ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026
Curated set of tool compounds to probe PYK2 and FAK signaling in Alzheimer's disease.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionProline-rich tyrosine kinase 2 (PYK2) and focal adhesion kinase (FAK) are non-receptor tyrosine kinases implicated in Alzheimer's disease (AD), but their functional role in microglia remains understudied. Selective pharmacological tools are required for preclinical studies leading to translational therapeutic development.
methodsWe evaluated potent and selective inhibitors described in publications and patents, synthesized or procured representative compounds, and profiled them in kinase assays. In vitro physicochemical and pharmacokinetic (PK) properties were assessed, and functional effects were studied in microglial phagocytosis assays using HMC3 and BV2 microglia cellular models.
resultsBiochemical profiling confirmed potent and selective inhibition, consistent with reported data, though assay-dependent differences in apparent selectivity were observed. Most compounds showed favorable physicochemical and PK properties. In HMC3 assay, the PYK2-selective tool compounds showed that strong stimulation of phagocytosis and parallel cell counts declined at non-toxic concentrations. DISCUSSION: This curated set of well-characterized inhibitors provides a validated toolkit to probe PYK2/FAK biology in AD-relevant models.
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