EC21
EC21 is a PROTAC degrader that binds to CDK6, thereby targeting EYA2 for degradation. EC21 enhances the interaction between CDK6 and EYA2, thereby driving ubiquitin-proteasome-dependent degradation of EYA2. EC21 reduces EYA2 protein levels in tumor tissues without obvious toxicity. EC21 disrupts the DNA damage repair pathway and inhibits cancer cell proliferation. EC21 can be used in breast cancer-related research.
(Pink: EYA2 ligand (HY-184746); Blue: CDK6 ligand (HY-50767); Black: linker).
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 分子式: C53H60N10O11
- 分子量:1013.10
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- 純度とドキュメンテーション
- 参考文献
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PROTACs アイソフォーム固有の製品をすべて表示
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生物活性
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CDK6 |
EYA2 |
EC21 (72 h) potently inhibits the proliferation of MDA-MB-231 and 4T1 triple-negative breast cancer cells, with IC50 values of 7.84 μM and 6.56 μM, respectively, after 72 h of treatment[1].
EC21 (10 μM; 0-24 h) induces time-dependent degradation of EYA2 protein in MDA-MB-231 and 4T1 triple-negative breast cancer cells (following treatment with 10 μM for up to 24 h)[1].
EC21 (5-20 μM; 24 h) induces concentration-dependent degradation of EYA2 protein in MDA-MB-231 and 4T1 triple-negative breast cancer cells[1].
EC21 (10 μM EC21 + 100 μg/mL Cycloheximide (HY-12320); 12 h) accelerates the degradation of pre-existing EYA2 protein in MDA-MB-231 and 4T1 triple-negative breast cancer cells[1].
EC21 (10 μM EC21; 4 h co-incubation following 2 h pre-treatment with 10 μM MG132 (HY-13259)) induces EYA2 degradation in MDA-MB-231 and 4T1 triple-negative breast cancer cells, and this process is dependent on the ubiquitin-proteasome system[1].
EC21 (10 μM; 6 h) enhances the physical interaction between endogenous CDK6 and EYA2 in MDA-MB-231 and 4T1 triple-negative breast cancer cells in a reciprocal co-immunoprecipitation assay[1].
EC21 (10 μM; 6 h) increases the colocalization level of CDK6 and EYA2 in MDA-MB-231 and 4T1 triple-negative breast cancer cells, with Pearson correlation coefficients of 0.680 and 0.699, respectively[1].
EC21 (10 μM; 24 h) inhibits the migration of MDA-MB-231 and 4T1 triple-negative breast cancer cells[1].
EC21 (10 μM; 14 days) potently inhibits the clonogenic capacity of MDA-MB-231 and 4T1 triple-negative breast cancer cells[1].
Treatment with EC21 (10 μM; 24 h) induces apoptosis in MDA-MB-231 and 4T1 triple-negative breast cancer cells, and the total apoptosis rate is higher than that of the control group[1].
EC21 (10 μM; 24 h) induces G1 phase arrest and impairs G1/S cell cycle transition in MDA-MB-231 and 4T1 triple-negative breast cancer cells when treated at 10 μM for 24 h[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:0, 6, 12, 24 h
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Result:Induced a time-dependent reduction in EYA2 protein levels in both cell lines.
Caused significant decreases observed at 12 h and 24 h compared to the 0 h control.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:5, 10, 20 μM
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Incubation Time:24 h
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Result:Induced a concentration-dependent reduction in EYA2 protein levels in both cell lines.
Caused significant decreases observed at all tested concentrations compared to the 0 μM control.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM, 100 μg/mL CHX
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Incubation Time:12 h
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Result:Resulted in markedly lower EYA2 protein levels in cells co-treated with EC21 and CHX compared to cells treated with CHX alone.
Indicated acceleration of degradation of pre-existing EYA2 protein.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM,10 μM MG132
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Incubation Time:2 h (MG132 pre-incubation); 4 h ( co-incubation)
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Result:Pre-treatment with MG132 effectively rescued the EC21-induced reduction in EYA2 protein levels.
Confirmed proteasome involvement in EYA2 degradation.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:6 h
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Result:Markedly enhanced the association of endogenous EYA2 with CDK6 in both cell lines compared to untreated controls.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:2 h (pre-treatment with single-target inhibitors); 24 h (EC21 co-incubation)
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Result:Pre-incubation with either palbociclib or ETC-616 significantly attenuated EC21-induced EYA2 degradation in both cell lines.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:6 h; 4 h co-incubation after 2 h pre-treatment with single-target inhibitors
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Result:Significantly increased intracellular co-localization of CDK6 and EYA2, raising the Pearson correlation coefficient to 0.680 in MDA-MB-231 and 0.699 in 4T1 cells.
Had enhanced co-localization blocked by pre-treatment with palbociclib or ETC-616.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Markedly suppressed wound closure in both cell lines at 24 h compared to control treatments.
Indicated reduced cell migration.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:14 days
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Result:Resulted in the lowest number of surviving colonies compared to control treatments.
Indicated stronger inhibition of clonogenic growth.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Induced a higher rate of total apoptosis (early + late apoptotic cells) compared to control treatments in both cell lines.
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Cell Line:MDA-MB-231, 4T1 triple-negative breast cancer cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Induced pronounced G1-phase arrest in both cell lines.
Impaired the G1/S transition more effectively than control treatments.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female, 6-8 weeks old, 18-22 g, subcutaneous 4T1 murine mammary carcinoma cell implantation)[1]
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Dosage:10 mg/kg; 30 mg/kg
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Administration:i.p.; every two days; 21 days
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Result:Dose-dependently inhibited tumor growth and reduced tumor weight and intratumoral EYA2.
Decreased Ki67 and increased γ-H2AX.
No significant body-weight loss or major-organ pathology was observed at 10 mg/kg; 30 mg/kg caused a nonsignificant downward trend in body weight.
化学情報
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分子量 1013.10
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分子式 C53H60N10O11
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SMILES
O=C(C1=CC(OC2=CC=CC=C2)=CC=C1)N/N=C/C(O3)=CC=C3C(NCCOCCOCCOCCOCC(N(CC4)CCN4C(C=N5)=CC=C5NC(N=C6N7C8CCCC8)=NC=C6C(C)=C(C(C)=O)C7=O)=O)=O
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
EC21 関連分類
HY-184678 関連分類
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