Key result
SP1999-null mice exhibited highly prolonged bleeding times (>30 minutes compared to 3.5 minutes in wild-type mice) and impaired ADP-induced platelet aggregation, identifying SP1999 as the P2Y12 receptor.
Population
SP1999-null mice
Comparison
Genetic knockout of SP1999 and oral clopidogrel… vs Normal/wild-type mice (implied)
Design
Preclinical
Authors
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Confirms SP1999 as P2Y12 in mice; leaves open human validation and antithrombotic translation.
Absolute Event Rate: 30% vs 3.5%
This preclinical study identifies the orphan receptor SP1999 as the P2Y12 receptor, the molecular target of thienopyridine antithrombotic drugs such as clopidogrel.
Foster et al. (2001) studied Thrombosis and Hemostasis (Preclinical) (n=14). SP1999 (P2Y12) gene knockout vs. Wild-type was evaluated on Bleeding time. SP1999-null mice exhibited highly prolonged bleeding times (>30 minutes compared to 3.5 minutes in wild-type mice) and impaired ADP-induced platelet aggregation, identifying SP1999 as the P2Y12 receptor.
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