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Documentos Principais

SML0021

Sigma-Aldrich

PDI inhibitor 16F16

≥98% (HPLC)

Sinônimo(s):

2-(2-Chloroacetyl)-2,3,4,9-tetrahydro-1-methyl-1H-pyrido[3,4-b]indole-1-carboxylic acid methyl ester, Methyl 2-(2-chloroacetyl)-1-methyl-2,3,4,9-tetrahydro-1H-pyrido[3,4-b]indole-1-carboxylate

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About This Item

Fórmula empírica (Notação de Hill):
C16H17ClN2O3
Número CAS:
Peso molecular:
320.77
Número MDL:
Código UNSPSC:
12352200
ID de substância PubChem:
NACRES:
NA.77

Nível de qualidade

Ensaio

≥98% (HPLC)

Formulário

powder

cor

white to tan

solubilidade

DMSO: 12 mg/mL, clear

temperatura de armazenamento

2-8°C

cadeia de caracteres SMILES

COC(=O)C1(C)N(CCc2c1[nH]c3ccccc23)C(=O)CCl

InChI

1S/C16H17ClN2O3/c1-16(15(21)22-2)14-11(7-8-19(16)13(20)9-17)10-5-3-4-6-12(10)18-14/h3-6,18H,7-9H2,1-2H3

chave InChI

BCSIRYFYAKLJDK-UHFFFAOYSA-N

Aplicação

PDI inhibitor 16F16 has been used to inhibit PDI (protein disulfide isomerase) function to examine the functional conservation of PDIs in human embryonic kidney cells.
PDI inhibitor 16F16 may be used in protein disulfide isomerase-mediated cell signaling studies.

Ações bioquímicas/fisiológicas

16F16 is a protein disulfide isomerase (PDI) inhibitor, first identified in a screen for compounds that prevent apoptosis induced by mutant huntingtin protein. 16F16 not only suppressed apoptosis induced by the misfolded protein mutant hungtingtin, it also protected rat neurons from cell death triggered by Aβ peptide. The actions of this inhibitor helped to identify a new mechanism in which a cell death pathway is regulated by protein misfolding via PDI upregulation.
Protein disulfide isomerase (PDI) inhibitor; suppresses apoptosis induced by misfolded proteins

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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A Protein Disulfide Isomerase Controls Neuronal Migration through Regulation of Wnt Secretion
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Tissue factor (TF) can be present in a non-coagulant and coagulant form. Whether the coagulant activity is affected by the plasma membrane microenvironment is unexplored. This article studies the presence and coagulant activity of human TF in plasma membrane micro-domains.
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Appropriate Wnt morphogen secretion is required to control animal development and homeostasis. Although correct Wnt globular structure is essential for secretion, proteins that directly mediate Wnt folding and maturation remain uncharacterized. Here, we report that protein disulfide isomerase-1 (PDI-1), a protein-folding
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Hypoxic tumor microenvironment (TME) plays critical roles in induction of cancer stem cell-like phenotype in breast cancer and contribute to chemoresistance. However, the mechanism underlying stemness reprogramming of breast cancer cells (BCs) by hypoxic TME remains largely unknown. In the

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