ReviewMedicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents2026
Advances in nucleotide-based P2Y₁ antagonism: implications for cardiovascular therapeutics.
Review in Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases (CVDs) remain a leading cause of global mortality, emphasizing the need for novel, mechanism-driven therapeutics. The P2Y₁ receptor (P2Y₁R), a G protein-coupled purinergic receptor activated by extracellular nucleotides, has emerged as a key regulator of cardiovascular function and dysfunction. Upon activation, P2Y₁R triggers phospholipase C (PLC)-dependent signaling, modulating platelet activation, vascular tone, endothelial integrity, and fibrotic remodeling. Dysregulated P2Y₁R signaling is implicated in thrombosis, atherosclerosis, hypertension, and abnormal platelet reactivity, highlighting its therapeutic potential. Nucleotide bisphosphate antagonists have played a pivotal role in elucidating P2Y₁R pharmacology and guiding drug discovery. The first-generation antagonist MRS2179 demonstrated proof-of-concept for competitive inhibition, but was limited by low potency and metabolic instability. Structural optimization led to MRS2279, exhibiting improved receptor affinity and enzymatic stability. Further refinement produced MRS2500, a highly potent and selective antagonist with nanomolar activity and robust in vivo antithrombotic efficacy without compromising hemostasis. This review integrates advances in P2Y₁R signaling, pharmacology, and structure-based design, emphasizing the evolution of nucleotide antagonists and their translational potential. These insights establish P2Y₁R antagonism as a promising strategy for next-generation cardiovascular therapeutics.
Indexed as
Identifiers
42566009What 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.