ArticleFrontiers in immunology2026
Selpercatinib mitigates microglia-mediated neuroinflammation by inhibiting RET signaling and NLRP3 inflammasome activation.
Article in Frontiers in immunology, 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
Background: Selpercatinib is a highly selective rearranged during transfection (RET) receptor tyrosine kinase inhibitor approved for RET fusion-positive cancers and known to penetrate the blood-brain barrier. Although RET signaling has been implicated in neural development and cell survival, its role in microglia-mediated neuroinflammation and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation remains poorly understood. This study investigated whether Selpercatinib attenuates neuroinflammatory signaling in microglia by modulating RET-dependent kinase cascades. Methods: Neuroinflammation was induced in BV2 microglial cells using lipopolysaccharide (LPS; 200 ng/mL), followed by post-treatment with Selpercatinib (5 μM). For Results: Selpercatinib reduced RET phosphorylation at Tyr1062 in LPS-stimulated BV2 microglia and reduced the mRNA expression of proinflammatory mediators, including Conclusion: Selpercatinib attenuated the development of microglia-mediated neuroinflammatory responses through modulation of RET-associated AKT/ERK-NF-κB/CREB signaling and suppression of NLRP3 inflammasome activation. These findings provide a mechanistic basis for further investigating Selpercatinib as an early intervention agent for neuroinflammatory responses.
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