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Cat. No.: HY-184678

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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).

연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.

화학식: C₅₃H₆₀N₁₀O₁₁
분자량:1013.10

보관:

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

EC21 Chemical Structure

Amount: USD 0.00

* 장바구니에 담기 전 물품의 수량을 선택해 주십시오.

Use of MCE Products

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

Biological Activity
- 제품 설명
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

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^[1]. (Pink: EYA2 ligand (HY-184746); Blue: CDK6 ligand (HY-50767); Black: linker).

IC₅₀ & Target^[1]

CDK6

EYA2

All PROTACs Isoforms :

In Vitro

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.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

0, 6, 12, 24 h
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.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

5, 10, 20 μM
Incubation Time:

24 h
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.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM, 100 μg/mL CHX
Incubation Time:

12 h
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.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM,10 μM MG132
Incubation Time:

2 h (MG132 pre-incubation); 4 h ( co-incubation)
Result:

Pre-treatment with MG132 effectively rescued the EC21-induced reduction in EYA2 protein levels.
Confirmed proteasome involvement in EYA2 degradation.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

6 h
Result:

Markedly enhanced the association of endogenous EYA2 with CDK6 in both cell lines compared to untreated controls.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

2 h (pre-treatment with single-target inhibitors); 24 h (EC21 co-incubation)
Result:

Pre-incubation with either palbociclib or ETC-616 significantly attenuated EC21-induced EYA2 degradation in both cell lines.

Immunofluorescence^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

6 h; 4 h co-incubation after 2 h pre-treatment with single-target inhibitors
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.

Cell Migration Assay ^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Markedly suppressed wound closure in both cell lines at 24 h compared to control treatments.
Indicated reduced cell migration.

Cell Proliferation Assay^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

14 days
Result:

Resulted in the lowest number of surviving colonies compared to control treatments.
Indicated stronger inhibition of clonogenic growth.

Apoptosis Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Induced a higher rate of total apoptosis (early + late apoptotic cells) compared to control treatments in both cell lines.

Cell Cycle Analysis^[1]

Cell Line:

MDA-MB-231, 4T1 triple-negative breast cancer cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Induced pronounced G1-phase arrest in both cell lines.
Impaired the G1/S transition more effectively than control treatments.

In Vivo

EC21 (10-30 mg/kg; i.p.; every two days; 21 days) suppresses breast tumor growth in a dose-dependent manner, induces on-target EYA2 degradation in tumor tissues, reduces tumor cell proliferation, and increases DNA damage, with significant efficacy observed at 10 mg/kg and enhanced activity at 30 mg/kg^[1].

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

Animal Model:

BALB/c (female, 6-8 weeks old, 18-22 g, subcutaneous 4T1 murine mammary carcinoma cell implantation)^[1]
Dosage:

10 mg/kg; 30 mg/kg
Administration:

i.p.; every two days; 21 days
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.

Chemical Information

분자량 1013.10
화학식 C₅₃H₆₀N₁₀O₁₁
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
선적

Room temperature in continental US; may vary elsewhere.
보관

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

순도&문서

Handling Instructions (2659 KB)

References

[1]. Zhang Y, et al. A PROTAC-inspired bifunctional small molecule recruits CDK6 to target EYA2 degradation and suppress breast tumor growth. European journal of medicinal chemistry. 2026 Jun 18;317:119065. [Content Brief]

Calculators

몰농도 계산기

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

농도 희석 계산기

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

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.

Bioz

Keywords

MOQ

Minimum order quantity

100 mg

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Other size

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Amount: USD 0.00

Biological Activity
- 제품 설명
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
순도&문서
References

상품명:
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수량:
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상품명:
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수량:

EC21

All PROTACs Isoforms

Biological Activity

Chemical Information

순도&문서

References

Calculators

Help & FAQs

EC21 Related Classifications

HY-184678 Related Classifications

Bioz