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SML0021

Sigma-Aldrich

PDI inhibitor 16F16

≥98% (HPLC)

Synonyme(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

Formule empirique (notation de Hill):
C16H17ClN2O3
Numéro CAS:
922507-80-0
Poids moléculaire :
320.77
Numéro MDL:
MFCD20134198
Code UNSPSC :
12352200
ID de substance PubChem :
329825093
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to tan

Solubilité

DMSO: 12 mg/mL, clear

Température de stockage

2-8°C

Chaîne 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

Clé InChI

BCSIRYFYAKLJDK-UHFFFAOYSA-N

Application

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.

Actions biochimiques/physiologiques

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.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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A Protein Disulfide Isomerase Controls Neuronal Migration through Regulation of Wnt Secretion
Torpe N, et al.
Cell Reports, 26(12), 3183-3190 (2019)
Suma Yarapureddy et al.
Neoplasia (New York, N.Y.), 21(6), 516-532 (2019-04-28)
Patients with metastatic or relapsed/refractory osteosarcoma (OS) have a 5-year survival rate of <30%. This has remained unchanged over several decades. One of the factors contributing to lack of improvement in survival is the development of chemoresistance. Hence, elucidating and
Yuanjie Yu et al.
Thrombosis and haemostasis, 118(6), 990-1000 (2018-04-22)
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.
Nanna Torpe et al.
Cell reports, 26(12), 3183-3190 (2019-03-21)
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
Yuanyuan Yan et al.
Cell death and differentiation, 29(9), 1769-1789 (2022-03-19)
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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