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480402

Sigma-Aldrich

NFAT Inhibitor

The NFAT Inhibitor controls the biological activity of NFAT. This small molecule/inhibitor is primarily used for Inflammation/Immunology applications.

Sinónimos:

NFAT Inhibitor, MAGPHPVIVITGPHEE

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About This Item

Fórmula empírica (notación de Hill):
C75H118N20O22S
Número de CAS:
Peso molecular:
1683.93
UNSPSC Code:
51111800
NACRES:
NA.77

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)
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.

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


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Sami I Said
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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