MNP2
MNP2 is a NLRP3-ASC interaction inhibitor. MNP2 selectively binds to the PYD domain of ASC (Ka=149 nM) and blocks ASC-PYM binding (Ka=58 nM), thereby inhibiting the interaction between ASC and NLRP3 and suppressing the formation of the NLRP3 inflammasome. MNP2 inhibits IL-1β release and caspase-1 maturation, and reduces the efflux of potassium and chloride ions. MNP2 prevents mitochondrial damage and reactive oxygen species production, and significantly decreases NLRP3 inflammasome formation in neurodegenerative pathologies induced by β-amyloid, Tau protein and α-synuclein. MNP2 is applicable for the research of neurodegenerative diseases.
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- Formule: C56H94N18O12
- Masse moléculaire:1211.46
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
IC50 & Target
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Caspase-1 |
IL-1β |
NLRP3 inflammasome |
α-synuclein |
In Vitro
MNP2 (20-100 μM; 24 h) potently inhibits NLRP3 inflammasome activation in N9 microglia, with an IC50 of 2.57 μM for IL-1β and 16.23 μM for caspase-1, while also resisting pyroptosis induced by 1 μg/mL LPS+ATP or LPS+Aβ/Tau/α-Syn[1].
MNP2 (100 μM; 24-48 h) remains stable for 48 hours in fetal bovine serum (FBS) and for 24 hours in human serum[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:N9 microglial cells
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Concentration:100 μM; stimulated with LPS (1 μg/mL), ATP (5 mM), Aβ oligomer (10 μM), Tau oligomer (5 μM), and α- Syn (5 μM)
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Incubation Time:24 h
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Result:Protected cells against pyroptosis induced by LPS+ATP or LPS+Aβ/Tau/α-Syn.
Chemical Information
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Masse moléculaire 1211.46
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Formule C56H94N18O12
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Sequence
Val-Trp-Ile-Leu-Ala-Ala-Ile-Asn-Arg-Arg
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Sequence Shortening
VWILAAINRR
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Amyloid: Congo Red Amyloid Staining
Congo red amyloid staining is a histochemical method used to detect extracellular amyloid deposits in tissue sections based on the affinity of Congo red dye for β-pleated sheet-rich protein aggregates. When bound to amyloid, Congo red produces characteristic apple-green birefringence under polarized light microscopy, which is widely regarded as a diagnostic feature of amyloid deposition in histopathology. The diagnostic principle relies on the combination of dye binding (congophilia) and optical anisotropy under polarized illumination, which distinguishes amyloid from most non-amyloid eosinophilic extracellular deposits in routine histological evaluation. Amyloid identification by Congo red staining remains a cornerstone in diagnostic pathology despite the availability of adjunct methods such as immunohistochemistry and mass spectrometry, particularly because of its ability to localize deposits directly within tissue architecture. The specificity of Congo red-positive deposits is incre
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)