Dipyridamole

Category: pharmacological

Aliases: Persantine, Aggrenox (+ASA)

Pharmacological Mechanism

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.

Half-Life (t½)

PO: 12h, IV: 12h

Dosing Guidelines

PO: Typical 200 mg (Range: 200–200 mg)
IV: Typical 200 mg (Range: 200–200 mg)

Target Organ Systems

cardiovascular
immune-hematologic

Interactions

Caffeine (caution): Caffeine antagonises adenosine at A2A → reduces dipyridamole stress-test sensitivity. Hold caffeine 24 h prior.
Adenosine (major): Dipyridamole potentiates adenosine effects by blocking its reuptake — profound response to exogenous IV adenosine. [Meester 1998]

Pathways It Modulates

Adenosine receptor signaling (activator) — adenosine (indirect — blocks ENT1 uptake → ↑extracellular)
cAMP / PKA second-messenger signaling (inhibitor) — PDE3 + PDE5 + adenosine reuptake
PDE5 / NO-cGMP axis (inhibitor) — PDE3 + PDE5 (broad) + adenosine reuptake
Platelet aggregation (inhibitor) — PDE3 + adenosine reuptake
Purinergic signaling (activator) — ENT1 inhibition → ↑extracellular adenosine → P1 activation

Chemical Identifiers

PubChem CID: 3108
Formula: C24H40N8O4
Molecular weight: 504.62 g/mol
InChIKey: IZEKFCXSFNUWAM-UHFFFAOYSA-N
SMILES: C1CCN(CC1)C2=NC(=NC3=C2N=C(N=C3N4CCCCC4)N(CCO)CCO)N(CCO)CCO