ArticleJournal of medicinal chemistry2025
A Novel Class of Complement 3a Receptor Agonists and Antagonists Derived from the TLQP-21 Peptide.
Article in Journal of medicinal chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Molecular basis of diverse ligand recognition and species-specific pharmacology at the complement anaphylatoxin receptor C3aR.Nature communications · 2026Article
- Complement 3a Receptor mediates high fat diet induced hypothalamic accumulation of lipid associated microglia to regulate neuroinflammation and obesity.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The complement 3a receptor (C3aR) is a G-protein-coupled receptor (GPCR) involved in inflammatory, metabolic, and neurological diseases. Two endogenous ligands (C3a and TLQP-21) and small molecules (SB290157 and JR14a) differentially signal at C3aR, but these properties are not fully understood and need to be optimized with medicinal chemistry. Here, we generated rationally designed peptidergic analogues of TLQP-21 in an effort to extend the range of compounds with therapeutic potential beyond C3a-derived peptidergic agonists or small-molecule antagonists. We identified key arginines in the central portion of the peptide and the C-terminus, where mutation confers enhanced plasma stability. Mutations at the C-terminal motif alanine-arginine (-AlaArg), with unnatural amino acids and stereoisomers conferred signaling selectivity, enhanced peptide potency (e.g., DArg10_DAla20), or resulted in a functional antagonist (DArg10_Aib20). Overall, we increased our understanding of the C3aR mechanism of action, expanding and differentiating the range of therapeutic potentials for this GPCR.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.