Triciribine hydrate

≥97% (HPLC)

API-2, Akt/PKB Signaling Inhibitor-2, NSC 154020, VD-0002, Inhibitor V, TCN
Empirical Formula (Hill Notation):
C13H16N6O4 · xH2O
Número de CAS:
Peso molecular:
320.30 (anhydrous basis)
MDL number:
PubChem Substance ID:
En este momento no podemos mostrarle ni los precios ni la disponibilidad


≥97% (HPLC)






DMSO: >10 mg/mL

storage temp.


SMILES string




InChI key


Gene Information

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


5, 25 mg in glass bottle


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.


NONH for all modes of transport

WGK Germany


Flash Point F

Not applicable

Flash Point C

Not applicable

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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...
L Mavroeidis et al.
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Information regarding Helicobacter pylori antibiotic resistance in Indonesia was previously inadequate. We assessed antibiotic susceptibility for H. pylori in Indonesia, and determined the association between virulence genes or genetic mutations and antibiotic resistance. We recruited 849 dyspeptic patients who underwent...
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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...
We present an article about how proliferating cells require the biosynthesis of structural components for biomass production and for genomic replication.
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