Catalog No.S1117 Synonyms: NSC 154020, VD-0002, vqd-002

Triciribine Chemical Structure

Molecular Weight(MW): 320.3

Triciribine is a DNA synthesis inhibitor, also inhibits Akt in PC3 cell line and HIV-1 in CEM-SS, H9, H9IIIB, U1 cells with IC50 of 130 nM and 20 nM, respectively; does not inhibit PI3K/PDK1; 5000-fold less active in cells lacking adenosine kinase. Phase 1/2.

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In DMSO USD 150 In stock
USD 120 In stock
USD 170 In stock
USD 570 In stock
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2 Customer Reviews

  • Effects of FAK A., PI3K B. or Akt C. inhibition in D-Hep2/AURKA cells on dormancy-related protein expression as analyzed by western blotting. P130 and E2F4 levels were increased, while P107 and Ki67 were decreased. Dormancy-related protein ratio in D-Hep2/AURKA cells treated with TAE226 D., Omipalisib E. or Triciribine F.

    Oncotarget, 2016, 7(30):48346-48359. Triciribine purchased from Selleck.

    Effect of triciribine on the migration of (A) FaDu and (B) Hep2 cells. The cells were treated with 5 µM triciribine for different periods of time. *P<0.05 vs. control. Hpf, high-power field.

    Oncol Lett, 2016, 11(3):1889-1894.. Triciribine purchased from Selleck.

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Biological Activity

Description Triciribine is a DNA synthesis inhibitor, also inhibits Akt in PC3 cell line and HIV-1 in CEM-SS, H9, H9IIIB, U1 cells with IC50 of 130 nM and 20 nM, respectively; does not inhibit PI3K/PDK1; 5000-fold less active in cells lacking adenosine kinase. Phase 1/2.
HIV-1 [2]
(CEM-SS, H9, H9IIIB, U1 cells)
Akt [1]
(PC3 cells)
20 nM 130 nM
In vitro

Triciribine exhibits maximum growth inhibition around 1-10 μM and inhibits phosphorylation of Akt, as well as downstream p70S6K, to basal levels at 100μM (IC50 = 130 nM). Triciribine shows particular promise for inhibiting growth in Nf1 and Trp53 mutant astrocytoma cells in a grade-dependent manner. The WHO II K1861-10 line is inhibited, incompletely (69% maximum inhibition), with a GI50 value of 1.7 μM for Triciribine, whereas higher-grade tumor lines (KR158, KR130, and SF295) are inhibited to a greater extent (>80% maximum inhibition) at lower GI50 values (0.4–1.1 mM). Importantly, Triciribine is much less effective at inhibiting primary astrocytes (GI5013.6 mM), suggesting that this inhibitor may show specificity for tumor cells. [1] Triciribine inihibits HIV-1with an IC50 of 20 nM. Greater than 90% inhibition is achieved at 0.1μM and complete inhibition of syncytia formation is achieved at 5μM. Associated cell toxicity in the same cell line for Triciribine is 46 μM, resulting in selectivity indices of 2250. Triciribine markedly inhibits HIV-1-induced p24 core antigen production, reverse transcriptase, and infectious virus production in a dose-dependent manner using HIV-1 acutedly infected CEM-SS, H9, and persistently infected H9III B and U1 cells. [2] Triciribine inhibits Akt phosphorylation at Thr308 and Ser473 and Akt activity in the human prostate cancer cell line PC-3. Triciribine sensitizes PC-3 cells to TRAIL- and anti-CD95-induced apoptosis, whereas the cells remain resistant to DNA damaging chemotherapeutics. [3] Triciribine is highly selective for Akt and does not inhibit the activation of phosphatidylinositol 3-kinase, phosphoinositide-dependent kinase-1, protein kinase C, serum and glucocorticoid-inducible kinase, protein kinase A, signal transducer and activators of transcription 3, extracellular signal-regulated kinase-1/2, or c-Jun NH2-terminal kinase. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human ACH2 cells NIizNJhEgXSxdH;4bYPDqGG|c3H5 MULDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBR2gzKGOnbHzzJIlv\mWldHXkJJdqfGhibHH0[Y51KEi3bXHuJIludXWwb3Tl[olkcWWwY4mgeolzfXNiMTDifUBOXFNiYYPzZZktKEOFNUC9NE4xOSEQvF2= MnjqNlAxQDZzNEm=
L1210 leukemic cells MWfDfZRwfG:6aXRCpIF{e2G7 NIXld4FV\XO2ZXSgbY4hfmm2cn:g[o9zKGO7dH;0c5hq[2m2eTDh[4FqdnO2IH31dolv\SCOMUKxNEBt\XWtZX3pZ{Bk\WyuczygTWM2OD1yLkCzOUDPxE1? NVe0OGVXOTB6OEKzO|E>
human H9 cells NIOzRnFHfW6ldHnvckBie3OjeR?= MlHrRY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgTJVu[W5iaX3teY5w\GWoaXPp[Y5kgSC4aYL1d{AyKFONMTDpcoZm[3SnZDDpckBpfW2jbjDIPUBk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oII\pdoFtKFKndnXyd4UhfHKjboPjdolxfGG|ZTDifUBcO0ifVGTQJIlv[2:{cH;yZZRqd25iYYPzZZktKEmFNUC9NE4xOzZizszN MXKyNFA5PjF2OR?=
human MCF7 cells NFzNe41EgXSxdH;4bYPDqGG|c3H5 NHfDeZhEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOS0Z5IHPlcIx{KGmwIIDy[ZNmdmOnIH;mJFIxKHWPIHPocI9zd3G3aX7lJIJ6KFOUQjDhd5NigSxiR1m1NF0xNjB3IN88US=> M4XGRlE5PjlzOEm0
AA5 cells MnnoSpVv[3Srb36gZZN{[Xl? MYLBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDv[kBJfW2jbjDpcY12dm:mZX\pZ4lmdmO7II\pdpV{KDFiM1KgbY5n\WO2ZXSgbY4hSUF3IHPlcIx{KGmwZnXjeIVlKHerdHigN{4yOyC3TDDv[kB3cXK3czDzeI9kcyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKH[rcnHsJHJmfmW{c3WgeJJidnOlcnnweIF{\SCkeTDbN2heXFSSIHnuZ49zeG:{YYTpc44h[XO|YYmsJGlEPTB;MD6xO{DPxE1? MXuyNFA5PjF2OR?=
human U1 cells NEe1UpJHfW6ldHnvckBie3OjeR?= NF71TWxCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJfW2jbjDpcY12dm:mZX\pZ4lmdmO7II\pdpV{KDFiaX7m[YN1\WRiaX6gbJVu[W5iVUGgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iC4aYLhcEBT\X[ncoPlJJRz[W6|Y4LpdJRie2ViYomgX|NJZVSWUDDpcoNwenCxcnH0bY9vKGG|c3H5MEBKSzVyPUKuN{DPxE1? MmTONlAxQDZzNEm=
human MDM cells M2HiVmN6fG:2b4jpZ:Kh[XO|YYm= NV[4N2tDS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUSPIHPlcIx{KGmwZnXjeIVlKHerdHigTJVu[W5iaX3teY5w\GWoaXPp[Y5kgSC4aYL1d{AyKEKDTDDifUBOXFNiYYPzZZktKFSFNUC9NE43PiEQvF2= Mo\KNlAxQDZzNEm=
human MDA-MB-231 cells NHjwOI1EgXSxdH;4bYPDqGG|c3H5 NFLnPYpEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOTEFvTVKtNlMyKGOnbHzzJIlvKHC{ZYPlcoNmKG:oIEKwJJVOKGOqbH;yc5F2cW6nIHL5JHNTSiCjc4PhfUwhT0l3ME2wMlY6KM7:TR?= MmnPNVg3QTF6OUS=
Huh-7 cells NYnDXWp[TnWwY4Tpc44h[XO|YYm= NGHPZVlEd22yb4Xu[EB4[XNidHXzeIVlKG[xcjDpeJMh[WKrbHn0fUB1dyCrbnjpZol1KGincHH0bZRqeyCFII\pdoFtKFKQQTDy[ZBtcWOjdHnvckBqdiCKdXitO{Bk\WyuczCobJVu[W5iaHXwZZRwdWFiY3XscJMqNCCHQ{WwQVIh|ryP MYSxOVE4PzR4NB?=
HFF cells NXHQXYtyTnWwY4Tpc44h[XO|YYm= M2fkemhEVVZicHzhdZVmKGG|c3H5JJdieyCyZYLmc5Ju\WRidYPpcochUE[IIHPlcIx{KGGwZDDl[oZm[3Rid3HzJINidGO3bHH0[YQh[XNiYTDw[ZJk\W62YXflJI9nKHKnZIXjeIlwdiCrbjDueY1j\XJib3[gdIxieXWnczygTWM2OD1{LkWg{txO M3T6SlExQDh{M{ex
human MDA-MB-468 cells MWLDfZRwfG:6aXRCpIF{e2G7 NXm5TnNoS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUSDLV3CMVQ3QCClZXzsd{BqdiCycnXz[Y5k\SCxZjCyNEB2VSClaHzvdo9yfWmwZTDifUBUWkJiYYPzZZktKEeLNUC9NVAvOjlizszN NWruXm9bOTh4OUG4PVQ>
human 184B5 cells NVv0VXBPS3m2b4TvfIlkyqCjc4PhfS=> MkPOR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gNVg1SjViY3XscJMh[nliU2LCJIF{e2G7LDDHTVUxRTRyIN88US=> NFrYXHcyQDZ7MUi5OC=>

... Click to View More Cell Line Experimental Data

In vivo 1 mg/kg/day i.p. treated Triciribine inhibits OVCAR3, OVCAR8 and PANC1 tumor growth, which overexpressing Akt, by 90%, 88% and 80% in nude mice, respectively. However, Triciribine has little effect on the growth of OVCAR5 and COLO357 cells. [4]


Kinase Assay:[1]
+ Expand

Akt Phosphorylation Changes Assay:

Cells are grown to 80%–90% confluency and stimulated for 5–10 minutes with 1–10 ng/mL of epidermal growth factor or platelet derived growth factor (PDGF)–AA with or without 10–20 mM of U0126 or LY-294002. Protein lysates (5–20 μg) are separated by 12%–15% SDS PAGE and analyzed by Western blot for Akt, phosphorylated Akt (phospho-Ser 473), MAPK, and phosphorylated MAPK (p44/42 phospho-Thr202/Tyr204) antibodies (1:1000).
Cell Research:[2]
+ Expand
  • Cell lines: CEM-SS cells
  • Concentrations: 0-500 μM
  • Incubation Time: 48 hours
  • Method: Triciribine is evaluated for cytotoxicity by seeding CEM-SS cells at a density of 1 × 104 cells/well in growth medium, using a 96-well flat-bottom plate. Serial fivefold dilutions of Triciribine are prepared in growth medium and added to the wells as a second overlay. After a 48-hours incubation at 37 °C, the cells are pulse labeled with [3H]dThd (1 μCi per well, specific activity 20 Ci/mmol) for 6 hours and the cells are harvested to measure total DNA synthesis.
    (Only for Reference)
Animal Research:[4]
+ Expand
  • Animal Models: OVCAR3, OVCAR8, PANC1, OVCAR5 and COLO357 tumor cells are injected s.c. into 80week-old female nude mice.
  • Formulation: Triciribine is dissolved in 20% DMSO.
  • Dosages: 1 mg/kg/day
  • Administration: Triciribine is administrated through i.p. injection once a day.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 64 mg/mL (199.81 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% DMSO+30% polyethylene glycol+1% Tween 80
For best results, use promptly after mixing.
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 320.3


CAS No. 35943-35-2
Storage powder
in solvent
Synonyms NSC 154020, VD-0002, vqd-002

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02930109 Recruiting Acute Leukemia Prescient Therapeutics Ltd. September 2016 Phase 1|Phase 2
NCT01697293 Recruiting Breast Adenocarcinoma|Estrogen Receptor Positive|HER2/Neu Negative|Recurrent Breast Carcinoma|Stage IIB Breast Cancer|Stage IIIA Breast Cancer|Stage IIIB Breast Cancer|Stage IIIC Breast Cancer|Stage IV Breast Cancer Prescient Therapeutics Ltd.|National Cancer Institute (NCI) January 2012 Phase 1|Phase 2
NCT00642031 Completed Hematologic Malignancies|Leukemia Prescient Therapeutics Ltd.|VioQuest Pharmaceuticals August 2006 Phase 1
NCT00363454 Completed Cancer Prescient Therapeutics Ltd.|VioQuest Pharmaceuticals April 2006 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID