Cat. No.: HY-148334

MS8815

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MS8815 is a EZH2 PROTAC degrader, with a DC₅₀ of 140 nM in MDA-MB-453 triple-negative breast cancer (TNBC) cells and an IC₅₀ of 8.6 nM against human EZH2. MS8815 induces ubiquitin-proteasome system-mediated degradation of EZH2, reduces the levels of EED, SUZ12, FOXM1, H3K27me3 and global m₆A, and increases the protein level of HMGCS2. MS8815 can be used in the research of breast cancer and prostate cancer.
(Pink: EZH2 ligand (HY-147230); Blue: VHL ligand (HY-125845); Black: linker).

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

Purity: 99.95%
CAS No.: 2855085-25-3
Formula: C₆₅H₈₇N₉O₈S
Molecular Weight:1154.51

Storage:

-20°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

MS8815 Chemical Structure

CAS No.: 2855085-25-3

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Fluorescent Dye

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

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

MS8815 is a EZH2 PROTAC degrader, with a DC₅₀ of 140 nM in MDA-MB-453 triple-negative breast cancer (TNBC) cells and an IC₅₀ of 8.6 nM against human EZH2. MS8815 induces ubiquitin-proteasome system-mediated degradation of EZH2, reduces the levels of EED, SUZ12, FOXM1, H3K27me3 and global m₆A, and increases the protein level of HMGCS2. MS8815 can be used in the research of breast cancer and prostate cancer^[1]^[2]^[3]^[4]^[5]^[6]^[7]. (Pink: EZH2 ligand (HY-147230); Blue: VHL ligand (HY-125845); Black: linker).

IC₅₀ & Target^[1]

EZH2

8.6 nM (IC₅₀)

All Histone Methyltransferase Isoforms :

All PROTACs Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
EOL1	IC₅₀	0.42 μM Compound: MS8815	Anti-proliferative activity against human EOL1 cells assessed as cell viability measured after 5 days incubation by CCK-8 assay Anti-proliferative activity against human EOL1 cells assessed as cell viability measured after 5 days incubation by CCK-8 assay	[PMID: 38295690]
MDA-MB-453	IC₅₀	2.3 μM Compound: 27	Antiproliferative activity against human MDA-MB-453 cells assessed as inhibition of cell viability incubated for 5 days by CCK8 assay Antiproliferative activity against human MDA-MB-453 cells assessed as inhibition of cell viability incubated for 5 days by CCK8 assay	[PMID: 38056296]
MV4-11	IC₅₀	1 μM Compound: MS8815	Anti-proliferative activity against human MV4-11 cells assessed as cell viability measured after 5 days incubation by CCK-8 assay Anti-proliferative activity against human MV4-11 cells assessed as cell viability measured after 5 days incubation by CCK-8 assay	[PMID: 38295690]
RS4-11	IC₅₀	1.4 μM Compound: MS8815	Anti-proliferative activity against human RS4-11 cells assessed as cell viability measured after 5 days incubation by CCK-8 assay Anti-proliferative activity against human RS4-11 cells assessed as cell viability measured after 5 days incubation by CCK-8 assay	[PMID: 38295690]

In Vitro

MS8815 (0.1-10 μM; 6 days) inhibits the growth of luminal breast cancer T47D cells, with an IC₅₀ of 2 μM after 6 days of treatment^[1].
MS8815 (0.1-10 μM; 6 days) inhibits the growth of luminal breast cancer CAMA1 cells, with an IC₅₀ of 2.4 μM after 6 days of treatment^[1].
MS8815 (2.5 μM; until colony formation) reduces colony formation in luminal breast cancer T47D cells^[1].
MS8815 (0.1-5 μM; 48 h) reduces the protein levels of EZH2, EED and H3K27me3 in luminal breast cancer T47D cells in a dose-dependent manner^[1].
MS8815 (0.1-5 μM; 48 h) reduces the protein levels of FOXM1 and EZH2 in luminal breast cancer T47D cells in a dose-dependent manner^[1].
MS8815 (0.1-10 μM; 6 days) inhibits the growth of tamoxifen-resistant luminal breast cancer T47D-TR cells, with an IC₅₀ of 1.9 μM after 6 days of treatment^[1].
MS8815 (2.5 μM; 48 h) reduces the protein levels of EED, FOXM1 and EZH2 in tamoxifen-resistant luminal breast cancer T47D-TR cells^[1].
MS8815 (0.1-10 μM; 2-6 days) inhibits the growth of luminal breast cancer T47D cells in a time-dependent manner, with gradually increased activity observed after 2, 4, and 6 days of treatment^[1].
MS8815 (0.1-100 μM; 72 h) potently inhibits the proliferation of human prostate cancer C4-2 cells, with an IC₅₀ of 2.17 μM^[2].
MS8815 (0.01-3 μM; 3-72 h) induces potent, time-dependent, concentration-dependent, and ubiquitin-proteasome system-dependent degradation of EZH2 in MDA-MB-453 triple-negative breast cancer (TNBC) cells, with a DC₅₀ of 140 nM. It also degrades SUZ12 and EED, and reduces the level of H3K27me3^[4].
MS8815 (0.3-3 μM; 48 h) potently induces EZH2 degradation in BT549 triple-negative breast cancer (TNBC) cells, with nearly complete degradation observed at a concentration of 0.3 μM after 48 h of treatment^[4].
MS8815 (0.03-1 μM; 48 h) does not induce EZH1 degradation in MDA-MB-453 cells, although it inhibits EZH1 methyltransferase activity in biochemical assays^[4].
MS8815 (serially diluted starting from 10 μM; 5 days) potently inhibits the proliferation of triple-negative breast cancer (TNBC) cell lines BT549, MDA-MB-468, MDA-MB-453 and SUM159, with GI₅₀ values ranging from 1.7 to 2.3 μM. It exhibits better activity than EZH2 inhibitors and slightly higher potency than YM281^[4].
MS8815 (serial dilution starting from 10 μM; 5-day proliferation assay; 0.1-1 μM; 48 h degradation assay) potently inhibits the proliferation of primary patient-derived 515a TNBC cells, with a GI₅₀ of 1.4 μM; moreover, after 48 h of treatment, it induces nearly complete degradation of EZH2 at a concentration of 100 nM^[4].
MS8815 efficiently degrades EZH2 in MDA-MB-453 cells (DC₅₀ = 140 nM) and potently inhibits the growth of multiple TNBC cell lines (GI₅₀ = 1.7-2.3 μM) as well as patient-derived primary TNBC ductal adenocarcinoma 515a cells (GI₅₀ = 1.4 μM), overcoming the limitations of traditional EZH2 catalytic inhibitors^[5].
MS8815 (administered for 3 days) acts synergistically with STM2457 to reduce the viability of human prostate cancer C4-2 and PC-3 cells, while only exerting an additive effect in human benign prostatic hyperplasia BPH-1 cells^[6].
MS8815 (2.5 μM; 30 h) reduces the expression of cell cycle-related gene sets and FOXM1 target gene sets in tamoxifen-resistant luminal breast cancer T47D-TR cells^[1].
MS8815 (0.1-2 μM) dose-dependently degrades EZH2, reduces H₃K₂₇me₃ levels and disrupts the PRC2 complex in human prostate cancer C4-2 cells, without altering the level of ADAR1p110^[2].
MS8815 potently inhibits the methyltransferase activity of EZH2 in biochemical assays, with an IC₅₀ value of 8.6 nM^[4].
MS8815 inhibits the methyltransferase activity of EZH1 in biochemical assays, with an IC₅₀ of 62 nM^[4].
MS8815 (10 μM) exhibits selectivity for EZH2 over a panel of 20 protein methyltransferases, and only exerts partial inhibitory activity against MLL1 at 10 μM^[4].
MS8815 (1 μM; 3 days) significantly reduces the global mRNA m⁶A level in human prostate cancer C4-2 cells^[6].
MS8815 (1 μM; 3 days) significantly reduces the global mRNA m⁶A level in human prostate cancer PC-3 cells^[6].
MS8815 (1 μM; 3 days) reduces the protein levels of EZH2, YTHDF1, METTL14, WTAP and H3K27me3 in human prostate cancer C4-2 and PC-3 cells^[6].
MS8815 (20 mg/mL; immediately post-preparation, 5 days postsynthesis) form stable fucoidan-functionalized nanoparticles, and the length of PEG linker is positively correlated with nanoparticle size. A higher GATS1i score correlates with a more significant decrease in colloidal stability over time^[7].

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

Cell Proliferation Assay^[1]

Cell Line:

Luminal breast cancer T47D cells
Concentration:

0.1 μM; 1 μM; 10 μM
Incubation Time:

6 days
Result:

Potently inhibited T47D cell growth with an IC₅₀ of 2 μM, as measured by reduced relative absorbance compared to DMSO control.
Showed significantly greater inhibitory effect than control compounds (MS8815-N, EPZ-6438).

Cell Proliferation Assay^[1]

Cell Line:

Luminal breast cancer CAMA1 cells
Concentration:

0.1 μM; 1 μM; 10 μM
Incubation Time:

6 days
Result:

Inhibited CAMA1 cell growth with an IC₅₀ of 2.4 μM, as measured by reduced relative absorbance compared to DMSO control.
Showed significantly greater inhibitory effect than control compounds (MS8815-N, EPZ-6438).

Western Blot Analysis^[1]

Cell Line:

Luminal breast cancer T47D cells
Concentration:

0.1μM; 0.5 μM; 1 μM; 2.5 μM; 5 μM
Incubation Time:

48 h
Result:

Reduced EZH2 and EED protein levels, and reduced H3K27me3 levels in T47D cells at 2.5 μM.
Caused dose-dependent reductions in EZH2 protein levels with increasing concentrations (0.1 to 5 μM).\n
Reduced FOXM1 and EZH2 protein levels in T47D cells at 2.5 μM, while control compounds did not produce similar reductions.
Caused dose-dependent reductions in FOXM1 protein levels with increasing concentrations (0.1 to 5 μM).

Cell Proliferation Assay^[1]

Cell Line:

Tamoxifen-resistant luminal breast cancer T47D-TR cells
Concentration:

0.1 μM; 1 μM; 10 μM
Incubation Time:

6 days
Result:

Inhibited T47D-TR cell growth with an IC₅₀ of 1.9 μM, as measured by reduced relative absorbance compared to DMSO control.
Showed significantly greater inhibitory effect than control compounds (MS8815-N, EPZ-6438).

Western Blot Analysis^[1]

Cell Line:

Tamoxifen-resistant luminal breast cancer T47D-TR cells
Concentration:

2.5 μM
Incubation Time:

48 h
Result:

Reduced EZH2 and EED protein levels in T47D-TR cells.
Reduced FOXM1 and EZH2 protein levels in T47D-TR cells, while control compounds did not produce similar reductions.

Cell Proliferation Assay^[1]

Cell Line:

Luminal breast cancer T47D cells
Concentration:

0.1 μM; 1 μM; 10 μM
Incubation Time:

2 days; 4 days; 6 days
Result:

Inhibited T47D cell growth in a time-dependent manner, with greater inhibition observed at 6 days compared to 2 or 4 days of treatment.

Cell Viability Assay^[2]

Cell Line:

Human prostate cancer C4-2 cells
Concentration:

0.1 μM; 1 μM; 10 μM; 100 μM
Incubation Time:

72 h
Result:

Potently inhibited C4-2 cell proliferation with an IC₅₀ of 2.17 μM, which was significantly more potent than MS177 (IC₅₀ = 11.78 μM) and EPZ6438 (IC₅₀ = 45.50 μM).

Western Blot Analysis^[4]

Cell Line:

MDA-MB-453 TNBC cells
Concentration:

0.01 μM; 0.03 μM; 0.1 μM; 0.3 μM; 1 μM; 3 μM
Incubation Time:

3 h; 6 h; 12 h; 24 h; 48 h; 72 h
Result:

Induced time-dependent EZH2 degradation, with noticeable degradation at 6 h and maximal degradation at 48 h.
Induced concentration-dependent EZH2 degradation with a DC₅₀ of 140 nM.
Co-treated with EPZ-6438 or VHL-1 completely rescued EZH2 degradation.
Pre-treated with MG132 fully recovered EZH2 degradation, while pre-treated with MLN4924 partially rescued EZH2 degradation.
Degraded PRC2 components SUZ12 and EED, and reduced the H3K27me3 mark at 48-72 h post-treatment.

Western Blot Analysis^[4]

Cell Line:

BT549 TNBC cells
Concentration:

0.3 μM; 3 μM
Incubation Time:

48 h
Result:

Induced nearly complete EZH2 degradation at 0.3 μM, with more effective activity than shorter-linker analogs and PEG-linker analogs.

Western Blot Analysis^[4]

Cell Line:

MDA-MB-453 and SUM159 TNBC cells
Concentration:

0.03 μM; 0.1 μM; 0.3 μM; 1 μM
Incubation Time:

48 h
Result:

Did not induce significant EZH1 degradation in either cell line, despite potent biochemical inhibition of EZH1.

Cell Proliferation Assay^[4]

Cell Line:

BT549, MDA-MB-468, MDA-MB-453, SUM159 TNBC cell lines
Concentration:

serial dilutions starting from 10 μM (2-fold dilutions)
Incubation Time:

5 days
Result:

Effectively suppressed cell proliferation with GI₅₀ values of 2.0 μM (BT549), 1.7 μM (MDA-MB-468), 2.3 μM (MDA-MB-453), and 2.0 μM (SUM159).
This activity was superior to that of the EZH2 inhibitor EPZ-6438 and negative control MS8815N, and slightly more potent than the EZH2 PROTAC YM281.

ELISA Assay^[6]

Cell Line:

Human prostate cancer C4-2 cells
Concentration:

1 μM
Incubation Time:

3 days
Result:

Reduced the global m⁶A level in total RNA to approximately 0.38%, compared to the DMSO control value of approximately 0.52%.

ELISA Assay^[6]

Cell Line:

Human prostate cancer PC-3 cells
Concentration:

1 μM
Incubation Time:

3 days
Result:

Reduced the global m⁶A level in total RNA to approximately 0.3%, compared to the DMSO control value of approximately 0.5%.

Western Blot Analysis^[6]

Cell Line:

human prostate cancer C4-2 and PC-3 cells
Concentration:

1 μM
Incubation Time:

3 days
Result:

Reduced protein levels of EZH2, YTHDF1, METTL14, and WTAP, and decreased H3K27me3 levels compared to DMSO-treated controls.
Left METTL3 protein levels unchanged.

In Vivo

MS8815 (25-200 mg/kg/day; i.p.; five times weekly; 28 days) dose-dependently represses C4-2 PCa xenograft tumor growth in SCID mice, with significant efficacy starting at 50 mg/kg/day, and is well tolerated at all tested doses^[2].
MS8815 (50 mg/kg/day; i.p.; five times weekly; 35 days) exerts significant anti-tumor activity in C4-2 PCa xenografts, and combining MS8815 with ADAR1 knockdown achieves a synergistic reduction in tumor growth in SCID mice^[2].
MS8815 (25-100 mg/kg; i.p.; daily, 5 days per week; 28 days) increases HMGCS2 protein levels and reduces EZH2 and H3K27me3 protein levels in a dose-dependent manner in C4-2 xenograft tumors, with the highest dose (100 mg/kg) achieving the greatest magnitude of effect^[3].
MS8815 (50 mg/kg; i.p.; twice weekly; 5 days on/2 days off for 30 days) reduces tumor burden in a castration-resistant prostate cancer patient-derived xenograft model, with significant decreases in tumor volume and weight relative to vehicle control^[6].
MS8815 (50 mg/kg; i.p.; single dose) achieves high, sustained plasma exposure following a single 50 mg/kg intraperitoneal injection in male Swiss Albino mice and is well tolerated at this dose^[4].

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

Animal Model:

SCID mice (male, 5 weeks old)^[2]
Dosage:

25 mg/kg/day; 50 mg/kg/day; 100 mg/kg/day; 200 mg/kg/day
Administration:

i.p.; five times weekly; 28 days
Result:

Triggered tumor repression, with more significant effects at 50 mg/kg/day and higher doses.
Showed no sudden death or evident weight loss in any treatment group.
Confirmed EZH2 degradation in xenograft tumors.

Animal Model:

SCID mice (male, 5 weeks old)^[2]
Dosage:

50 mg/kg/day
Administration:

i.p.; five times weekly; 35 days
Result:

Significantly reduced tumor volume and weight compared to vehicle control.
Achieved synergistic reduction in tumor volume and weight when co-administered with doxycycline-induced ADAR1 knockdown, with significantly greater efficacy than MS8815 alone or ADAR1 knockdown alone.

Animal Model:

NCG (male, 4 weeks old, immunodeficient, precastrated, C4-2 human prostate cancer cell xenograft)^[3]
Dosage:

25 mg/kg; 50 mg/kg; 100 mg/kg
Administration:

i.p.; daily, 5 days per week; 28 days
Result:

Increased HMGCS2 protein levels to ~11-fold relative to vehicle.
Reduced EZH2 protein levels to ~0.7-fold relative to vehicle.
Reduced H3K27me3 protein levels to ~1.1-fold relative to vehicle (25 mg/kg).
Increased HMGCS2 protein levels to ~16-fold relative to vehicle.
Reduced EZH2 protein levels to ~0.6-fold relative to vehicle.
Reduced H3K27me3 protein levels to ~0.6-fold relative to vehicle (50 mg/kg).
Increased HMGCS2 protein levels to ~19-fold relative to vehicle.
Reduced EZH2 protein levels to ~0.7-fold relative to vehicle.
Reduced H3K27me3 protein levels to ~0.3-fold relative to vehicle (100 mg/kg).

Animal Model:

Swiss Albino (male)^[4]
Dosage:

50 mg/kg
Administration:

i.p.; single dose
Result:

Achieved peak plasma concentration (Cₘₐₓ) of 3.7 μM at 1 hour post-administration.
Maintained plasma concentrations at approximately 3 μM over 4 hours and above 250 nM over 12 hours post-injection.
Displayed no obvious clinical signs of toxicity at the tested dose.

Animal Model:

NCG mice (male, 4-week-old, castrated, subcutaneous implantation of LuCaP 35CR castration-resistant prostate cancer patient-derived xenograft bits)^[6]
Dosage:

50 mg/kg
Administration:

i.p.; twice weekly; 5 days on/2 days off for 30 days
Result:

Reduced final mean tumor volume to approximately 950 mm³ (vs. ~1350 mm³ for vehicle).
Reduced final mean tumor weight to approximately 400 mg (vs. ~700 mg for vehicle).
Reduced EZH2 protein levels and global m⁶A levels in harvested tumors.

Chemical Information

CAS No. 2855085-25-3
Appearance Solid
Molecular Weight 1154.51
Formula C₆₅H₈₇N₉O₈S
Color White to off-white
SMILES

CC(C=C(C)N1)=C(CNC(C2=C(C)C(N(CC)C3CCOCC3)=CC(C4=CC=C(CN5CCN(C(CCCCCCCC(N[C@@H](C(C)(C)C)C(N6[C@H](C(NCC7=CC=C(C8=C(C)N=CS8)C=C7)=O)C[C@@H](O)C6)=O)=O)=O)CC5)C=C4)=C2)=O)C1=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

-20°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (86.62 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

0.8662 mL

4.3308 mL

8.6617 mL

5 mM

0.1732 mL

0.8662 mL

1.7323 mL

10 mM

0.0866 mL

0.4331 mL

0.8662 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

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

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Concentration Concentration

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Molecular Weight Molecular Weight

Dilution Calculator

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 3.25 mg/mL (2.82 mM); Clear solution

This protocol yields a clear solution of ≥ 3.25 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (32.5 mg/mL) to 900 μL Corn oil, and mix evenly.

Working Solution

For the following dissolution methods, please prepare the working solution directly:

It is recommended to prepare fresh solutions and use them promptly within a short period of time.

The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 50% PEG300 50% Saline

Solubility: 2.5 mg/mL (2.17 mM); Suspended solution; Need ultrasonic

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (297 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 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]. Corbin J, et al. EZH2 PROTACs target EZH2- and FOXM1-associated oncogenic nodes, suppressing breast cancer cell growth. Oncogene. 2024 Aug;43(36):2722-2736. [Content Brief]

[2]. Yi Y, et al. A dual role of EZH2 in regulating A-to-I RNA editing and mRNA stability through ADAR. Nature communications. 2026 Mar 26;17(1):4421. [Content Brief]

[3]. Yum C, et al. Ketone drink enhances therapeutic efficacy in prostate cancer by targeting EZH2. Oncogenesis. 2025 Jul 12;14(1):24. [Content Brief]

[4]. Dale B, et al. Targeting Triple-Negative Breast Cancer by a Novel Proteolysis Targeting Chimera Degrader of Enhancer of Zeste Homolog 2. ACS pharmacology & translational science. 2022 Jul 08;5(7):491-507. [Content Brief]

[5]. Sun D, et al. Blocking Non-enzymatic Functions by PROTAC-Mediated Targeted Protein Degradation. Journal of medicinal chemistry. 2022 Nov 10;65(21):14276-14288. [Content Brief]

[6]. Yi Y, et al. EZH2 crosstalk with RNA methylation promotes prostate cancer progression through modulation of m6A autoregulation pathway. The Journal of clinical investigation. 2026 Jan 16;136(2):e195840. [Content Brief]

[7]. Vogt KC, et al. Tumor microenvironment-targeted PROTAC nanoparticle self-assembly broadly predicted by structural descriptors. Science advances. 2025 Dec 05;11(49):eadu2292. [Content Brief]

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.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	0.8662 mL	4.3308 mL	8.6617 mL	21.6542 mL
	5 mM	0.1732 mL	0.8662 mL	1.7323 mL	4.3308 mL
	10 mM	0.0866 mL	0.4331 mL	0.8662 mL	2.1654 mL
	15 mM	0.0577 mL	0.2887 mL	0.5774 mL	1.4436 mL
	20 mM	0.0433 mL	0.2165 mL	0.4331 mL	1.0827 mL
	25 mM	0.0346 mL	0.1732 mL	0.3465 mL	0.8662 mL
	30 mM	0.0289 mL	0.1444 mL	0.2887 mL	0.7218 mL
	40 mM	0.0217 mL	0.1083 mL	0.2165 mL	0.5414 mL
	50 mM	0.0173 mL	0.0866 mL	0.1732 mL	0.4331 mL
	60 mM	0.0144 mL	0.0722 mL	0.1444 mL	0.3609 mL
	80 mM	0.0108 mL	0.0541 mL	0.1083 mL	0.2707 mL

Keywords

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent:

Product Name:
CAS No.:
Species:
Purity:
Quantity:

MS8815

PROTAC Library

All Histone Methyltransferase Isoforms

All PROTACs Isoforms

Biological Activity

Chemical Information

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

MS8815 Related Classifications

HY-148334 Related Classifications