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B2311

Sigma-Aldrich

5-(2-Benzothiazolyl)-3-ethyl-2-[2-(methylphenylamino)ethenyl]-1-phenyl-1H-benzimidazolium iodide

≥98% (HPLC)

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About This Item

Formula empirica (notazione di Hill):
C31H27IN4S
Numero CAS:
681281-88-9
Peso molecolare:
614.54
Numero MDL:
MFCD00570739
Codice UNSPSC:
12352200
ID PubChem:
24724416
NACRES:
NA.77

Livello qualitativo

100

Saggio

≥98% (HPLC)

Stato

powder

Colore

yellow to orange

Solubilità

DMSO: 5 mg/mL, clear

Temperatura di conservazione

2-8°C

Stringa SMILE

[I-].CC[n+]1c(\C=C\N(C)c2ccccc2)n(-c3ccccc3)c4ccc(cc14)-c5nc6ccccc6s5

InChI

1S/C31H27N4S.HI/c1-3-34-28-22-23(31-32-26-16-10-11-17-29(26)36-31)18-19-27(28)35(25-14-8-5-9-15-25)30(34)20-21-33(2)24-12-6-4-7-13-24;/h4-22H,3H2,1-2H3;1H/q+1;/p-1
NAYRELMNTQSBIN-UHFFFAOYSA-M

Azioni biochim/fisiol

5-(2-Benzothiazolyl)-3-ethyl-2-[2-(methylphenylamino)-ethenyl]-1-phenyl-1H-benzimidazolium, or Akt Inhibitor IV, is a cell-permeable benzimidazole compound that inhibits Akt phosphorylation/activation by targeting the ATP binding site of a kinase upstream of Akt, but downstream of PI3K. Shown to block Akt-mediated FOXO1a nuclear export (IC50 = 0.625μM) and cell proliferation (IC50 < 1.25μM) in 786-O cells. Unlike phosphatidylinositol analog-based Akt inhibitors, this inhibitor does not affect PI3K.

Caratteristiche e vantaggi

This compound is featured on the PKB/Akt page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Dispositivi di protezione individuale

dust mask type N95 (US), Eyeshields, Gloves

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Certificati d'analisi (COA)

Lot/Batch Number
065M4757V
077K47083
077K47082
077K47081
077K4708

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Jinxia Liu et al.
Oncogenesis, 9(9), 84-84 (2020-09-26)
β-Adrenergic receptor (β-AR) signalling is strongly associated with tumour progression by the coupling of β-ARs with either a G protein or β-arrestin; however, the related mechanism underlying hepatocellular carcinoma (HCC) metastasis is not clear. Here, we reveal that the transcription
Emmanuel Chautard et al.
Neuro-oncology, 12(5), 434-443 (2010-04-22)
Radiation therapy plays a central role in the treatment of glioblastoma, but it is not curative due to the high tumor radioresistance. Phosphatidyl-inositol 3-kinase/protein kinase B (Akt) and Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathways serve
Pavithra Lakshminarasimhan Chavali et al.
The Journal of biological chemistry, 286(11), 9393-9404 (2010-12-08)
Hypoxia promotes neural stem cell proliferation, the mechanism of which is poorly understood. Here, we have identified the nuclear orphan receptor TLX as a mediator for proliferation and pluripotency of neural progenitors upon hypoxia. We found an enhanced early protein
Kenji Hayata et al.
Journal of pharmacological sciences, 108(3), 348-354 (2008-11-15)
To obtain compounds that promote glucose uptake in muscle cells, the novel cell lines A31-IS derived from Balb/c 3T3 A31 and C2C12-IS from mouse myoblast C2C12 were established. In both cell lines, glucose consumption was induced by insulin and suppressed
Mei-Tsz Su et al.
Journal of hypertension, 37(12), 2461-2469 (2019-07-25)
Recent studies suggested that prophylactic aspirin prior to 16 weeks of gestation in high-risk patients may reduce the risk of developing preeclampsia; however, the exact mechanism of aspirin's effect on the pathophysiology of preeclampsia is not clear. This study was
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Articoli

Oncogenes and Tumor Suppressors Reprogram Metabolism

We present an article about how proliferating cells require the biosynthesis of structural components for biomass production and for genomic replication.

Protocolli

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