Fig. 1 · Structure

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CCT128930

Cat. No. A11031 CAS 885499-61-6

AKT Inhibitor

CCT128930 is an ATP-competitive AKT inhibitor that is a potent, advanced lead pyrrolopyrimidine compound exhibiting selectivity for AKT over PKA, achieved by targeting a single amino acid difference.

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Biological Activity

Target & Activity

Target Activity Value
Akt2 (Cell-free assay) 6 nM
p70 S6K (Cell-free assay) 120 nM
PKA (Cell-free assay) 168 nM

Cellular Effect

Cell Line Activity Value Description Reference
PC-3M GI50 12 nM Antiproliferative activity against human PC3M cells after 96 hrs by SRB assay [PMID: 20151677]
PC-3M IC50 12 μM Growth inhibition of human PC3M cells by SRB assay [PMID: 18345609]
U-87MG ATCC IC50 0.66 nM Inhibition of PKB in human U87MG cells assessed as GSK3-beta phosphorylation by ELISA [PMID: 20151677]
U-87MG ATCC IC50 0.66 μM Inhibition of GSK3-beta in human U87MG cells by ELISA [PMID: 18345609]
U-87MG ATCC GI50 5 nM Antiproliferative activity against human U87MG cells after 96 hrs by SRB assay [PMID: 20151677]
U-87MG ATCC IC50 5 μM Growth inhibition of human U87MG cells by SRB assay [PMID: 18345609]
U-87MG ATCC GI50 6.3 μM Antiproliferative activity against human U87MG cells after 96 hrs by SRB assay [PMID: 30583248]

In Vitro Studies

In HeyA8 and SKOV3 cells, higher concentrations of BX795 and CCT128930 induced stronger inhibition of pS6 (S240/S244) and pS6 (S235/S236) expression. In macrophages, CCT128930 treatment significantly reduced supernatant lactate levels compared with trained immunity (TI) and control groups, with the compound effect isolated by the comparison: TI + LPS + CCT128930 vs TI + LPS. In sorted MDA-MB-231 tdTomato− cells under serum free low attachment conditions, increasing CCT128930 concentrations were associated with fewer tumorspheres. [1,2,3]

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

Protein expression inhibition in HeyA8 cells

Cell-based study · HeyA8 cells [1]

HeyA8 cells in three-dimensional culture were treated with CCT128930 at 3.33 μM or 10 μM for 24 hours. Higher concentrations of BX795 and CCT128930 induced stronger inhibition of pS6 (S240/S244) and pS6 (S235/S236) expression.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteinsReported result The higher concentration of BX795 and CCT128930 induced stronger inhibition of pS6 (S240/S244) and pS6 (S235/S236) expression in HeyA8 and SKOV3 cells.[1]

Literature-Reported Treatment Conditions

Treatment concentration
3.33 μM or 10 μM
Exposure duration
24 hours
Method
three-dimensional cell culture
Reported limits
Not stated in the sentences used: vehicle, control.
Methods and source locations

Compound reported in the paper: CCT128930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results (S48); Fig 4 legend (S70)

Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteins: Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteins — Results (S48); Fig 4 legend (S70)

Lactate secretion in macrophages

Cell-based study · macrophages [2]

Macrophages received CCT128930 treatment for 24 h. Treatment significantly reduced lactate levels in cellular supernatants compared with trained immunity (TI) and control groups, with the compound effect isolated by the comparison: TI + LPS + CCT128930 vs TI + LPS.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Lactate secretion levelsReported result CCT128930 treatment significantly reduced lactate levels in cellular supernatants compared to both trained immunity (TI) and control groups[2]

Literature-Reported Treatment Conditions

Exposure duration
24 h
Co-treatment
Other interventions in this design: β-glucan 5 μg/mL; LPS 100 ng/mL. Compound effect isolated by the comparison: TI + LPS + CCT128930 vs TI + LPS.
Reported limits
Not stated in the sentences used: dose, route, vehicle.
Methods and source locations

Compound reported in the paper: CCT128930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > β-glucan induced trained immunity ameliorates acute lung injury via PDK1-dependent metabolic modulation (S16); Results > Akt2 phosphorylation promotes the activation of PDK1 in ALI (S29); Fig. 4 legend (S119); Fig. 5 legend (S128, S134)

Lactate secretion levels: Lactate secretion levels; comparator: trained immunity (TI) and control groups — Results > Akt2 phosphorylation promotes the activation of PDK1 in ALI (S29); Fig. 5 legend (S128)

Tumorsphere formation in sorted breast cancer cells

Cell-based study · Sorted MDA-MB-231 tdTomato− cells [3]

Sorted MDA-MB-231 tdTomato− cells were treated with CCT128930 at 6.25 µM, 12.5 µM, and 25 µM under serum free low attachment conditions. Fewer tumorspheres formed with increasing CCT128930 concentrations.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
formation of tumorspheresReported result With increasing concentrations of CCT128930, there were fewer tumorspheres[3]

Literature-Reported Treatment Conditions

Treatment concentration
6.25 µM, 12.5 µM, and 25 µM
Exposure duration
monitored over time
Method
in serum free low attachment conditions
Reported limits
Not stated in the sentences used: vehicle, control.
Methods and source locations

Compound reported in the paper: CCT128930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Figure 8 legend (S161, S162)

formation of tumorspheres: formation of tumorspheres — Figure 8 legend (S161, S162)

Protein expression inhibition in SKOV3 cells

Cell-based study · SKOV3 cells [1]

SKOV3 cells in three-dimensional culture were treated with CCT128930 at 3.33 μM or 10 μM for 24 hours. Higher concentrations of BX795 and CCT128930 induced stronger inhibition of pS6 (S240/S244) and pS6 (S235/S236) expression.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteinsReported result The higher concentration of BX795 and CCT128930 induced stronger inhibition of pS6 (S240/S244) and pS6 (S235/S236) expression in HeyA8 and SKOV3 cells.[1]

Literature-Reported Treatment Conditions

Treatment concentration
3.33 μM or 10 μM
Exposure duration
24 hours
Method
three-dimensional cell culture
Reported limits
Not stated in the sentences used: vehicle, control.
Methods and source locations

Compound reported in the paper: CCT128930

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results (S48); Fig 4 legend (S70)

Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteins: Western blot analysis of pPRAS40 (T246), pS6 (S240/S244), and pS6 (S235/S236) proteins — Results (S48); Fig 4 legend (S70)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 885499-61-6
Applications AKT Inhibitor
Formula C18H20ClN5
Molecular Weight 341.8
SMILES
C1CN(CCC1(CC2=CC=C(C=C2)Cl)N)C3=NC=NC4=C3C=CN4

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 59 mg/mL (172.59 mM)
Water Insoluble
Ethanol 5 mg/mL (14.63 mM)

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
3 mg/mL
Vehicle
2% DMSO+30% PEG 300+2% Tween 80+ddH2O

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] Choi JI, Park SH, Lee HJ, et al. Inhibition of Phospho-S6 Kinase, a Protein Involved in the Compensatory Adaptive Response, Increases the Efficacy of Paclitaxel in Reducing the Viability of Matrix-Attached Ovarian Cancer Cells. PLoS One (2016). PMID: 27148873 DOI: 10.1371/journal.pone.0155052 Source material
  2. [2] Sun Z, Meng H, Wang X, et al. Trained immunity attenuated acute lung injury by activating alveolar macrophages via AKT2-PDK1 axis-mediated metabolic reprogramming. J Transl Med (2025). PMID: 41437043 DOI: 10.1186/s12967-025-06879-4 Source material
  3. [3] Gener P, Rafael D, Seras-Franzoso J, et al. Pivotal Role of AKT2 during Dynamic Phenotypic Change of Breast Cancer Stem Cells. Cancers (Basel) (2019). PMID: 31357505 DOI: 10.3390/cancers11081058 Source material

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