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T3830

Sigma-Aldrich

Triciribine hydrate

≥97% (HPLC)

Sinónimos:

API-2, Akt/PKB Signaling Inhibitor-2, Inhibitor V, NSC 154020, TCN, VD-0002

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About This Item

Fórmula empírica (notación de Hill):
C13H16N6O4 · xH2O
Número de CAS:
35943-35-2
Peso molecular:
320.30 (anhydrous basis)
MDL number:
MFCD16879015
UNSPSC Code:
12352200
PubChem Substance ID:
329826778
NACRES:
NA.77

Quality Level

100

assay

≥97% (HPLC)

form

powder

color

tan

solubility

DMSO: >10 mg/mL

storage temp.

2-8°C

SMILES string

O.Cn1nc(N)c2cn([C@@H]3O[C@H](CO)[C@@H](O)[C@H]3O)c4ncnc1c24

InChI

1S/C13H16N6O4.H2O/c1-18-11-7-5(10(14)17-18)2-19(12(7)16-4-15-11)13-9(22)8(21)6(3-20)23-13;/h2,4,6,8-9,13,20-22H,3H2,1H3,(H2,14,17);1H2/t6-,8-,9-,13-;/m1./s1

InChI key

SPGRLWCWHWRPHX-DOKXERMVSA-N

Gene Information

human ... AKT1(207)
mouse ... AKT1(11651)
rat ... AKT1(24185)

Application

Triciribine hydrate has been used to study the effect of diethyldithiocarbamate (DDC) on matrix metalloproteinase-1 (MMP-1) in hepatic stellate cells1. It has also been used to analyze ADAM 10 activation by (-)-epigallocatechin-3-gallate (EGCG) in N2a cells overexpressing Swedish mutant APP (SweAPP N2a cells)2.

Biochem/physiol Actions

Triciribine is a highly selective Akt/PKB inhibitor, that selectively inhibits the cellular phosphorylation/activation of Akt1/2/3.

Features and Benefits

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.

Preparation Note

Triciribine hydrate is soluble in DMSO at a concentration that is greater than 10 mg/ml.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number
0000239716
096M4741V
042M4710V
031M4732V
090M47091

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Physiology & behavior, 168, 20-23 (2016-11-05)
Autonomic nervous system (ANS) imbalances are involved in the etiology of cancer, allergy, and collagen diseases. Previously, we hypothesized that FoxO and HSF-1 limit autonomic stress responses via negative feedback on the ANS. Here, we evaluated the role of AKT
Camilla Evangelisti et al.
Journal of cellular physiology, 226(3), 822-831 (2010-09-22)
Over the past 20 years, survival rates of T-cell acute lymphoblastic leukemia (T-ALL) patients have improved, mainly because of advances in polychemotherapy protocols. Despite these improvements, we still need novel and less toxic treatment strategies targeting aberrantly activated signaling networks
Hiroaki Kamijo et al.
The Journal of investigative dermatology, 140(3), 636-644 (2019-08-30)
Whereas atopic dermatitis (AD) is considered as a T helper 2 (Th2)-centered disease, IL-17-producing Th (Th17) cells are also activated in AD lesional skin. However, the relationship between Th17 responses and Th2 responses in AD is still to be elucidated.
Amanda Martins Baviera et al.
Molecular and cellular endocrinology, 315(1-2), 104-112 (2009-10-07)
Very little is known about the signaling pathways by which catecholamines exert anabolic effects on muscle protein metabolism, stimulating protein synthesis and suppressing proteolysis. The present work tested the hypothesis that epinephrine-induced inhibition of muscle proteolysis is mediated through the
A Griveau et al.
Oncogene, 35(38), 5033-5042 (2016-04-05)
Little is known about the biological role of the phospholipase A2 receptor (PLA2R1) transmembrane protein. In recent years, PLA2R1 has been shown to have an important role in regulating tumor-suppressive responses via JAK2 activation, but the underlying mechanisms are largely
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