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Conflicts of Interest The authors declare no conflicts of interest. Data Availability Statement The data that support the findings of this study are available from the corresponding author upon reasonable request. Supporting Information Filename Description cbf70177-sup-0001-07_Supplementary_material.docx67.7 KB Figure 1S: IC50 values of 6-MP, 6MP/propolis, 5-FU, and 5-FU/propolis in MCF-7 and HepG2.
Abstract Pharmacogenetics can enhance cardiovascular disease (CVD) treatment by tailoring drug therapy to genetic profiles and minimising trial-and-error approaches. Genetic variability influences responses to common CVD drugs, including antiplatelet drugs (clopidogrel and aspirin), anticoagulants (warfarin), statins, and antihypertensives (ACE inhibitors and β-blockers). Understanding genetic polymorphisms can improve efficacy and safety.
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