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Merck

SML2475

Sigma-Aldrich

Larazotide acetate salt

≥95% (HPLC)

Sinónimos:

AT-1001, AT1001, GGVLVQPG acetate, Glycylglycyl-L-valyl-L-leucyl-L-valyl-L-glutaminyl-L-prolyl-glycine acetate

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About This Item

Fórmula empírica (notación de Hill):
C32H55N9O10 · xC2H4O2
Número de CAS:
Peso molecular:
725.83 (free base basis)
Código UNSPSC:
12352200
NACRES:
NA.77

Ensayo

≥95% (HPLC)

Formulario

powder

color

white to beige

Condiciones de envío

wet ice

temp. de almacenamiento

−20°C

cadena SMILES

N1([C@@H](CCC1)C(=O)NCC(=O)O)C(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)CN)C(C)C)CC(C)C)C(C)C)CCC(=O)N.OC(=O)C

InChI

1S/C32H55N9O10.C2H4O2/c1-16(2)12-20(38-30(49)26(17(3)4)39-24(44)14-35-23(43)13-33)28(47)40-27(18(5)6)31(50)37-19(9-10-22(34)42)32(51)41-11-7-8-21(41)29(48)36-15-25(45)46;1-2(3)4/h16-21,26-27H,7-15,33H2,1-6H3,(H2,34,42)(H,35,43)(H,36,48)(H,37,50)(H,38,49)(

Clave InChI

NYGCNONRVCGHAT-UFIKZEAMSA-N

Acciones bioquímicas o fisiológicas

Larazotide acetate (AT1001) is a Zonulin receptor antagonist, a tight junction modulator. Larazotide inhibition of zonulin results in reducing trafficking across epithelial cells in the intestines and reducing intestinal permeability and "leaky gut," thought to be a gateway to multiple autoimmune diseases, including celiac disease, irritable bowel syndrome (IBS), inflammatory bowel diseases (IBD, Crohn′s and ulcerative colitis), type 1 diabetes mellitus (T1DM), nonalcoholic steatohepatitis (NASH), chronic kidney disease (CKD) and several others. It has been shown to inhibit the effect of inflammatory cytokines such as tumor necrosis factor (TNF-alpha) and interleukin (IL-4), blocking their increase of intestinal epithelial permeability.
Zonulin receptor antagonist; tight junction modulator

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


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Masoumeh Sadat Mousavi Maleki et al.
Amino acids, 55(11), 1601-1619 (2023-10-07)
Enzyme therapy for celiac disease (CeD), which digests gliadin into non-immunogenic and non-toxic peptides, can be an appropriate treatment option for CeD. Here, we have investigated the effectiveness of bromelain and ficin on gliadin digestion using in vitro, such as
Craig Sturgeon et al.
Annals of the New York Academy of Sciences, 1397(1), 130-142 (2017-04-20)
Increased small intestinal permeability (IP) has been proposed to be an integral element, along with genetic makeup and environmental triggers, in the pathogenies of chronic inflammatory diseases (CIDs). We identified zonulin as a master regular of intercellular tight junctions linked
Shahryar Khaleghi et al.
Therapeutic advances in gastroenterology, 9(1), 37-49 (2016-01-16)
Celiac disease (CD) is a common chronic immune disease triggered by gluten. Gliadin peptides pass through the epithelial layers, either paracellularly or transcellularly, to launch a potent adaptive immune response in the lamina propria. This aberrant immune response leads to
Alessio Fasano
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 10(10), 1096-1100 (2012-08-21)
One of the most important and overlooked functions of the gastrointestinal tract is to provide a dynamic barrier to tightly controlled antigen trafficking through both the transcellular and paracellular pathways. Intercellular tight junctions (TJ) are the key structures regulating paracellular

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