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10.1016/j.xcrm.2025.102336 http://scihub22266oqcxt.onion/10.1016/j.xcrm.2025.102336 40914167!ä!40914167 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=40914167&cmd=llinks): Failed to open stream: HTTP request failed! 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ENPP1 inhibitor with ultralong drug-target residence time as an innate immune checkpoint blockade cancer therapy |pdf=|usr=}}{{40914167}} gab.com Text ENPP1 inhibitor with ultralong drug-target residence time as an innate immune checkpoint blockade cancer therapy JO: Cell Rep Med http://www.kidney.de/pget.php?&tw=1&pmid=40914167 #FOAvip Only one in five patients respond to immune checkpoint inhibitors, which primarily target adaptive immunity. Ectonucleotide pyrophosphatase/phophodiesterase 1 (ENPP1), the dominant hydrolase of 2'3'-cyclic-GMP-AMP (cGAMP) that suppresses downstream stimulator of interferon genes (STING) signaling, has emerged as a promising innate immunotherapy target. However, existing ENPP1 inhibitors have been optimized for prolonged systemic residence time rather than effective target inhibition within tumors. Here, we report the characterization of STF-1623, a highly potent ENPP1 inhibitor with an exceptionally long tumor residence time despite rapid systemic clearance, enabled by its high ENPP1 binding affinity and slow dissociation rate. We show that membrane-bound ENPP1 on tumor cells, not the abundant soluble ENPP1 in serum, drives tumor progression. Consequently, STF-1623 unleashes anti-tumor immunity to produce robust anti-tumor and anti-metastatic effects across multiple tumor models. Conceptually, this work establishes a noncovalent small-molecule inhibitor of ENPP1 with ultralong drug-target engagement as a safe and precise strategy to activate STING within tumors. Twit Text FOAVip ENPP1 inhibitor with ultralong drug-target residence time as an innate immune checkpoint blockade cancer therapy ????Cell Rep Med http://www.kidney.de/pget.php?&tw=1&pmid=40914167 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=40914167 #FOAvip English Wikipedia <ref>{{Cite pmid|40914167}}</ref> ENPP1 inhibitor with ultralong drug-target residence time as an innate immune checkpoint blockade cancer therapy #MMPMID40914167 Wang S; Johnson RM; Carozza JA; Fernandez D; Scicinski J; Verity NA; Mardjuki R; Cao X; Guo Y; Papkoff J; Ray N; Li L Cell Rep Med 2025[Aug]; ä (ä): 102336 PMID40914167show ga Only one in five patients respond to immune checkpoint inhibitors, which primarily target adaptive immunity. Ectonucleotide pyrophosphatase/phophodiesterase 1 (ENPP1), the dominant hydrolase of 2'3'-cyclic-GMP-AMP (cGAMP) that suppresses downstream stimulator of interferon genes (STING) signaling, has emerged as a promising innate immunotherapy target. However, existing ENPP1 inhibitors have been optimized for prolonged systemic residence time rather than effective target inhibition within tumors. Here, we report the characterization of STF-1623, a highly potent ENPP1 inhibitor with an exceptionally long tumor residence time despite rapid systemic clearance, enabled by its high ENPP1 binding affinity and slow dissociation rate. We show that membrane-bound ENPP1 on tumor cells, not the abundant soluble ENPP1 in serum, drives tumor progression. Consequently, STF-1623 unleashes anti-tumor immunity to produce robust anti-tumor and anti-metastatic effects across multiple tumor models. Conceptually, this work establishes a noncovalent small-molecule inhibitor of ENPP1 with ultralong drug-target engagement as a safe and precise strategy to activate STING within tumors. äENPP1 inhibitor with ultralong drug-target residence time as an innate(epmc).pdf DeepDyve Pubget Overpricing