Key result
Sustained-release aspirin 50 mg achieves equivalent steady-state platelet inhibition vs enteric-coated aspirin 100 mg.
Why the study?
The pharmacodynamic effects of enteric-coated sustained-release aspirin under multiple-dose conditions remained unknown.
Does 50 mg enteric-coated sustained-release aspirin provide equivalent steady-state platelet inhibition compared to 100 mg enteric-coated aspirin in healthy Chinese males?
RCT (n=12)
Open-label
Block randomization
No
Does 50 mg enteric-coated sustained-release aspirin provide equivalent steady-state platelet inhibition compared to 100 mg enteric-coated aspirin in healthy Chinese males?
Effect estimate: GMR 1.11 (95% CI 0.96-1.27)
p-value: p=>0.05
A 50 mg dose of enteric-coated sustained-release aspirin achieves equivalent steady-state platelet inhibition to 100 mg conventional enteric-coated aspirin, offering a potentially safer low-dose option for cardiovascular prevention in Asian populations.
Supports lower-dose sustained-release aspirin for equivalent steady-state platelet inhibition; extends single-dose PK/PD observations to repeated dosing in an RCT.
Whereas our previous single-dose study characterized the distinct pharmacokinetic (PK) profile of enteric-coated sustained-release (ECSR) aspirin compared with enteric-coated (EC) aspirin, featuring prolonged absorption and reduced variability, its pharmacodynamic (PD) effects under multiple-dose conditions remain unknown. This study was designed to compare the multiple-dose PK and PD profiles of 50 mg ECSR aspirin versus 100 mg EC aspirin. An open-label, randomized, two-sequence, crossover study was conducted in 12 healthy Chinese male subjects. Participants received either 100 mg EC or 50 mg ECSR aspirin daily for 10 consecutive days. PK parameters and PD biomarkers, including serum thromboxane B 2 (TXB 2 ), urinary 11-dehydro-thromboxane B 2 (11-dehydro-TXB 2 ) and 2,3-dinor-6-keto prostaglandin F 1α (2,3-dinor-6-keto PGF 1α ), were assessed. PK analysis revealed that dose-normalized systemic exposure to the parent drug (acetylsalicylic acid, ASA) for the ECSR formulation was only 37% of that for the EC formulation, indicative of extensive pre-systemic first-pass metabolism. However, the total extent of absorption was well preserved, with the primary metabolite (salicylic acid, SA) exposure reaching 77% of the EC group. Pharmacodynamically, although ECSR exhibited a delayed onset of platelet inhibition during Day 1 and Day 2, its efficacy progressively accumulated. By steady state (Days 9–10), the 50 mg ECSR achieved statistically equivalent inhibition of serum TXB 2 and urinary 11-dehydro-TXB 2 compared to 100 mg EC. Furthermore, both formulations showed no significant difference in urinary 2,3-dinor-6-keto PGF 1α excretion throughout the study, indicating comparable preservation of vascular endothelial prostacyclin synthesis. Despite a 50% dose reduction and a delayed initial onset, 50 mg ECSR aspirin achieves equivalent steady-state platelet inhibition to 100 mg EC aspirin. Given the higher bleeding risk in Asian populations, this lower-dose formulation with more predictable absorption may provide a safer and more reliable option for long-term cardiovascular prevention in Chinese populations. ChiCTR2500112317, retrospectively registered in https://www.chictr.org.cn/ on 12 November 2025.
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Xu et al. (2026) conducted an RCT in Healthy (n=12). Enteric-coated sustained-release aspirin vs. Enteric-coated aspirin 100 mg daily was evaluated on Urinary 11-dehydro-TXB2 excretion at Day 10 (GMR 1.11, 95% CI 0.96-1.27, p=>0.05). Enteric-coated sustained-release aspirin 50 mg achieved equivalent steady-state platelet inhibition compared to 100 mg enteric-coated aspirin after 10 consecutive days of administration.
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