IMMUNE MODULATION AND ApTOLL
After a stroke, cell damage induced by the lack of blood supply causes the release of endogenous cell components to the extracellular medium, triggering central nervous system alarms. One of the primary sensors of these brain damage-associated molecular patterns (DAMPs) is TLR4, a central receptor in innate immunity and expressed on the plasmatic membrane of immune cells such as microglia, neutrophils, monocytes, macrophages, among others. TLR4’s activation initiates a cascade of triggers that ultimately leads to the production and release of pro-inflammatory mediators, causing inflammation, further cell damage, and subsequent worsening of the brain lesion. ApTOLL has a powerful immunomodulatory effect through antagonistic action on TLR4 receptors, inhibiting the inflammatory cascade.
Scientific publications
ApTOLL: A new therapeutic aptamer for cytoprotection and (re)myelination after multiple sclerosis
British Journal of Pharmacology (2024)
Beneficial effect of TLR4 blockade by a specific aptamer antagonist after acute myocardial infarction
Biomedicine & Pharmacotherapy (2023)
Targeting TLR4 with ApTOLL Improves Heart Function in Response to Coronary Ischemia Reperfusion in Pigs Undergoing Acute Myocardial Infarction
Biomolecules (2020)
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