| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C18H20ClN5 |
| Purity | |
| Activity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
CCT128930 is an ATP-competitive, selective inhibitor of AKT, with an IC50 of 6 nM against AKT2. It shows 28-fold selectivity over the closely related PKA kinase (IC50 168 nM) by targeting Met282 of AKT (Met173 of the PKA-AKT chimera), and 20-fold selectivity over p70S6K (IC50 120 nM). Antitumor activity has been reported. It is supplied as an off-white to yellow solid (C18H20ClN5, MW 341.84) at 98.95% purity.
Physical & Chemical Properties
| CAS Number | 885499-61-6 |
|---|---|
| Molecular Formula | C18H20ClN5 |
| Molecular Weight | 341.84 g/mol |
| Purity | 98.95% |
| Appearance | Solid |
| Color | Off-white to yellow |
| SMILES | ClC1=CC=C(C=C1)CC2(CCN(CC2)C3=NC=NC4=C3C=CN4)N |
| Target | Akt2, p70S6K, PKA |
| Signaling Pathway | PI3K/Akt/mTOR; Autophagy; Apoptosis |
| Bioactivity Class | Autophagy, Apoptosis |
| Solubility | In Vitro: DMSO: 33.33 mg/mL (97.50 mM; Requires sonication and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
Akt2 6 nM (IC50) |
p70S6K 120 nM (IC50) |
PKA 168 nM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 33.33 mg/mL (97.50 mM) | requires sonication and warming and heat to 60°C; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.08 mg/mL (6.08 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.08 mg/mL (6.08 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.08 mg/mL (6.08 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
CCT128930 inhibits growth of the PTEN-deficient human tumor cell lines U87MG (human glioblastoma), LNCaP (human prostate cancer), and PC3 (human prostate cancer), with GI50 values of 6.3 μM, 0.35 μM, and 1.9 μM, respectively[1]. In U87MG human glioblastoma cells, CCT128930 (0.1-60 μM; 1 hour) first induces AKT phosphorylation at serine 473, up to 20 μM, and phosphorylation then declines at higher concentrations[1]. At ≥5 μM, CCT128930 inhibits direct AKT substrates (Ser9 GSK3β, pThr246 PRAS40 and pT24 FOXO1/p32 FOXO3a); the downstream target pSer235/236 S6RP is inhibited at ≥ 10 μM. Total protein levels and GAPDH remain generally constant[1]. In U87MG human glioblastoma cells, CCT128930 (18.9 μM) increases pSer473 AKT phosphorylation after 30 minutes, and the increase persists for 48 hours. Total AKT protein signal declines gradually between 8 hours and 48 hours of treatment[1]. In PTEN-null U87MG human glioblastoma cells, CCT128930 (over a 24-hour time period) raises the proportion of cells in G0/G1 phase from 43.6% to 64.8% after 24 hours of treatment[1]. In HepG2 and A549 cells, CCT128930 (0-10 μM; 24 hours) increases Akt phosphorylation rather than inhibiting it. Cell proliferation is inhibited by CCT128930 (0-20 μM; 24 hours) through G1 phase cell cycle arrest, achieved by downregulating cyclinD1 and Cdc25A and upregulating p21, p27 and p53. Apoptosis is triggered by CCT128930 (20 μM), accompanied by activation of caspase-3, caspase-9, and PARP. ERK and JNK phosphorylation is increased in HepG2 cells by CCT128930 (0-20 μM; 24 hours). In HepG2 cells, CCT128930 (0-20 μM; 24 hours) activates a DNA damage response marked by phosphorylation affecting H2AX, ATM (ataxia-telangiectasia mutated), Chk1 and Chk2[2].
In Vivo
In U87MG and BT474 human breast cancer xenografts, CCT128930 (i.p.; 25 or 40 mg/kg, daily or twice daily for 5 days) shows antitumor activity[1]. Pharmacokinetic parameter summary for CCT128930 (25 mg/kg) in CrTacNCr-Fox1nu mice[1]
| Tissue | Route | T1/2 (h) | Tmax (h) | Cmax (μM) | Vss (L) | Cl (L/h) | AUC0-∞ (μMh) | Bioavailability (%) |
| Plasma | i.v. | 0.95 | 0.083 | 6.36 | 0.25 | 0.325 | 4.62 | 100 |
| Plasma | i.p. | 2.33 | 0.5 | 1.28 | N/A | 0.372 | 1.33 | 28.8 |
| Tumor | i.p. | 3.89 | 1 | 8.02 | N/A | 0.06* | 25.8 | N/A |
| Plasma | p.o. | 0.57 | 0.5 | 0.432 | N/A | 0.317 | 0.392 | 8.5 |
*Apparent clearance.
| Animal Model | 6-8 weeks old female CrTacNCr-Fox1nu mice[1] |
|---|---|
| Dosage | 25 mg/kg (U87MG human glioblastoma xenografts) or 40 mg/kg (BT474 human breast cancer xenografts) |
| Administration | i.p. daily for 5 days (U87MG human glioblastoma xenografts); i.p. twice daily for 5 days (BT474 human breast cancer xenografts) |
| Result | Giving a treated:control (T/C) ratio on day 12 of 48%. There was no weight loss associated with this regime in U87MG human glioblastoma xenografts. Had a profound antitumor effect with complete growth arrest and a T/C ratio of 29% on day 22. This regimen was associated with minimal weight loss, with a nadir of only 94.8% of the initial body weight on day 15 of treatment in BT474 human breast cancer xenografts. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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PEBP4 alleviates muscle wasting in lung cancer cachexia via KEAP1-NRF2-mediated redox homeostasis. Cell Death Dis 2026 Jun 3. PMID: 42236665
Trained immunity attenuated acute lung injury by activating alveolar macrophages via AKT2-PDK1 axis-mediated metabolic reprogramming. J Transl Med 2025 Dec 23;23(1):1412. PMID: 41437043
AKT Inhibition Sensitizes to Polo-Like Kinase 1 Inhibitor Onvansertib in Prostate Cancer. Mol Cancer Ther 2024 Oct 1;23(10):1404-1417. PMID: 38894678
CCT128930 is a novel and potent antagonist of TRPM7 channel. Biochem Biophys Res Commun 2021 Jun 30:560:132-138. PMID: 33989904
Patent. US20240066113A1.
Study on Toll-Like Receptor 2-Mediated Inflammation-Induced Familial Hypertension Combined with Hyperlipemia and Its Mechanism. J Healthc Eng 2022 Jan 5:2022:1473597. PMID: 35035808
Dual inhibition of AKT/FLT3-ITD by A674563 overcomes FLT3 ligand-induced drug resistance in FLT3-ITD positive AML. Oncotarget 2016 May 17;7(20):29131-42.
