Carbonic Anhydrase II inhibitors, such as acetazolamide, can significantly increase effects of aspirin by prolonging it's half-life.
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Aspirin is a potent performance-enhancing and anti-aging drug (Unveiling the anti-glycation properties of acetylsalicylic acid: targeted inhibition of albumin glycation. Amino Acids. 2026 Feb 6;58(1):11. doi: 10.1007/s00726-026-03501-9). However, it's effectiveness is limited by it's very short half-life and metamorphosis into metabolite, salicylic acid, that lacks many beneficial properties of aspirin and is cytotoxic at high doses (Too much of a good thing: Long-term treatment with salicylate strengthens outer hair cell function but impairs auditory neural activity. Hear Res. 2010 June 14; 265(0): 63–69. doi:10.1016/j.heares.2010.02.010).
In article "Aspirin: A Suicide Inhibitor of Carbonic Anhydrase II" (Biomolecules. 2020 Mar 31;10(4):527. doi: 10.3390/biom10040527) researchers found that aspirin inhibits Carbonic Anhydrase II, enzyme that metabolizes carbon dioxide, and in this process it is converted into salicylic acid. Quote:
"we provide kinetic data to support the observation that CAII converts Aspirin to its deacetylated form, SA. This data may also explain the short half-life of Aspirin, with CAII so abundant in blood, and that Aspirin could act as a suicide inhibitor of CAII. ... We have identified CAII as the carboxylesterase responsible for Aspirin’s short half-life in the blood. Therefore, perhaps a combined therapy with a CA inhibitor and Aspirin could improve Aspirin’s efficacy in the treatment of heart disease." -
does the free acetyl also have this interactions with CAII?
