Cat. No.: HY-111045

CG0009

CG0009 is a GSK3 inhibitor. CG0009 activates p53 transcriptional activity, depletes Cyclin D1, induces Caspase-dependent Apoptosis, and activates Wnt/β-catenin target genes. CG0009 does not induce epithelial-mesenchymal transition, does not increase Vimentin/N-cadherin, and does not decrease E-cadherin. CG0009 exhibits anticancer activity against breast cancer and colorectal cancer.

For research use only. We do not sell to patients.

CAS No.: 944744-57-4
Formula: C₂₆H₃₁N₇O
Molecular Weight:457.58

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (292 KB)

CG0009 Chemical Structure

CAS No.: 944744-57-4

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- Cellular Effect
- In Vitro
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

All GSK-3 Isoforms :

All CDK Isoforms :

All Caspase Isoforms :

All Wnt Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
MCF7	IC50	0.49 μM	Cytotoxicity against human MCF7 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human MCF7 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
Hs-578T	IC50	1 μM	Cytotoxicity against human HS578T breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human HS578T breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
MDA-MB-435	IC50	4.3 μM	Cytotoxicity against human MDA-MB-435 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human MDA-MB-435 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
MDA-MB-231	IC50	4.9 μM	Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
NCI/ADR-RES	IC50	11 μM	Cytotoxicity against human NCI/ADR-RES breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human NCI/ADR-RES breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
BT-549	IC50	11 μM	Cytotoxicity against human BT549 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human BT549 breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
T47D	IC50	>100 μM	Cytotoxicity against human T47D breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human T47D breast cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238
HCT-116	IC50	0.22 μM	Cytotoxicity against human HCT116 colon cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay. Cytotoxicity against human HCT116 colon cancer cells assessed as viability reduction after 48 hrs exposure by CellTiter-Glo luminescent assay.	23565238

In Vitro

Anti-cancerCell Cycle RegulationApoptosisOthers

Anti-cancer

CG0009 (0.001-100 μM; 48 h) reduces viability most potently in HCT116 (IC₅₀ 0.22 μM) and MCF7 (0.49 μM), while T47D remains resistant (>100 μM)^[1].

Anti-cancer

Cell Cycle Regulation

CG0009 (1 μM; 0-48 h) depletes cyclin D1 in ERα-negative HS578T, MDA-MB-435, MDA-MB-231, and NCI/ADR-RES cells, with complete loss by 40 h in moderately sensitive lines^[1].
CG0009 decreases proliferation and survival in different breast cancer cell lines, reduces cyclin D1 expression, and activates p53^[2].

Apoptosis

CG0009 (1 μM; 0-32 h) induces caspase-9/PARP apoptosis in MCF7 but only delayed PARP cleavage without detectable caspase-9 activation in T47D^[1].

Cell Cycle Regulation

CG0009 (1 μM; 0-48 h) reduces ERα and cyclin D1 transcripts in MCF7 but causes oscillatory ERα/cyclin D1 expression in T47D^[1].
CG0009 (1 μM; 0-48 h) completely depletes ERα and cyclin D1 protein in MCF7 but not T47D^[1].

Others

CG0009 (1 μM; 0-24 h) inactivates GSK3α/β in HCT116, MCF7, and T47D by increasing Ser21/Ser9 phosphorylation and decreasing Tyr216 phosphorylation^[1].
CG0009 (1 μM; 0-24 h) does not sustain AKT Ser473 phosphorylation in MCF7 cells^[1].
CG0009 (1 μM; 0-48 h) does not increase AKT kinase activity in MCF7 lysates^[1].
CG0009 (1 μM; 0-24 h) induces p53 and p21 protein in MCF7 but not T47D^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:

human breast cancer cell lines (MCF7, HS578T, MDA-MB-435, MDA-MB-231, NCI/ADR-RES, BT549, T47D) and HCT116 colon cancer cells
Concentration:

0.001, 0.01, 0.1, 1, 10, 100 μM
Incubation Time:

48 h (after 24 h seeding)
Result:

IC₅₀ values were 0.49 μM in MCF7, 1 μM in HS578T, 4.3 μM in MDA-MB-435, 4.9 μM in MDA-MB-231, 11 μM in NCI/ADR-RES, 11 μM in BT549, >100 μM in T47D, and 0.22 μM in HCT116.
Growth was suppressed across the panel, with HCT116 and MCF7 most sensitive and T47D resistant.

Western Blot Analysis^[1]

Cell Line:

HCT116, MCF7, and T47D cells
Concentration:

1 μM
Incubation Time:

0, 8, 16, 24 h
Result:

Inactivating phosphorylation of GSK3α Ser21 and GSK3β Ser9 was enhanced, activating phosphorylation of GSK3β Tyr216 was suppressed in all three cell lines, and total GSK3α/β was slightly decreased.

Western Blot Analysis^[1]

Cell Line:

MCF7 and T47D cells
Concentration:

1 μM
Incubation Time:

0, 8, 16, 24, 32 h
Result:

In MCF7, caspase-9 and PARP were activated after 8 h.
In T47D, PARP activation was delayed until 32 h, and caspase-9 activation was not detectable.

Western Blot Analysis^[1]

Cell Line:

MCF7 cells
Concentration:

1 μM
Incubation Time:

0, 8, 16, 24 h
Result:

Normalized pAKT Ser473 values were 1, 0.9, 1, and 0.8 at 0, 8, 16, and 24 h, respectively.

Real Time qPCR^[1]

Cell Line:

MCF7 and T47D cells
Concentration:

1 μM
Incubation Time:

0, 8, 16, 24, 32, 40, 48 h
Result:

In MCF7, ERα and cyclin D1 transcripts were significantly reduced approximately 5-fold up to 48 h.
In T47D, ERα initially decreased at 8 h, increased to approximately 8-fold at 24 h, and decreased again at 48 h; cyclin D1 showed a decrease followed by a subsequent increase.
T47D expressed approximately 10-fold higher cyclin D1 transcripts than MCF7.

Western Blot Analysis^[1]

Cell Line:

MCF7 and T47D cells
Concentration:

1 μM
Incubation Time:

0, 8, 16, 24, 32, 40, 48 h
Result:

Complete ablation of ERα and cyclin D1 proteins occurred in MCF7, but not in T47D.

Related Protocols :

Chemical Information

CAS No. 944744-57-4
Molecular Weight 457.58
Formula C₂₆H₃₁N₇O
SMILES

O=C(NC=1C=NC=CC1C)C=2C=CN=C3N=C(NC32)C=4C=CC(=CC4)N(C)CCN(CC)CC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (292 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Kim HM, et al. CG0009, a novel glycogen synthase kinase 3 inhibitor, induces cell death through cyclin D1 depletion in breast cancer cells. PloS one. 2013;8(4):e60383.

[2]. Tecalco-Cruz AC, et al. Mechanisms that Increase Stability of Estrogen Receptor Alpha in Breast Cancer. Clinical breast cancer. 2017 Feb;17(1):1-10.

[3]. Pal K, et al. Inhibition of GSK-3 induces differentiation and impaired glucose metabolism in renal cancer. Molecular cancer therapeutics. 2014 Feb;13(2):285-96.

[4]. Trnski D, et al. GSK3β and Gli3 play a role in activation of Hedgehog-Gli pathway in human colon cancer - Targeting GSK3β downregulates the signaling pathway and reduces cell proliferation. Biochimica et biophysica acta. 2015 Dec;1852(12):2574-84.

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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CG0009

All GSK-3 Isoforms

All CDK Isoforms

All Caspase Isoforms

All Wnt Isoforms