from the context , extract pharmakokinetic parameters and create a table that contains (parameter , value ,pharmacokinetic phase , target  )  . context:"Pharmacokinetics
Aspirin, ASA; dipyridamole is administered orally. Aggrenox is formulated to provide 25 mg of aspirin for immediate-release and 200 mg of dipyridamole for extended-release. There are no significant interactions between aspirin and dipyridamole. The kinetics of the components are unchanged by their coadministration as Aggrenox.
Aspirin: Aspirin is poorly bound to plasma proteins with an apparent volume of distribution (Vd) of 10 L. Its metabolite, salicylic acid, is highly bound to plasma proteins, but its binding is concentration-dependent (nonlinear). At low concentrations (less than 100 mcg/mL), approximately 90% of salicylic acid is bound to albumin. Salicylic acid is widely distributed to all tissues and fluids in the body, including the central nervous system, breast milk, and fetal tissues. Aspirin is rapidly hydrolyzed to salicylic acid and other metabolites, with a half-life of about 20 minutes. Salicylic acid, but not aspirin itself, undergoes saturable kinetics resulting in a decrease in total body clearance at higher serum concentrations. At low doses, the elimination is first-order and the half-life remains constant at 2 to 3 hours. At higher doses, salicylic acid elimination follows zero-order kinetics, with an apparent half-life of 6 hours or greater. Salicylic acid and its metabolites are excreted primarily by the kidneys. Almost all the ingested dose is excreted in the urine. Following therapeutic doses, about 75% is excreted as salicyluric acid, as phenolic and acyl glucuronides, and 10% as salicylic acid in the urine. The excretion of salicylic acid (but not other metabolites) is enhanced by alkalinization of the urine which is used in the management of aspirin overdose. As urinary pH rises above 6.5, the renal clearance of free salicylate increases from less than 5% to greater than 80%.
Dipyridamole: Dipyridamole distributes widely throughout the body tissues, crosses the placenta, and is secreted into breast milk. Approximately 99% of dipyridamole is bound to plasma proteins, predominantly to alpha 1-acid glycoprotein and albumin. Dipyridamole is highly lipophilic; however, the drug does not cross the blood-brain barrier to any significant extent in animal models. The steady-state Vd of dipyridamole is approximately 92 L. Dipyridamole undergoes hepatic metabolism, primarily glucuronidation, and these glucuronide conjugates are eliminated mainly in the feces, although enterohepatic circulation can occur. Renal excretion of dipyridamole is negligible and urinary excretion of the glucuronide metabolite is low (about 5%). The terminal phase plasma half-life following oral administration is 13.6 hours.
 
Affected cytochrome P450 (CYP) isoenzymes and drug transporters: none

Oral Route
Aspirin; dipyridamole: When aspirin, ASA; dipyridamole capsules are taken with a high-fat meal, the AUC for aspirin is unchanged and the Cmax for aspirin is decreased by 50%; this effect is not considered clinically significant based on a similar degree of cyclooxygenase inhibition for the fed versus the fasted state. Coadministration of aspirin, ASA; dipyridamole capsules with a high-fat meal decreases dipyridamole Cmax and AUC values by 20 to 30% compared to fasting; this effect is not considered clinically significant based on similar inhibition of adenosine uptake at these dipyridamole plasma concentrations. Following twice-daily oral administration of aspirin, ASA 25 mg; dipyridamole 200 mg, peak plasma levels of salicylic acid and dipyridamole are achieved in 0.63 hours (0.5 to 1 hours) and 2 hours (range 1 to 6 hours), respectively. The peak plasma concentration at steady-state for salicylic acid is 319 ng/mL (175 to 463 ng/ml); the dipyridamole peak plasma concentration at steady-state is 1.98 mcg/mL (1.01 to 3.99 mcg/mL), and the steady-state trough concentration is 0.53 mcg/mL (0.18 to 1.01 mcg/mL).

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