decreasing RPA's DNA binding activity via a SMI may disrupt RPA's role in cell cycle regulation. Thus, RPA SMIs hold the potential to be used as single agent chemotherapeutics or in combination with current chemotherapeutic regimens to increase their efficacy.
priorityDate 2010-09-17-04:00^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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