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MCC950

Catalog No. T3701 CAS 210826-40-7

Synonyms: CP-456773

CP-456773 (MCC950 (CP-456773) and CRID3) is an effective and specific cytokine release inhibitor and NLRP3 inflammasome inhibitor. CP-456773 inhibits IL-1β secretion and caspase 1 processing. MCC950 blocked canonical and noncanonical NLRP3 activation at nanomolar concentrations. MCC950 specifically inhibited activation of NLRP3 but not the AIM2, NLRC4 or NLRP1 inflammasomes. MCC950 reduced IL-1β production in vivo and attenuated the severity of experimental autoimmune encephalomyelitis (EAE), a disease model of multiple sclerosis.

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MCC950, CAS 210826-40-7

Pack Size	Availability	Price/USD
2 mg	In stock	$ 42.00
5 mg	In stock	$ 53.00
10 mg	In stock	$ 89.00
25 mg	In stock	$ 190.00
50 mg	In stock	$ 344.00
100 mg	In stock	$ 612.00
1 mL * 10 mM (in DMSO)	In stock	$ 57.00

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Biological Description

Chemical Properties

Storage & Solubility Information

Description	CP-456773 (MCC950 (CP-456773) and CRID3) is an effective and specific cytokine release inhibitor and NLRP3 inflammasome inhibitor. CP-456773 inhibits IL-1β secretion and caspase 1 processing. MCC950 blocked canonical and noncanonical NLRP3 activation at nanomolar concentrations. MCC950 specifically inhibited activation of NLRP3 but not the AIM2, NLRC4 or NLRP1 inflammasomes. MCC950 reduced IL-1β production in vivo and attenuated the severity of experimental autoimmune encephalomyelitis (EAE), a disease model of multiple sclerosis.
Targets&IC50	HMDM:8.1 nM, BMDM:7.5nM
In vitro	MCC950 effectively inhibits both canonical and non-canonical NLRP3 activators at nanomolar concentrations, distinguishing its specificity towards NLRP3 inhibition while not affecting AIM2, NLRC4, or NLRP1 activations. Its impact on NLRP3 inflammasome activity was evaluated in both mouse bone marrow-derived macrophages (BMDM) and human monocyte-derived macrophages (HMDM), demonstrating similar IC50 values of approximately 7.5 nM and 8.1 nM, respectively. MCC950 selectively reduces IL-1β secretion without influencing TNF-α levels, and it uniquely prevents caspase-11-mediated NLRP3 and IL-1β activation in the non-canonical pathway. However, MCC950 does not suppress NLRC4-induced IL-1β and TNF-α secretion, even at concentrations up to 10 μM, and fails to block caspase-1 activation or IL-1β processing following Salmonella typhimurium exposure. Furthermore, MCC950 does not markedly alter the expression levels of pro-caspase-1 and pro-IL-1β in treated cell lysates[1].
In vivo	MCC950 effectively lowers production of Interleukin-1β (IL-1β) and lessens the severity of experimental autoimmune encephalomyelitis (EAE), serving as a model for multiple sclerosis. It not only reduces serum levels of IL-1β and IL-6 without significantly affecting TNF-α concentrations but also delays the onset and diminishes the severity of EAE in treated mice. Furthermore, analysis through intracellular cytokine staining and FACS of brain mononuclear cells from mice euthanized on day 22 reveals that MCC950 treatment slightly decreases the prevalence of IL-17 and IFN-γ producing CD3+ T cells, in comparison to PBS-treated controls. Notably, the numbers of cells producing IFN-γ and especially IL-17 are lower in both CD4+ and γδ+ subsets of CD3+ T cells.
Kinase Assay	Disk diffusion is conducted, except that 10 μg of each antibiotic compound is used per filter. Growth in liquid medium in the presence of CHIR-090 is evaluated as follows: cells from overnight cultures are inoculated into 50 mL portions of LB broth at an A600 of 0.02 and grown with shaking at 30°C. When the A600 reaches 0.15, parallel cultures are treated with either 6 μL of 500 μg/mL CHIR-090 in DMSO or 6 μL of DMSO. To assess cumulative growth, cultures are maintained in log phase growth by 10-fold dilution into pre-warmed medium, containing the same concentrations of DMSO or DMSO/CHIR-090, whenever the A600 reaches 0.4. The minimal inhibitory concentration is defined as the lowest antibiotic concentration at which no measurable bacterial growth is observed in LB medium containing 1% DMSO (v/v), when inoculated at a starting density of A600=0.01. Cultures are incubated with shaking for 24 h at 30°C in the presence of CHIR-090. Experiments are performed in triplicate[1].
Cell Research	MCC950 is dissolved in DMSO and stored, and then diluted with appropriate media before use[1]. 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].

Synonyms	CP-456773
Molecular Weight	404.48
Formula	C20H24N2O5S
CAS No.	210826-40-7

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 28 mg/mL

References and Literature

1. Coll RC, et al. A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nat Med. 2015 Mar;21(3):248-55. 2. Li L H, Chen T L, Chiu H W, et al. Critical Role for the NLRP3 Inflammasome in Mediating IL-1β Production in Shigella sonnei-Infected Macrophages[J]. Frontiers in Immunology. 2020, 11: 1115. 3. Li L H, Lin J S, Chiu H W, et al. Mechanistic insight into the activation of the NLRP3 inflammasome by Neisseria gonorrhoeae in macrophages[J]. Frontiers in Immunology. 2019, 10: 1815. 4. Li S, Hui Y, Yuan J, et al. Syk-Targeted, a New 3-Arylbenzofuran Derivative EAPP-2 Blocks Airway Inflammation of Asthma–COPD Overlap in vivo and in vitro[J]. Journal of Inflammation Research. 2021, 14: 2173-2185. 5. Wu C H, Gan C H, Li L H, et al. A Synthetic Small Molecule F240B Decreases NLRP3 Inflammasome Activation by Autophagy Induction[J]. Frontiers in Immunology. 2020, 11. 6. Xie D, Ge X, Ma Y, et al. Clemastine improves hypomyelination in rats with hypoxic–ischemic brain injury by reducing microglia-derived IL-1β via P38 signaling pathway[J]. Journal of Neuroinflammation. 2020, 17(1): 1-17. 7. Chen Y Q, Wang S N, Shi Y J, et al. CRID3, a blocker of apoptosis associated speck like protein containing a card, ameliorates murine spinal cord injury by improving local immune microenvironment[J]. Journal of Neuroinflammation. 2020, 17(1): 1-18. 8. Wei Shi, Guang Xu, Xiaoyan Zhan, Yuan Gao, Zhilei Wang, Shubin Fu, Nan Qin, Xiaorong Hou, Yongqiang Ai, Chunyu Wang, Tingting He, Hongbin Liu, Yuanyuan Chen, Yan Liu, Jiabo Wang, Ming Niu, Yuming Guo, Xiaohe Xiao & Zhaofang Bai. Carnosol inhibits inflammasome activation by directly targeting HSP90 to treat inflammasome-mediated diseases. Cell death & disease. 2020 9. Zhilei Wang, Guang Xu, Yuan Gao, Xiaoyan Zhan, Nan Qin, Shubin Fu, Ruisheng Li et al. Cardamonin from a medicinal herb protects against LPS-induced septic shock by suppressing NLRP3 inflammasome [J]. Acta Pharmaceutica Sinica B. 2019 Feb 14.

Citations

1. Shi W, Xu G, Gao Y, et al.Novel role for epalrestat: protecting against NLRP3 inflammasome-driven NASH by targeting aldose reductase.Journal of Translational Medicine.2023, 21(1): 1-17. 2. Li N, Jiang X, Zhang R, et al.Discovery of Triazinone Derivatives as Novel, Specific, and Direct NLRP3 Inflammasome Inhibitors for the Treatment of DSS-Induced Ulcerative Colitis.Journal of Medicinal Chemistry.2023 3. Cao X, Di G, Bai Y, et al.Aquaporin5 Deficiency Aggravates ROS/NLRP3 Inflammasome-Mediated Pyroptosis in the Lacrimal Glands.Investigative Ophthalmology & Visual Science.2023, 64(1): 4-4. 4. Li Q, Zhao P, Wen Y, et al.POLYDATIN AMELIORATES TRAUMATIC BRAIN INJURY–INDUCED SECONDARY BRAIN INJURY BY INHIBITING NLRP3-INDUCED NEUROINFLAMMATION ASSOCIATED WITH SOD2 ACETYLATION.Shock.2023, 59(3): 460-468. 5. Chen Y Q, Wang S N, Shi Y J, et al. CRID3, a blocker of apoptosis associated speck like protein containing a card, ameliorates murine spinal cord injury by improving local immune microenvironment. Journal of Neuroinflammation. 2020, 17(1): 1-18. 6. Li S, Hui Y, Yuan J, et al. Syk-Targeted, a New 3-Arylbenzofuran Derivative EAPP-2 Blocks Airway Inflammation of Asthma–COPD Overlap in vivo and in vitro. Journal of Inflammation Research. 2021, 14: 2173-2185. 7. Zhang H, Gao J, Fang W, et al. Role of NINJ1 in Gout Flare and Potential as a Drug Target. Journal of Inflammation Research. 2022, 15: 5611-5620. 8. Gao Y, Xu G, Ma L, et al. Icariside I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity. Cell Communication and Signaling. 2021 Feb 11;19(1):13. doi: 10.1186/s12964-020-00647-1. 9. Yang S R, Hua K F, Yang C Y, et al. Cf‐02, a novel benzamide‐linked small molecule, blunts NF‐κB activation and NLRP3 inflammasome assembly and improves acute onset of accelerated and severe lupus nephritis in mice. The FASEB Journal. 2021, 35(8): e21785. 10. Qin N, Xu G, Wang Y, et al. Bavachin enhances NLRP3 inflammasome activation induced by ATP or nigericin and causes idiosyncratic hepatotoxicity. Frontiers of Medicine. 2021 Aug;15(4):594-607.

11. Niu L, Luo S S, Xu Y, et al. The critical role of the hippocampal NLRP3 inflammasome in social isolation-induced cognitive impairment in male mice. Neurobiology of Learning and Memory. 2020: 107301 12. Gao Y, Xu G, Ma L, et al. Icarisid I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity. Cell Communication and Signaling. 2020 13. Wu C H, Gan C H, Li L H, et al. A Synthetic Small Molecule F240B Decreases NLRP3 Inflammasome Activation by Autophagy Induction. Frontiers in Immunology. 2020 Dec 18;11:607564. doi: 10.3389/fimmu.2020.607564. eCollection 2020. 14. Meng Z, Liu H, Zhang J, et al. Sesamin promotes apoptosis and pyroptosis via autophagy to enhance antitumour effects on murine T-cell lymphoma. Journal of Pharmacological Sciences. 2021 15. Wei Shi, Guang Xu, Xiaoyan Zhan, Yuan Gao, Zhilei Wang, Shubin Fu, Nan Qin, Xiaorong Hou, Yongqiang Ai, Chunyu Wang, Tingting He, Hongbin Liu, Yuanyuan Chen, Yan Liu, Jiabo Wang, Ming Niu, Yuming Guo, Xiaohe Xiao & Zhaofang Bai Carnosol inhibits inflammasome activation by directly targeting HSP90 to treat inflammasome-mediated diseases. Cell Death & Disease. 2020 16. Tian C, Han X, He L, et al. Transient receptor potential ankyrin 1 contributes to the ATP-elicited oxidative stress and inflammation in THP-1-derived macrophage. Molecular and Cellular Biochemistry. 2020: 1-14 17. Li L H, Chen T L, Chiu H W, et al. Critical Role for the NLRP3 Inflammasome in Mediating IL-1β Production in Shigella sonnei-Infected Macrophages. Frontiers in Immunology. 2020, 11: 1115 18. Li L H, Lin J S, Chiu H W, et al. Mechanistic insight into the activation of the NLRP3 inflammasome by Neisseria gonorrhoeae in macrophages. Frontiers in Immunology. 2019, 10: 1815 19. Wang Z, Xu G, Gao Y, et al. Cardamonin from a medicinal herb protects against LPS-induced septic shock by suppressing NLRP3 inflammasome. Acta Pharmaceutica Sinica B. 2019, 9(4): 734-744 20. Tian C, Huang R, Tang F, et al. Transient Receptor Potential Ankyrin 1 Contributes to Lysophosphatidylcholine-Induced Intracellular Calcium Regulation and THP-1-Derived Macrophage Activation. The Journal of Membrane Biology. 2019: 1-13 21. Xie D, Ge X, Ma Y, et al. Clemastine improves hypomyelination in rats with hypoxic–ischemic brain injury by reducing microglia-derived IL-1β via P38 signaling pathway. Journal of neuroinflammation. 2020, 17(1): 1-17. 22. Ni B, Pei W, Qu Y, et al. MCC950, the NLRP3 Inhibitor, Protects against Cartilage Degradation in a Mouse Model of Osteoarthritis. Oxidative Medicine and Cellular Longevity. 2021, 2021. 23. Yuan X, Chen P, Luan X, et al.NLRP3 deficiency protects against acetaminophen‑induced liver injury by inhibiting hepatocyte pyroptosis.Molecular Medicine Reports.2024, 29(4): 1-15. 24. Chiu H W, Wu C H, Lin W Y, et al.The Angiotensin II Receptor Neprilysin Inhibitor LCZ696 Inhibits the NLRP3 Inflammasome By Reducing Mitochondrial Dysfunction in Macrophages and Alleviates Dextran Sulfate Sodium-induced Colitis in a Mouse Model.Inflammation.2024: 1-22.

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Related compound libraries

This product is contained In the following compound libraries：

Inhibitor Library Bioactive Compound Library Anti-Breast Cancer Compound Library Anti-Prostate Cancer Compound Library Bioactive Compounds Library Max

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Keywords

MCC950 210826-40-7 Immunology/Inflammation NF-Κb NOD CP 456773 MCC 950 Inhibitor CRID-3 NOD-like Receptor (NLR) inhibit CP-456773 MCC-950 CRID3 CP456773 CRID 3 inhibitor

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