For research use only.

Catalog No.S1117 Synonyms: NSC 154020, VD-0002, vqd-002, API-2

23 publications

Triciribine Chemical Structure

CAS No. 35943-35-2

Triciribine (NSC 154020, VD-0002, vqd-002, API-2) 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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Selleck's Triciribine has been cited by 23 publications

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Biological Activity

Description Triciribine (NSC 154020, VD-0002, vqd-002, API-2) 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 NVrxNYNuS3m2b4TvfIlkyqCjc4PhfS=> MmewR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRWNJOiClZXzsd{Bqdm[nY4Tl[EB4cXSqIHzheIVvfCCKdX3hckBqdW23bn;k[YZq[2mnbnP5JJZqenW|IEGgZpkhVVSVIHHzd4F6NCCFQ{WwQVAvODFizszN NULFbmwxOjByOE[xOFk>
L1210 leukemic cells MXrDfZRwfG:6aXRCpIF{e2G7 NVvMOlM4XGW|dHXkJIlvKH[rdILvJIZweiCleYTveI95cWOrdImgZYdicW6|dDDteZJqdmViTEGyNVAhdGW3a3XtbYMh[2WubIOsJGlEPTB;MD6wN|Uh|ryP Mk\JNVA5QDJ|N{G=
human H9 cells NHzU[oFHfW6ldHnvckBie3OjeR?= NIHQNoJCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJfW2jbjDpcY12dm:mZX\pZ4lmdmO7II\pdpV{KDFiU1uxJIlv\mWldHXkJIlvKGi3bXHuJGg6KGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[geolz[WxiUnX2[ZJ{\SC2cnHud4NzcXC2YYPlJIJ6KFt|SG3UWHAhcW6lb4Lwc5JifGmxbjDhd5NigSxiSVO1NF0xNjB|NjFOwG0> NXvQV4ZbOjByOE[xOFk>
human MCF7 cells NV;aWnEyS3m2b4TvfIlkyqCjc4PhfS=> M{HnRWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1ETjdiY3XscJMhcW5icILld4Vv[2Vib3[gNlAhfU1iY3jsc5JweXWrbnWgZpkhW1KEIHHzd4F6NCCJSUWwQVAvODVizszN Mnj3NVg3QTF6OUS=
AA5 cells NGTsVpdHfW6ldHnvckBie3OjeR?= MVjBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDv[kBJfW2jbjDpcY12dm:mZX\pZ4lmdmO7II\pdpV{KDFiM1KgbY5n\WO2ZXSgbY4hSUF3IHPlcIx{KGmwZnXjeIVlKHerdHigN{4yOyC3TDDv[kB3cXK3czDzeI9kcyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKH[rcnHsJHJmfmW{c3WgeJJidnOlcnnweIF{\SCkeTDbN2heXFSSIHnuZ49zeG:{YYTpc44h[XO|YYmsJGlEPTB;MD6xO{DPxE1? M3K4dFIxODh4MUS5
human U1 cells MUTGeY5kfGmxbjDhd5NigQ>? NIjCclFCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJfW2jbjDpcY12dm:mZX\pZ4lmdmO7II\pdpV{KDFiaX7m[YN1\WRiaX6gbJVu[W5iVUGgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iC4aYLhcEBT\X[ncoPlJJRz[W6|Y4LpdJRie2ViYomgX|NJZVSWUDDpcoNwenCxcnH0bY9vKGG|c3H5MEBKSzVyPUKuN{DPxE1? MofwNlAxQDZzNEm=
human MDM cells MYfDfZRwfG:6aXRCpIF{e2G7 Mk\RR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWROKGOnbHzzJIlv\mWldHXkJJdqfGhiSIXtZY4hcW2vdX7v[IVncWOrZX7jfUB3cXK3czCxJGJCVCCkeTDNWHMh[XO|YYmsJHREPTB;MD62OkDPxE1? MXKyNFA5PjF2OR?=
human MDA-MB-231 cells M3jRd2N6fG:2b4jpZ:Kh[XO|YYm= MYrDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNSGEuVUJvMkOxJINmdGy|IHnuJJBz\XOnbnPlJI9nKDJyIIXNJINpdG:{b4H1bY5mKGK7IGPSRkBie3OjeTygS2k2OD1yLk[5JO69VQ>? M3K2WVE5PjlzOEm0
Huh-7 cells MX\GeY5kfGmxbjDhd5NigQ>? MmXlR49ueG:3bnSge4F{KHSnc4Tl[EBnd3JiaYTzJIFjcWyrdImgeI8hcW6qaXLpeEBp\XCjdHn0bZMhSyC4aYLhcEBTVkFicnXwcIlk[XSrb36gbY4hUHWqLUegZ4VtdHNiKHj1cYFvKGincHH0c41iKGOnbHzzLUwhTUN3ME2yJO69VQ>? MYixOVE4PzR4NB?=
HFF cells NIG1e25HfW6ldHnvckBie3OjeR?= M2O4VmhEVVZicHzhdZVmKGG|c3H5JJdieyCyZYLmc5Ju\WRidYPpcochUE[IIHPlcIx{KGGwZDDl[oZm[3Rid3HzJINidGO3bHH0[YQh[XNiYTDw[ZJk\W62YXflJI9nKHKnZIXjeIlwdiCrbjDueY1j\XJib3[gdIxieXWnczygTWM2OD1{LkWg{txO MmnpNVA5QDJ|N{G=
human MDA-MB-468 cells NXXrRWtTS3m2b4TvfIlkyqCjc4PhfS=> M2WwWGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1FSS2PQj20Olgh[2WubIOgbY4heHKnc3XuZ4Uhd2ZiMkCgeW0h[2iub4LvdZVqdmViYomgV3JDKGG|c3H5MEBIUTVyPUGwMlI6KM7:TR?= MUGxPFY6OTh7NB?=
human 184B5 cells NFrjWXdEgXSxdH;4bYPDqGG|c3H5 NU\5ZYRJS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hOTh2QkWgZ4VtdHNiYomgV3JDKGG|c3H5MEBIUTVyPUSwJO69VQ>? NIDQPY4yQDZ7MUi5OC=>

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
PUMA / p-FoxO3a / p-AKT ; 

PubMed: 20978166     

p53-KO cells were treated with the AKT inhibitor triciribine (1 μM) or MK-2206 (25 μM) for 1 hr (for analysis of p-FoxO3a and p-AKT) or 24 hr (for analysis of PUMA), and indicated proteins were analyzed by Western blotting.

TRF2 / 53BP1 ; 

PubMed: 23862686     

TIF analysis of HTC75 cells serum starved (0.01% FBS) for 16 h or treated with triciribine (1µM) for 3 hours. Cells were immunostained with anti-53BP1 (red) and TRF2 (green) antibodies. DMSO-treated cells were used as controls. Arrows indicate overlapping foci. 

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]
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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]
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  • 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]
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  • Animal Models: OVCAR3, OVCAR8, PANC1, OVCAR5 and COLO357 tumor cells are injected s.c. into 80week-old female nude mice.
  • 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, API-2
Smiles CN1C2=NC=NC3=C2C(=CN3C4C(C(C(O4)CO)O)O)C(=N1)N

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID