| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C19H18N4O2 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
AZD1080 is a potent, selective GSK3 inhibitor that inhibits recombinant human GSK3α and GSK3β, with pKi (IC50) values of 8.2 (6.9 nM) and 7.5 (31 nM), respectively. It is supplied as a light yellow to orange solid (C19H18N4O2, MW 334.37) at 99.16% purity.
Physical & Chemical Properties
| CAS Number | 612487-72-6 |
|---|---|
| Molecular Formula | C19H18N4O2 |
| Molecular Weight | 334.37 g/mol |
| Purity | 99.16% |
| Appearance | Solid |
| Color | Light yellow to orange |
| SMILES | OC(N1)=C(C2=CC=C(CN3CCOCC3)C=N2)C4=C1C=CC(C#N)=C4 |
| Target | GSK-3α, GSK-3β, cdk5, cdk2, cdk1 |
| Signaling Pathway | PI3K/Akt/mTOR; Stem Cell/Wnt |
| Solubility | In Vitro: DMSO: 21.35 mg/mL (63.85 mM; Requires sonication and warming; 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, 6 months; -20°C, 1 month. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
GSK-3α 8.2 (pKi) |
GSK-3β 7.5 (pKi) |
cdk5 6.4 (pKi) |
cdk2 5.9 (pKi) |
cdk1 5.7 (pKi) |
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 | 21.35 mg/mL (63.85 mM) | requires sonication and warming; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); 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 | ≥ 2.5 mg/mL (7.48 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 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 | ≥ 2.5 mg/mL (7.48 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 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). |
Data provided by the manufacturer.
In Vitro
AZD1080 selectivity: 37-fold over cdk2 (pKi=5.9; 1150 nM), 14-fold over cdk5 (pKi=6.4; 429 nM), 64-fold over cdk1 (pKi=5.7; 1980 nM), and >323-fold over Erk2 (pKi< 5; >10 μM). AZD1080 (at 10 μM) is also evaluated for pan-kinase selectivity and shows good overall selectivity versus 23 kinases and against 65 different receptors, enzymes and ion channels in the MDS Pharma screen (< 50% effect at 10 μM AZD1080). Tau phosphorylation is inhibited in a concentration-dependent manner by AZD1080 (IC50=324 nM) and by the non-selective reference GSK3 inhibitor LiCl (IC50=1.5 mM), showing AZD1080 to be more potent than LiCl by several orders of magnitude[1].
In Vivo
Pharmacokinetic analysis of blood after oral administration revealed good oral bioavailability of AZD1080 in rats (15-24%) and a 7.1 h half-life, which makes AZD1080 an attractive candidate for additional in vivo testing. In mice, oral treatment with AZD1080 for 3 days (subchronic) at 4 or 15 μmol/kg significantly prevented the memory deficit induced by MK-801 (AZD1080 vs. MK-801, p<0.05 at 4 μmol/kg and p<0.01 at 15 μmol/kg), which raises the possibility that a longer treatment period may be needed for synapses to be primed to work effectively[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Animal Administration[1]
Mice[1] Use a total of 161 male C57BL/6 mice, 8-12 weeks of age. Keep the animals in conventional housing (3-5 mice per cage) with standard rodent chew and tap water ad libitum. Typically include 9-12 mice per experimental group and 2-4 mice per satellite group (for determination of compound exposure in plasma and brain, see below). Dose mice with AZD1080 at 4.0 or 15 μmol/kg, or with vehicle (water with 0.5% ascorbic acid, 0.01% EDTA, pH 2.0), by oral gavage (10 mL/kg), acutely or subchronically (twice daily) for 3 days. Perform the training trial at 1.5, 3, or 5 h after the final administration of AZD1080. To disrupt learning, give mice subcutaneous MK-801 (0.1 or 0.15 mg/kg; (+)-MK-801 hydrogen maleate) or vehicle (saline) 30 min prior to the training trial. Rats[1] Use a total of 71 adult male Sprague-Dawley rats (250-300 g). Give the rats a single acute oral-gavage dose of AZD1080 at 1, 3 or 10 μmol/kg, or vehicle (water with 0.5% ascorbic acid, 0.01% EDTA, pH 2.0), at a dosing volume of 5 mL/kg. At 1, 2, 3, 6, or 24 h after administration, anesthetize the rats and sample blood from the abdominal aorta into heparin micro tainer tubes. Isolate peripheral blood mononuclear cells (PBMC) from the blood samples. Obtain separate blood samples for plasma processing and subsequent bioanalysis.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. Sci Transl Med 2018 Jul 18;10(450):eaaq1093.
Transcriptome analysis of newly established carboplatin-resistant ovarian cancer cell model reveals genes shared by drug resistance and drug-induced EMT. Br J Cancer 2023 Mar;128(7):1344-1359. PMID: 36717670
Evidence for investigating GSK-3 inhibitors as potential therapeutics for severe COVID-19. Biochem Biophys Res Commun 2022 May 21;605:171-176. PMID: 35367865
bioRxiv. 2026 May 7.
University of Rijeka. 2023.
Patent. US20170165230A1.
