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• W2897088921 endingPage "398" @default.
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• W2897088921 abstract "Blockade the interaction of the programmed cell death protein 1 (PD-1) and its ligand, programmed death-ligand 1 (PD-L1) can prevent immune evasion of tumor cells and significantly prolong the survival of cancer patients. Currently marketed drugs targeting PD-1/PD-L1 pathway are all monoclonal antibodies (mAbs) that have achieved great success in clinical trials. With the constantly emerging problems of antibody drugs, small molecule inhibitors have attracted the attention of pharmaceutical chemists due to their controllable pharmacological and pharmacokinetic properties, which make them potential alternatives or supplements to mAbs to regulate PD-1/PD-L1 pathway. However, the insufficient target structure information hinders the development of small molecule inhibitors. Since the publication of human-PD-1/human-PD-L1 (hPD-1/hPD-L1) crystal structure, more and more cocrystal structures of mAbs, cyclopeptides and small molecules with PD-1 and PD-L1 have been resolved. These complexes provide a valuable starting point for the rational design of peptide-based and small synthetic molecule inhibitors. Here we reviewed the non-antibody inhibitors that have been published so far and analyzed their structure-activity relationships (SAR). We also summarized the cocrystal structures with hot spots identified, with the aim to provide reference for future drug discovery." @default.
• W2897088921 created "2018-10-26" @default.
• W2897088921 creator A5020746135 @default.
• W2897088921 creator A5031755924 @default.
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• W2897088921 creator A5064248942 @default.
• W2897088921 creator A5069744037 @default.
• W2897088921 creator A5088889008 @default.
• W2897088921 date "2019-01-01" @default.
• W2897088921 modified "2023-10-18" @default.
• W2897088921 title "Peptide-based and small synthetic molecule inhibitors on PD-1/PD-L1 pathway: A new choice for immunotherapy?" @default.
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• W2897088921 doi "https://doi.org/10.1016/j.ejmech.2018.10.044" @default.
• W2897088921 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30384043" @default.
• W2897088921 hasPublicationYear "2019" @default.
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