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Fig. 1 · Structure
Cat. No.
A11033
CAS No.
61966-08-3
Formula
C13H17N6O7P
Mol. Weight
400.3

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Triciribine phosphate (NSC-280594)

Cat. No. A11033 CAS 61966-08-3

AKT Inhibitor

Triciribine phosphate inhibits the phosphorylation, activation, and signalling of Akt-1, -2, and -3, which may result in the inhibition of Akt-expressing tumor cell proliferation.

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Biological Activity

Cellular Effect

Cell Line Activity Value Description Reference
BSC-1 IC50 20 μM Antiviral activity was tested using an enzyme-linked immunosorbent assay (ELISA) to detect HSV-1 (herpes simplex virus type 1) using BSC-1 cells [PMID: 10882371]
BSC-1 IC50 20 μM Antiviral activity against HSV-1 was determined using BSC-1 cells by an enzyme-linked immunosorbent assay (ELISA) [PMID: 10882373]
HFF IC50 0.8 μM HCMV plaque assay was performed using HFF cells and effect was calculated as a percentage of reduction in number of plaques [PMID: 10882371]
HFF IC50 0.8 μM Antiviral activity against HCMV was determined by plaque reduction assay using HFF cells [PMID: 10882373]

In Vitro Studies

The Triciribine studies reported dose-dependent TCN-P binding to the Akt1-derived PH domain, with a KD of 690 nM. Treatment of ALL-SIL cell lysates with 100 μM TCN-P identified 199 candidate interacting proteins through protein solubility analysis. In an immunoprecipitated Akt1 assay, TCN-P did not inhibit GSK3-β phosphorylation at concentrations up to 30 μM. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

PH domain binding

Cell-based study · Akt1-derived PH domain [1]

In an Akt1-derived PH domain assay, TCN-P was tested at 46 nM to 11.1 μM. Binding was dose-dependent, with a KD of 690 nM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
bind the PH domain of AktKD 46 nM to 11.1 μM: KD of 690 nM[1]

Literature-Reported Treatment Conditions

Treatment concentration
46 nM to 11.1 μM
Exposure duration
The contact time was typically ≥ 3 min and the dissociation time ≥ 6 min.
Method
immobilized to the surface via ligand thiol coupling
Vehicle
PBS
Methods and source locations

Compound reported in the paper: Triciribine; Compound label in the paper: TCN-P

The paper names Triciribine without stating the salt or form; not verified as the phosphate form supplied as A11033. No dose conversion or lot validation.

Results > TCN-P, but not TCN, binds to the PH domain of Akt as demonstrated by SPR (S21, S22, S23); Materials and Methods > Surface plasmon resonance (SPR) (S130, S131); Figure 3 legend (S165)

bind the PH domain of Akt: bind the PH domain of Akt; comparator: solvent alone (which served as a blank) — Results > TCN-P, but not TCN, binds to the PH domain of Akt as demonstrated by SPR (S21, S22, S23)

Candidate interacting proteins in leukemia cell lysates

Cell-based study · ALL-SIL cell lysates [2]

ALL-SIL cell lysates were treated with 100 μM TCN-P. Protein solubility analysis identified 199 candidate TCN-P-interacting proteins.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
changes in protein solubilitycandidate interacting proteins 100 μM TCN-P: 199 candidate TCN-P-interacting proteins[2]

Literature-Reported Treatment Conditions

Treatment concentration
100 μM
Exposure duration
10 min at room temperature
Method
cell lysates were treated
Vehicle
DMSO
Methods and source locations

Compound reported in the paper: Triciribine; Compound label in the paper: TCN-P

The paper names Triciribine without stating the salt or form; not verified as the phosphate form supplied as A11033. No dose conversion or lot validation.

Results > PISA profiling identifies candidate triciribine-interacting proteins across the proteome (S49); Methods > Proteome integral solubility alteration assay (S175, S176); Fig. 3 legend (S244)

changes in protein solubility: changes in protein solubility; comparator: DMSO control — Results > PISA profiling identifies candidate triciribine-interacting proteins across the proteome (S49); Fig. 3 legend (S244)

Kinase activity in an immunoprecipitated Akt assay

Cell-based study · Akt1 immunoprecipitated from HEK293T cells transfected with Myc-tagged Akt [1]

Akt1 immunoprecipitated from HEK293T cells transfected with Myc-tagged Akt was tested with increasing TCN-P concentrations. Up to 30 μM TCN-P did not inhibit phosphorylation of GSK3-β in vitro.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
phosphorylation of the substrate GSK3-βReported result Up to 30 μM TCN-P does not inhibit in vitro the kinase activity; TCN-P did not inhibit the ability of Akt1 to phosphorylate its substrate GSK3-β in vitro.[1]

Literature-Reported Treatment Conditions

Treatment concentration
Up to 30 μM
Method
in the absence or presence of increasing TCN-P concentrations
Reported limits
Not stated in the sentences used: schedule, vehicle.
Methods and source locations

Compound reported in the paper: Triciribine; Compound label in the paper: TCN-P

The paper names Triciribine without stating the salt or form; not verified as the phosphate form supplied as A11033. No dose conversion or lot validation.

Results > TCN-P inhibits in vitro neither Akt kinase activity nor the phosphorylation of purified Akt by PDK1 and mTORC2 (S6); Figure 1 legend (S147, S149)

phosphorylation of the substrate GSK3-β: phosphorylation of the substrate GSK3-β; comparator: in the absence or presence of increasing TCN-P concentrations — Results > TCN-P inhibits in vitro neither Akt kinase activity nor the phosphorylation of purified Akt by PDK1 and mTORC2 (S6); Figure 1 legend (S149)

In Vivo Studies

Rag1−/− mice bearing tumors derived from shDsc2 SK-CO15 cells received daily intraperitoneal Triciribine at 1 mg/kg. Compared with vehicle alone, treatment markedly reduced tumor growth after 5 d. [3]

Tumor growth in mice

Animal study · Rag1−/− mice [3]

Rag1−/− mice bearing tumors derived from shDsc2 SK-CO15 cells received daily intraperitoneal Triciribine at 1 mg/kg. Compared with vehicle alone, treatment markedly reduced tumor growth after 5 d.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Fold change in tumor sizeReported result The Akt inhibitor triciribine (1 mg/kg) or DMSO was administered daily via intraperitoneal injection. After 5 d treatment, Akt inhibition markedly reduced the in vivo growth of tumors derived from shDsc2 SK-CO15 cells.[3]

Conditions shared by the study groups

Route
intraperitoneal injection
Treatment course
daily
Vehicle
DMSO
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Triciribine 1 mg/kgDMSOThe Akt inhibitor triciribine (1 mg/kg) or DMSO was administered daily via intraperitoneal injection. After 5 d treatment, Akt inhibition markedly reduced the in vivo growth of tumors derived from shDsc2 SK-CO15 cells.[3]
Triciribine 1 mg/kg
Model: Rag1−/− mice
Methods and source locations

Compound reported in the paper: Triciribine

The paper names Triciribine without stating the salt or form; not verified as the phosphate form supplied as A11033. No dose conversion or lot validation.

RESULTS > Down-regulation of Dsc2 promotes cell invasion and xenograft tumor formation in mice (S90, S91, S93, S94, S96, S97); MATERIALS AND METHODS > Tumor formation in Rag1−/− mice (S145); FIGURE 5: legend (S223)

Fold change in tumor size: Fold change in tumor size; comparator: DMSO — RESULTS > Down-regulation of Dsc2 promotes cell invasion and xenograft tumor formation in mice (S94, S96, S97); MATERIALS AND METHODS > Tumor formation in Rag1−/− mice (S145)

Triciribine 1 mg/kg · RESULTS > Down-regulation of Dsc2 promotes cell invasion and xenograft tumor formation in mice (S93, S94, S97); MATERIALS AND METHODS > Tumor formation in Rag1−/− mice (S145)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 61966-08-3
Applications AKT Inhibitor
Formula C13H17N6O7P
Molecular Weight 400.3
Synonyms VQD-002,TCN-P; NSC-280594
SMILES
CN1C2=NC=NC3=C2C(=CN3[C@H]4[C@@H]([C@@H]([C@H](O4)COP(=O)(O)O)O)O)C(=N1)N

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 60 mg/mL (187.32 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
1% DMSO+30% polyethylene glycol+1% Tween 80

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Berndt N, Yang H, Trinczek B, et al. The Akt activation inhibitor TCN-P inhibits Akt phosphorylation by binding to the PH domain of Akt and blocking its recruitment to the plasma membrane. Cell Death Differ (2010). PMID: 20489726 DOI: 10.1038/cdd.2010.63 Source material
  2. [2] Qi X, Mermelekas G, Hodek O, et al. Multi-omics profiling identifies triciribine as a biomarker-guided antimetabolite therapy for acute lymphoblastic leukemia. NPJ Precis Oncol (2026). PMID: 42875447 DOI: 10.1038/s41698-026-01736-z Source material
  3. [3] Kolegraff K, Nava P, Helms MN, et al. Loss of desmocollin-2 confers a tumorigenic phenotype to colonic epithelial cells through activation of Akt/β-catenin signaling. Mol Biol Cell (2011). PMID: 21325624 DOI: 10.1091/mbc.E10-10-0845 Source material

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