480402
NFAT Inhibitor
The NFAT Inhibitor controls the biological activity of NFAT. This small molecule/inhibitor is primarily used for Inflammation/Immunology applications.
Synonym(s):
NFAT Inhibitor, MAGPHPVIVITGPHEE
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About This Item
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Quality Level
assay
≥95% (HPLC)
form
lyophilized solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
desiccated (hygroscopic)
solubility
water: soluble
shipped in
ambient
storage temp.
−20°C
General description
A highly selective NFAT (Nuclear Factor of Activated T-cells) inhibitor that interferes with calcineurin-NFAT interaction without affecting calcineurin (Cat. No. 539568) phosphatase activity. Inhibits NFAT activation and NFAT-dependent expression of endogenous cytokine genes in T cells, without affecting the expression of other cytokines that require calcineurin but not NFAT.
A highly selective NFAT inhibitor that prevents NFAT activation and NFAT-dependent expression of endogenous cytokine genes in T cells. Does not affect the expression of other cytokines requiring calcineurin, but not NFAT. Inhibits calcineurin-mediated dephosphorylation of NFAT1, NFAT2, and NFAT4 in cell extracts.
Biochem/physiol Actions
Cell permeable: no
Primary Target
NFAT (Nuclear Factor of Activated T-cells)
NFAT (Nuclear Factor of Activated T-cells)
Product does not compete with ATP.
Reversible: no
Packaging
Packaged under inert gas
Warning
Toxicity: Standard Handling (A)
Sequence
H-Met-Ala-Gly-Pro-His-Pro-Val-Ile-Val-Ile-Thr-Gly-Pro-His-Glu-Glu-OH
Other Notes
Noguchi, H., et al. 2004. Nat. Med.10, 305.
Kiani, A., et al. 2001. Blood98, 1480.
Aramburu, J., et al. 1999. Science285, 2129.
Kiani, A., et al. 2001. Blood98, 1480.
Aramburu, J., et al. 1999. Science285, 2129.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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Annals of the New York Academy of Sciences, 1144, 148-153 (2008-12-17)
Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate
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