1. MCC950 sodium

MCC950 sodium (Synonyms: CP-456773 sodium; CRID3 sodium salt)

目录号: HY-12815A 纯度: 99.43%

MCC950 sodium是一种有效,选择性的 NLRP3 抑制剂,在BMDMs 和 HMDMs中的 IC50 分别为 7.5 nM 和 8.1 nM。

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MCC950 sodium Chemical Structure

MCC950 sodium Chemical Structure

CAS No. : 256373-96-3

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10 mM * 1 mL in Water ¥657 In-stock
2 mg ¥500 In-stock
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10 mg ¥870 In-stock
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100 mg ¥6700 In-stock
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Other Forms of MCC950 sodium:

Top Publications Citing Use of Products

MCE 顾客使用本产品发表的科研文献

    MCC950 sodium purchased from MCE. Usage Cited in:

    Effects of MCC950 on hippocampal NLRP3 inflammasome activation in db/db mice. Western blot analysis of NLRP3 inflammasome-associated NLRP3, ASC, IL-1β, and β-actin are performed in the hippocampus of each group.

    MCC950 sodium purchased from MCE. Usage Cited in:

    The efficiency of MCC950, and its effect on caspase-1 activation and IL-1β production in As2O3-treated HepG2 cells.

    MCC950 sodium purchased from MCE. Usage Cited in:

    Cells are pretreated with YVAD(10 μM) or MCC950 (10 μM) for 2 hours, and then exposed to TMAO (600 μM) for a further 24 hours. Expression of IL-1β, ICAM-1, MMP-9, and caspase-1 p20 is detected via Western blot.

    MCC950 sodium purchased from MCE. Usage Cited in:

    The expression of various molecules in pyroptotic and apoptotic pathways is detected by western blot. Representative bands from densitometric analysis in experimental groups are presented. M, MCC950 group (an inhibitor of NLRP3).

    MCC950 sodium purchased from MCE. Usage Cited in:

    NLRP3, Casp1 p20, IL-1b, and ICAM-1 protein levels are assessed in the cell lysates by Western blotting.

    MCC950 sodium purchased from MCE. Usage Cited in:

    Chronic PVN infusion of MCC950 significantly decreases apoptosis-associated speck-like protein (ASC), pro-caspase-1, and IL-1β expression in high-salt diet rats.

    MCC950 sodium purchased from MCE. Usage Cited in:

    Effect of MCC950 on the expression of NLRP3 inflammasome components and substrates after traumatic brain injury (TBI).

    MCC950 sodium purchased from MCE. Usage Cited in:

    MCC950 treatment inhibits Nucleotide-binding, oligomerization domain (NOD)-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome pathway activation.

    MCC950 sodium purchased from MCE. Usage Cited in:

    MCC950 or vehicle control (PBS) is administered at 1, 4 and 6 day after Ang II infusion in the absence or presence of EMD638683. Representative images and quantification of picrosirius red-stained collagen in the heart at 7 days after Ang II infusion.

    MCC950 sodium purchased from MCE. Usage Cited in:

    Western analysis of NLRP3, Caspase-1 and IL-1β expression with or without the treatment of LPS, AS2O3 and MCC950.
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    • 实验参考方法

    • 技术信息

    • 纯度 & 产品资料

    • 参考文献


    MCC950 sodium is a potent, selective NLRP3 inhibitor with IC50s of 7.5 and 8.1 nM in BMDMs and HMDMs, respectively.

    IC50 & Target

    IC50: 7.5 nM (NLRP3, in BMDMs), 8.1 nM (NLRP3, in HMDMs)[1]

    In Vitro

    MCC950 blocks canonical and non-canonical NLRP3 activation at nanomolar concentrations. MCC950 specifically inhibits NLRP3 but not AIM2, NLRC4 or NLRP1 activation. The effect of MCC950 on NLRP3 inflammasome activation is tested in mouse bone marrow derived macrophages (BMDM) and human monocyte derived macrophages (HMDM). The IC50 of MCC950 in BMDM is approximately 7.5 nM, while in HMDM it has a similar inhibitory capacity (IC50=8.1 nM). MCC950 also dose dependently inhibit IL-1β but not TNF-α secretion.MCC950 specifically blocks caspase-11-directed NLRP3 activation and IL-1β secretion upon stimulation of the non-canonical pathway. NLRC4-stimulated IL-1β and TNF-α secretion (as activated by Salmonella typhimurium) are not inhibited by MCC950 even at a concentration of 10 µM. MCC950 does not inhibit caspase-1 activation or IL-1β processing in response to S. typhimurium. The expression of pro-caspase-1 and pro-IL-1β in cell lysates is not substantially affected by MCC950 treatment[1].

    In Vivo

    MCC950 reduces Interleukin-1p (IL-1β) production and attenuates the severity of experimental autoimmune encephalomyelitis (EAE), a disease model of multiple sclerosis. Pre-treatment with MCC950 reduces serum concentrations of IL-1β and IL-6 while it does not considerably decrease the amount of TNF-α. Treatment of mice with MCC950 delays the onset and reduced the severity of EAE. Intracellular cytokine staining and FACS analysis of brain mononuclear cells from mice sacrificed on day 22 shows modestly reduced frequencies of IL-17 and IFN-γ producing CD3+ T cells in MCC950 treated mice in comparison with PBS-treated mice. IFN-γ and particularly IL-17 producing cell numbers are also reduced in both the CD4+ and γδ+ sub-populations of CD3+ T cells[1].

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    H2O : ≥ 30 mg/mL (70.35 mM)

    * "≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.3449 mL 11.7244 mL 23.4489 mL
    5 mM 0.4690 mL 2.3449 mL 4.6898 mL
    10 mM 0.2345 mL 1.1724 mL 2.3449 mL
    * 请根据产品在不同溶剂中的溶解度,选择合适的溶剂配制储备液,并请注意储备液的保存方式和期限。
    In Vivo:
    • 1.

      MCC950 sodium is prepared in PBS[2].

    • [1].


    Cell Assay

    BMDM are seeded at 5×105/mL or 1×106/mL, HMDM at 5×105/mL and PBMC at 2×106/mL or 5×106/mL in 96 well plates. The following day the overnight medium is replaced and cells are stimulated with 10 ng/mL LPS from Escherichia coli serotype EH100 (ra) TLRgrad for 3 h. Medium is removed and replaced with serum free medium (SFM) containing DMSO (1:1,000), MCC950 (0.001-10 µM), glyburide (200 µM), Parthenolide (10 µM) or Bayer cysteinyl leukotriene receptor antagonist 1-(5-carboxy-2{3-[4-(3-cyclohexylpropoxy)phenyl]propoxy}benzoyl)piperidine-4-carboxylic acid (40 µM) for 30 min. Cells are then stimulated with inflammasome activators: 5 mM adenosine 5’-triphosphate disodium salt hydrate (ATP) (1 h), 1 µg/mL Poly(deoxyadenylic-thymidylic) acid sodium salt (Poly dA:dT) transfected with Lipofectamine 200 (3-4 h), 200 µg/mL MSU (overnight) and 10 µM nigericin (1 h) or S. typhimurium UK-1 strain. Cells are also stimulated with 25 µg/mL Polyadenylic-polyuridylic acid (4 h). For non-canonical inflammasome activation cells are primed with 100 ng/mL Pam3CSK4 for 4 h, medium is removed and replaced with SFM containing DMSO or MCC950 and 2 µg/mL LPS is transfected using 0.25% FuGENE for 16 h. Supernatants are removed and analysed using ELISA kits. LDH release is measured using the CytoTox96 non-radioactive cytotoxicity assay[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    C57BL/6 mice are immunized subcutaneously with 150 µg of MOG peptide 35-55 emulsified in CFA containing 4 mg/mL (0.4.mg/mouse) of heat-killed MTB. Mice are injected i.p. with 500 ng pertussis toxin (PT: kaketsuken) on days 0 and 2. MCC950 is administered i.p. to mice (10 mg/kg) at induction of the disease, day 0, 1 and 2 and every 2 days thereafter. Control mice are administered vehicle (PBS) at the same time points. Mice are observed for clinical signs of disease daily (unblinded). Disease severity is scored as follows: no clinical signs, 0; limp tail, 1; ataxic gait, 2; hind limb weakness, 3; hind limb paralysis, 4; and tetra paralysis, 5.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    • [1].


    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere

    Purity: 99.43%

    • [1].


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    This equation is commonly abbreviated as: C1V1 = C2V2

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    MCC950 sodium

    MCC950 sodium

    Cat. No.: HY-12815A

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