{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mazaleuskaya LL"],"funding":["National Center for Advancing Translational Sciences","Institute for Translational Medicine and Therapeutics","NCATS NIH HHS","NHLBI NIH HHS","National Institutes of Health","Perelman School of Medicine, University of Pennsylvania"],"pagination":["128313"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8484072"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["50"],"pubmed_abstract":["Activated macrophages overexpress the folate receptor β (FR-β) that can be used for targeted delivery of drugs conjugated to folic acid. FR-expressing macrophages contribute to arthritis progression by secreting prostaglandin E<sub>2</sub> (PGE<sub>2</sub>). Non-steroidal anti-inflammatory drugs (NSAIDs) block PGs and thromboxane by inhibiting the cyclooxygenase (COX) enzymes and are used for chronic pain and inflammation despite their well-known toxicity. New NSAIDs target an enzyme downstream of COXs, microsomal prostaglandin E synthase-1 (mPGES-1). Inhibition of mPGES-1 in inflammatory macrophages promises to retain NSAID efficacy while limiting toxicity. We conjugated a potent mPGES-1 inhibitor, MK-7285, to folate, but the construct released the drug inefficiently. Folate conjugation t"],"journal":["Bioorganic & medicinal chemistry letters"],"pubmed_title":["Targeted delivery of mPGES-1 inhibitors to macrophages via the folate receptor-β for inflammatory pain."],"pmcid":["PMC8484072"],"funding_grant_id":["U54 HL117798","HL117798","UL1TR001878","UL1 TR001878"],"pubmed_authors":["Lee S","Mazaleuskaya LL","Winkler JD","FitzGerald GA","Meng H"],"additional_accession":[]},"is_claimable":false,"name":"Targeted delivery of mPGES-1 inhibitors to macrophages via the folate receptor-β for inflammatory pain.","description":"Activated macrophages overexpress the folate receptor β (FR-β) that can be used for targeted delivery of drugs conjugated to folic acid. FR-expressing macrophages contribute to arthritis progression by secreting prostaglandin E<sub>2</sub> (PGE<sub>2</sub>). Non-steroidal anti-inflammatory drugs (NSAIDs) block PGs and thromboxane by inhibiting the cyclooxygenase (COX) enzymes and are used for chronic pain and inflammation despite their well-known toxicity. New NSAIDs target an enzyme downstream of COXs, microsomal prostaglandin E synthase-1 (mPGES-1). Inhibition of mPGES-1 in inflammatory macrophages promises to retain NSAID efficacy while limiting toxicity. We conjugated a potent mPGES-1 inhibitor, MK-7285, to folate, but the construct released the drug inefficiently. Folate conjugation t","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2025-04-22T12:09:50.855Z","creation":"2025-04-06T00:12:58.254Z"},"accession":"S-EPMC8484072","cross_references":{"pubmed":["34390827"],"doi":["10.1016/j.bmcl.2021.128313"]}}