Dipyridamole
Dipyridamole. Inhibits adenosine uptake (ENT) + cyclic-GMP phosphodiesterase → raises extracellular adenosine + cGMP → platelet inhibition +… Oral half-life 12 h.
Inhibits adenosine uptake (ENT) + cyclic-GMP phosphodiesterase → raises extracellular adenosine + cGMP → platelet inhibition + vasodilation. IV use causes coronary vasodilation for pharmacologic stress testing. Weaker antiplatelet than aspirin alone; value is in secondary stroke prevention combined with low-dose ASA.
PK: F 0.52 is verbatim and stands. The stored 12 h was NOT the paper measurement but a CHRONIC-DOSING accumulation estimate in 20 bypass patients ("the terminal half-life averaged about half a day"), displacing that same paper single-dose intravenous figure of 11.6 h. V 175 L appears nowhere; the stated value is 141 L. The corrected triple is self-consistent — clearance 138 ml/min with 141 L implies 11.8 h against the stated 11.6 — whereas the stored 175 L with 12 h implied a clearance 22% above the measured one. EFFECT IS STRONGLY DECOUPLED AND THE PD LAYER SHOULD BE TREATED AS UNVALIDATED: the drug is 99.13% protein bound, acts by potentiating ENDOGENOUS adenosine, and one study states outright that "dipyridamole concentrations did not correlate with changes in diastolic or systolic blood pressure, or heart rate". A reference in this record is a GUINEA-PIG receptor paper with no pharmacokinetics at all. ka 2.59 dropped; absorption is pH-gated, and in one study two of twenty patients had UNDETECTABLE levels, which no first-order rate can represent.
Pharmacokinetics
- Oral — t½ 11.6 h · F 52% · Vd 141 L
- IV — t½ 11.6 h · F 100% · Vd 141 L
Related compounds
Sources: PMID:6579711, PMID:9690865, PMID:1570231