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Merck

SML1996

Sigma-Aldrich

S3226

≥98% (HPLC)

Sinónimos:

3,3′-(4-Methyl-1,2-phenylene)bis[N-(aminoiminomethyl)-2-methyl-2-propenamide] dihydrochloride, S 3226, S-3226

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About This Item

Fórmula empírica (notación de Hill):
C17H22N6O2 · 2HCl
Número de CAS:
Peso molecular:
415.32
Código UNSPSC:
12352200

Análisis

≥98% (HPLC)

formulario

powder

color

white to beige

solubilidad

H2O: 2 mg/mL, clear

Condiciones de envío

ambient

temp. de almacenamiento

2-8°C

cadena SMILES

O=C(N=C(N)N)C(C)=CC1=CC(C)=CC=C1C=C(C)C(NC(N)=N)=O.[H]Cl.[H]Cl

Acciones bioquímicas o fisiológicas

S3226 is a potent and selective NHE3 (NHE-3) inhibitor (IC50 = 20 nM/human NHE3, 3.6 μM/human NHE1, 80 μM/rabbit NHE2) for studying NHE3 physiological as well as pathophysiological roles in kidney and gastrointestinal disorders in vitro and in animal models in vivo.
S3226 is also known as {3-[2-(3-guanidino-2-methyl-3-oxo-propenyl)-5-methyl-phenyl]-N-isopropylidene-2-methyl-acrylamide dihydro-chloride}. S3226 is used to explore the physiological and pathophysiological functions of sodium-hydrogen exchanger 3 (NHE3) in animal models. It is a bismethacryloyl guanidine derivative.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


Certificados de análisis (COA)

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S3226, a novel inhibitor of Na+/H+ exchanger subtype 3 in various cell types
Schwark J R, et al.
Pflugers Archiv : European Journal of Physiology, 436(5), 797-800 (1998)
J R Schwark et al.
Pflugers Archiv : European journal of physiology, 436(5), 797-800 (1998-08-26)
Inhibition of Na+/H+ exchange (NHE) subtypes has been investigated in a study of the mouse fibroblast L cell line (LAP1) transfected with human (h) NHE1, rabbit (rb) NHE2, rat (rt) or human (h) NHE3 as well as an opossum kidney
Hiromitsu Miyazaki et al.
BMC physiology, 17(1), 1-1 (2016-08-16)
Disturbance of acid-base balance in the inner ear is known to be associated with hearing loss in a number of conditions including genetic mutations and pharmacologic interventions. Several previous physiologic and immunohistochemical observations lead to proposals of the involvement of
Jennifer Foulke-Abel et al.
Gastroenterology, 150(3), 638-649 (2015-12-19)
Human intestinal crypt-derived enteroids are a model of intestinal ion transport that require validation by comparison with cell culture and animal models. We used human small intestinal enteroids to study neutral Na(+) absorption and stimulated fluid and anion secretion under

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