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References from The ALK inhibitor lorlatinib attenuates lipopolysaccharide-induced neuroinflammation by inhibiting microglial activation and preserving blood–brain barrier integrity. Local targets link to admitted publications; unresolved targets remain external evidence.
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The semantics of microglia activation: neuroinflammation, homeostasis, and stress
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Innate immunity in the central nervous system
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Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets
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Dual microglia effects on blood brain barrier permeability induced by systemic inflammation
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Microglia at the blood brain barrier in health and disease
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The impact of microglial activation on blood-brain barrier in brain diseases
10.3389/fncel.2014.00362 · 2014 · External reference
Anaplastic lymphoma kinase (ALK): structure, oncogenic activation, and pharmacological inhibition
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The role of the ALK receptor in cancer biology
10.1093/annonc/mdw301 · 2016 · External reference
The anaplastic lymphoma kinase in the pathogenesis of cancer
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Emerging roles of ALK in immunity and insights for immunotherapy
2020 · External reference
ALK is a therapeutic target for lethal sepsis
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STING signaling in the brain: molecular threats, signaling activities, and therapeutic challenges
10.1016/j.neuron.2023.10.014 · 2024 · External reference
Inhibition of anaplastic lymphoma kinase protects from ischemic stroke
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Lorlatinib: first global approval
10.1007/s40265-018-1041-0 · 2019 · External reference
First macrocyclic 3rd-generation ALK inhibitor for treatment of ALK/ROS1 cancer: clinical and designing strategy update of lorlatinib
10.1016/j.ejmech.2017.04.032 · 2017 · External reference
Lorlatinib in patients with ALK-positive non-small-cell lung cancer: results from a global phase 2 study
10.1016/s1470-2045(18)30649-1 · 2018 · External reference
Therapeutic drug repositioning with special emphasis on neurodegenerative diseases: threats and issues
10.3389/fphar.2022.1007315 · 2022 · External reference
Lorlatinib protects dopaminergic neurons by inhibiting ALK-mediated neuroinflammation in a mouse model of Parkinson’s disease
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Anti-inflammatory mechanism of ginseng saponins in activated microglia
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Overcoming crizotinib resistance in ALK-rearranged NSCLC with the second-generation ALK-inhibitor ceritinib
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Cellular functions of cGAS-STING signaling
10.1016/j.tcb.2022.11.001 · 2023 · External reference
Reactive oxygen species in inflammation and tissue injury
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Emerging roles of Nrf2 and phase II antioxidant enzymes in neuroprotection
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The role of STING signaling in central nervous system infection and neuroinflammatory disease
2023 · External reference
Type I interferon response is mediated by NLRX1-cGAS-STING signaling in brain injury
2022 · External reference
Signaling by cGAS-STING in neurodegeneration, neuroinflammation, and aging
10.1016/j.tins.2020.10.008 · 2021 · External reference
STING-mediated type-I interferons contribute to the neuroinflammatory process and detrimental effects following traumatic brain injury
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10.1021/acsnano.3c03390 · 2023 · External reference
Blockade of STING activation alleviates microglial dysfunction and a broad spectrum of Alzheimer's disease pathologies
10.1038/s12276-024-01295-y · 2024 · External reference
STING mediates neurodegeneration and neuroinflammation in nigrostriatal a-synucleinopathy
10.1073/pnas.2118819119 · 2022 · External reference
Effect of chronic oxidative stress on neuroinflammatory response mediated by CD4+ T cells in neurodegenerative diseases
10.3389/fncel.2018.00114 · 2018 · External reference
The relationship between reactive oxygen species and the cGAS/STING signaling pathway in the inflammaging process
10.3390/ijms232315182 · 2022 · External reference
STING enhances cell death through regulation of reactive oxygen species and DNA damage
10.1038/s41467-021-22572-8 · 2021 · External reference
Oxidative stress-induced disruption of epithelial and endothelial tight junctions
10.2741/3223 · 2008 · External reference
The role of reactive oxygen species in integrin and matrix metalloproteinase expression and function
10.1080/03008200802143166 · 2008 · External reference
The blood-brain barrier: structure, regulation, and drug delivery
10.1038/s41392-023-01481-w · 2023 · External reference
Matrix metalloproteinases in neuroinflammation
10.1002/glia.10108 · 2002 · External reference
Implications of MMP9 for blood brain barrier disruption and hemorrhagic transformation following ischemic stroke
10.3389/fncel.2016.00056 · 2016 · External reference
Lipopolysaccharide-induced blood-brain barrier disruption: roles of cyclooxygenase, oxidative stress, neuroinflammation, and elements of the neurovascular unit
10.1186/s12974-015-0434-1 · 2015 · External reference
Lipopolysaccharide-induced middle ear inflammation disrupts the cochlear intra-strial fluid-blood barrier through down-regulation of tight junction proteins
2015 · External reference
10.1021/jm500261q
10.1021/jm500261q · 2014 · External reference
Evaluation of lorlatinib cerebrospinal fluid concentrations in relation to target concentrations for anaplastic lymphoma kinase (ALK) inhibition
10.1002/jcph.2056 · 2022 · External reference
Brain penetration of lorlatinib: cumulative incidences of CNS and non-CNS progression with lorlatinib in patients with previously treated ALK-positive non-small-cell lung cancer
10.1007/s11523-020-00702-4 · 2020 · External reference
CNS drug design: balancing physicochemical properties for optimal brain exposure
10.1021/jm501535r · 2015 · External reference
Cyp3a4-mediated in vitro metabolism and in vivo disposition of lorlatinib in rats
10.2147/dddt.s565228 · 2025 · External reference
Prediction of ALK mutations mediating ALK-TKIs resistance and drug re-purposing to overcome the resistance
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