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c1q inhibitor  (Sanquin)

 
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    Sanquin c1q inhibitor
    C1q Inhibitor, supplied by Sanquin, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/c1q+inhibitor/c1+inhibitor/pmc13154114-54-0-9
    Average 86 stars, based on 1 article reviews
    c1q inhibitor - by Bioz Stars, 2026-10
    86/100 stars

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    Article Title: Engineering Liposomes and Polymer Conjugates: A Platform for Mechanistic Complement Activation Studies and Controlled Release Applications
    Article Snippet: C1q inhibitor (monoclonal mouse anti-C1q85 antibody) was obtained from Sanquin (Amsterdam, Netherlands).



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    Microglia-mediated synaptic plasticity (schematic diagram, created with BioRender). Under physiological conditions in the CNS, microglia precisely regulate synaptic plasticity through multiple canonical signaling pathways. (1) “Find-me” signals: CX3CL1 exists in membrane-bound (mCX3CL1) and soluble forms (sCX3CL1), mediating adhesion and chemotaxis, respectively, both of which bind to microglial CX3CR1 to promote targeted recruitment to synaptic sites. (2) “Eat-me” signals: PS exposure on less active synapses is recognized by microglial receptors such as GPR56 and MERTK, promoting synaptic engulfment. Complement signaling also plays a central role, with <t>C1q</t> and C3 deposition facilitating C3b generation and binding to CR3 on microglia, thereby driving phagocytosis. (3) “Do not-eat-me” signals: neuronal CD47 and CD200 interact with microglial SIRP α and CD200R, respectively, suppressing excessive synaptic pruning. In glaucoma, microglia show increased numbers and morphological activation, colocalizing with degenerating RGC synaptic elements, alongside abnormal complement activation (notably upregulated C1q), suggesting their involvement in synaptic remodeling, although the precise mechanisms remain to be elucidated.
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    Microglia-mediated synaptic plasticity (schematic diagram, created with BioRender). Under physiological conditions in the CNS, microglia precisely regulate synaptic plasticity through multiple canonical signaling pathways. (1) “Find-me” signals: CX3CL1 exists in membrane-bound (mCX3CL1) and soluble forms (sCX3CL1), mediating adhesion and chemotaxis, respectively, both of which bind to microglial CX3CR1 to promote targeted recruitment to synaptic sites. (2) “Eat-me” signals: PS exposure on less active synapses is recognized by microglial receptors such as GPR56 and MERTK, promoting synaptic engulfment. Complement signaling also plays a central role, with <t>C1q</t> and C3 deposition facilitating C3b generation and binding to CR3 on microglia, thereby driving phagocytosis. (3) “Do not-eat-me” signals: neuronal CD47 and CD200 interact with microglial SIRP α and CD200R, respectively, suppressing excessive synaptic pruning. In glaucoma, microglia show increased numbers and morphological activation, colocalizing with degenerating RGC synaptic elements, alongside abnormal complement activation (notably upregulated C1q), suggesting their involvement in synaptic remodeling, although the precise mechanisms remain to be elucidated.
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    Microglia-mediated synaptic plasticity (schematic diagram, created with BioRender). Under physiological conditions in the CNS, microglia precisely regulate synaptic plasticity through multiple canonical signaling pathways. (1) “Find-me” signals: CX3CL1 exists in membrane-bound (mCX3CL1) and soluble forms (sCX3CL1), mediating adhesion and chemotaxis, respectively, both of which bind to microglial CX3CR1 to promote targeted recruitment to synaptic sites. (2) “Eat-me” signals: PS exposure on less active synapses is recognized by microglial receptors such as GPR56 and MERTK, promoting synaptic engulfment. Complement signaling also plays a central role, with C1q and C3 deposition facilitating C3b generation and binding to CR3 on microglia, thereby driving phagocytosis. (3) “Do not-eat-me” signals: neuronal CD47 and CD200 interact with microglial SIRP α and CD200R, respectively, suppressing excessive synaptic pruning. In glaucoma, microglia show increased numbers and morphological activation, colocalizing with degenerating RGC synaptic elements, alongside abnormal complement activation (notably upregulated C1q), suggesting their involvement in synaptic remodeling, although the precise mechanisms remain to be elucidated.

    Journal: Frontiers in Neuroscience

    Article Title: Microglial regulation of synaptic plasticity in transsynaptic degeneration of glaucoma

    doi: 10.3389/fnins.2026.1828085

    Figure Lengend Snippet: Microglia-mediated synaptic plasticity (schematic diagram, created with BioRender). Under physiological conditions in the CNS, microglia precisely regulate synaptic plasticity through multiple canonical signaling pathways. (1) “Find-me” signals: CX3CL1 exists in membrane-bound (mCX3CL1) and soluble forms (sCX3CL1), mediating adhesion and chemotaxis, respectively, both of which bind to microglial CX3CR1 to promote targeted recruitment to synaptic sites. (2) “Eat-me” signals: PS exposure on less active synapses is recognized by microglial receptors such as GPR56 and MERTK, promoting synaptic engulfment. Complement signaling also plays a central role, with C1q and C3 deposition facilitating C3b generation and binding to CR3 on microglia, thereby driving phagocytosis. (3) “Do not-eat-me” signals: neuronal CD47 and CD200 interact with microglial SIRP α and CD200R, respectively, suppressing excessive synaptic pruning. In glaucoma, microglia show increased numbers and morphological activation, colocalizing with degenerating RGC synaptic elements, alongside abnormal complement activation (notably upregulated C1q), suggesting their involvement in synaptic remodeling, although the precise mechanisms remain to be elucidated.

    Article Snippet: Regarding complement-targeted inhibition strategies, the C1q inhibitor ANX007 (Annexon Biosciences) has completed a phase I clinical trial.

    Techniques: Protein-Protein interactions, Membrane, Chemotaxis Assay, Binding Assay, Activation Assay

    Pharmacological clinical trials registered at the World Health Organization (WHO) International Clinical Trials Research Platform (ICTRP) for people with Huntington’s disease (HD) since the first edition of the “Huntington’s Disease Clinical Trials Update”. N/S, not specified; HTT, Huntingtin; PD, Parkinson’s disease; SCA1, spinocerebellar ataxia 1; SCA3, spinocerebellar ataxia 3; VMAT2, Vesicular Monoamine Transporter 2. Note: IONIS-HTT Rx , ISIS 443139, RG6042 and tominersen refer to the same molecule. New trials added since the last Clinical Trials Update are indicated by *

    Journal: Journal of Huntington's Disease

    Article Title: Huntington’s Disease Clinical Trials Corner: March 2024

    doi: 10.3233/JHD-240017

    Figure Lengend Snippet: Pharmacological clinical trials registered at the World Health Organization (WHO) International Clinical Trials Research Platform (ICTRP) for people with Huntington’s disease (HD) since the first edition of the “Huntington’s Disease Clinical Trials Update”. N/S, not specified; HTT, Huntingtin; PD, Parkinson’s disease; SCA1, spinocerebellar ataxia 1; SCA3, spinocerebellar ataxia 3; VMAT2, Vesicular Monoamine Transporter 2. Note: IONIS-HTT Rx , ISIS 443139, RG6042 and tominersen refer to the same molecule. New trials added since the last Clinical Trials Update are indicated by *

    Article Snippet: NCT04514367 , – , ANX005 , C1q inhibitor , Early HD , None , Safety at 36 weeks , Single-dose open label trial , 28 , Annexon, Inc , USA (multi-center).

    Techniques: Clinical Proteomics, Small Interfering RNA, Activation Assay, Western Blot, Drug discovery, Comparison