Cat. No.: HY-114305

A1874

Name: A1874
Brand: MedChemExpress
SKU: HY-114305
Price: 250.00 USD
Availability: InStock
Rating: 5 (3 reviews)

3 Cited Publications

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Based on 3 publication(s) in Google Scholar

A1874 is an orally active BRD4 PROTAC degrader with a DC₅₀ of 32 nM. A1874 degrades BRD4 via the ubiquitin-proteasome system by recruiting the MDM2 E3 ligase, while disrupting the MDM2-p53 interaction to stabilize p53 and upregulate p21, thereby inducing cell cycle arrest and apoptosis. A1874 exhibits selectivity for wild-type p53 cells and MDM2-amplified tumors, and it can be used in research on breast cancer, colorectal cancer, melanoma, lung cancer, lymphoma, myeloid leukemia, osteosarcoma, and glioblastoma.
(Pink: BRD4 ligand (HY-13030); Blue: MDM-2/p53 ligand (HY-15676); Black: linker).

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

Purity: 99.77%
CAS No.: 2064292-12-0
Formula: C₅₈H₆₂Cl₃F₂N₉O₇S
Molecular Weight:1173.59

Storage:

4°C, stored under nitrogen

* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

A1874 Chemical Structure

CAS No.: 2064292-12-0

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Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (3)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

A1874 is an orally active BRD4 PROTAC degrader with a DC₅₀ of 32 nM. A1874 degrades BRD4 via the ubiquitin-proteasome system by recruiting the MDM2 E3 ligase, while disrupting the MDM2-p53 interaction to stabilize p53 and upregulate p21, thereby inducing cell cycle arrest and apoptosis. A1874 exhibits selectivity for wild-type p53 cells and MDM2-amplified tumors, and it can be used in research on breast cancer, colorectal cancer, melanoma, lung cancer, lymphoma, myeloid leukemia, osteosarcoma, and glioblastoma^[1]^[2]^[3]^[4]^[5]. (Pink: BRD4 ligand (HY-13030); Blue: MDM-2/p53 ligand (HY-15676); Black: linker).

IC₅₀ & Target

^[1]

BRD4

32 nM (DC₅₀)

MDM2

All PROTACs Isoforms :

All Epigenetic Reader Domain Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HCT-116	DC₅₀	32 nM	BRD4 degradation in wild-type p53 HCT116 colon cancer cells after 24-hour incubation measured by immunoblotting assay. BRD4 degradation in wild-type p53 HCT116 colon cancer cells after 24-hour incubation measured by immunoblotting assay.	32978368
SJSA-1	IC₅₀	46.5 nM	Antiproliferative activity against wild-type p53, MDM2-overexpressing SJSA1 osteosarcoma cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay. Antiproliferative activity against wild-type p53, MDM2-overexpressing SJSA1 osteosarcoma cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay.	32978368
HCT-116	IC₅₀	86.3 nM	Antiproliferative activity against wild-type p53 HCT116 colon cancer cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay. Antiproliferative activity against wild-type p53 HCT116 colon cancer cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay.	32978368
A-375	IC₅₀	236 nM	Antiproliferative activity against wild-type p53 A375 melanoma cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay. Antiproliferative activity against wild-type p53 A375 melanoma cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay.	32978368
U-87MG ATCC	DC₅₀	0.146 μM	Cytotoxicity against human U-87 MG glioblastoma cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay. Cytotoxicity against human U-87 MG glioblastoma cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.	42387117

In Vitro

A1874 exhibits nanomolar cytotoxic activity, induces BRD4 degradation, G1-phase arrest, and inhibits colony formation, proliferation and migration in p53 wild-type breast cancer cell lines, including Tamoxifen (HY-13757A)-resistant ER+ cells; whereas p53 mutant breast cancer cell lines only show micromolar sensitivity^[5].
A1874 (5-500 nM; 24 h-10 d) potently inhibits the viability, proliferation, cell cycle progression, migration and invasion abilities of primary human colon cancer cells (pCan1, pCan2, pCan3, pCan4) and established HCT116 colon cancer cells^[2].
A1874 (25 nM-10 μM; 24 h) potently degrades BRD4 (DC₅₀ = 32 nM, D_max = 98%), reduces c-Myc expression by 85%, stabilizes p53 up to 5.9-fold, and induces p21^CIP1/WAF1 expression in wild-type p53 HCT116 colon cancer cells after 24 h of incubation^[1].
A1874 (10 nM-10 μM; 48 h) reduces the viability of wild-type p53 HCT116 colon cancer cells by 97% after 48 h of incubation, and exhibits synergistic activity at concentrations of 100 nM and above^[1].
A1874 (10 nM-10 μM; 48 h) reduces the survival rate of wild-type p53 A375 melanoma cells by 98% after 48 h of incubation, and exhibits synergistic activity at concentrations of 250 nM and higher^[1].
A1874 (10 nM-10 μM; 48 h) exhibits only extremely low antiproliferative activity in p53-mutant NCI-H2030 lung cancer cells (with a 22.4% decrease in cell viability at 10 μM) and HT29 colon cancer cells (with no decrease in viability), and its activity is reduced in p53-deficient HCT116 colon cancer cells after 48 h of incubation^[1].
Incubation with A1874 (10 nM-10 μM; 48 h) reduces the viability of Daudi lymphoma cells by 70%, MOLM-13 myeloid leukemia cells by 95%, and wild-type p53 SJSA1 osteosarcoma cells overexpressing MDM2 by 97.5% (IC₅₀ = 46.5 nM)^[1].
A1874 (8-2000 nM; 18 h) induces concentration-dependent degradation of BRD4, and upregulates the protein levels of MDM2, p21 and p53 in MCF7 (p53 wild-type), HT1080 (p53 wild-type), LNCAP (p53 wild-type) and HFF (p53 wild-type) cells after 18 h of treatment^[3].
A1874 (8-2000 nM; 18 h at 32°C or 37°C) induces concentration-dependent degradation of BRD4 and upregulates the protein levels of MDM2 and p53 in HT1376 (p53^P250L) and H441 (p53^R158L) cells after 18 h of treatment at 32°C, while no such effects are observed after treatment at 37°C^[3].
A1874 (500 nM; 18 h) induces BRD4 degradation and upregulates the protein levels of MDM2 and p53 in HCT116 cells after 18 h of treatment; when combined with Doxorubicin (HY-15142A), Camptothecin (HY-16560) or Mitomycin C (HY-13316), it dose-dependently inhibits A1874-induced BRD4 degradation by downregulating MDM2 expression, whereas combination with Etoposide (HY-13629) does not interfere with the activity of A1874^[3].
A1874 (666 nM; 18 h) induces BRD4 degradation in A549, U2OS, SJSA, JAR and A875 cells after treatment at 666 nM for 18 h, with higher activity in cell lines with higher MDM2 expression levels; however, despite the high MDM2 expression level in CCF-STTG1 cells, A1874 fails to induce BRD4 degradation in JEG3 or CCF-STTG1 cells^[3].
A1874 (8-2000 nM; 18 h) induces BRD4 degradation and MDM2 expression in p53-functional JAR and CCF-STTG1 cells, but exerts no such effects in p53-inactivated JAR-E6 and CCF-STTG1-E6 cells^[3].
A1874 (72 h) potently reduces the viability of U-87 MG cells (IC₅₀ = 0.146 μM) and Temozolomide (HY-17364)-resistant U-87 MG TR cells (IC₅₀ = 0.319 μM)^[4].
After delivery via a targeted formulation, the intracellular level of A1874 (25 μM; 2 h) in bEnd.3 cells reaches 0.61 pg/cell, with an uptake over 5-fold higher than that delivered via a non-targeted formulation; free PC can partially inhibit this uptake process, indicating that its transport is mediated by OCTN2^[4].
A1874 induces significant degradation of nuclear BRD4 protein in U-87 MG cells and temozolomide-resistant U-87 MG TR cells, while it increases the expression levels of c-Myc and MDM2 proteins and elevates the content of nuclear TP53 in U-87 MG cells^[4].
A1874 upregulates BRD4 mRNA expression and downregulates p53 mRNA expression in U-87 MG cells, but exerts no significant effect on the mRNA expression of BRD4, c-Myc or p53 in Temozolomide-resistant U-87 MG TR cells^[4].
When tested in combination with PRONano, A1874 (200 nM; 24 h) alters the protein expression levels of BRD4, TP53, MDM2 and C-Myc in U-87 MG and U-87 MG TR glioblastoma cells^[5].
When tested together with PRONano, A1874 (100 μM) alters the gene expression levels of BRD4, MYC and TRP53 in cultured glioblastoma cells^[5].
When tested in combination with PRONano, A1874 (0.1 μM; administered once every two days for a total of 8 days) alters the growth of U-87 MG glioblastoma 3D multicellular tumor spheres, which can be detected by changes in diameter and surface area^[5].
A1874 (8-2000 nM; 18 h) requires functional wild-type p53 to induce MDM2 expression and achieve efficient BRD4 degradation in JAR and CCF-STTG1 cells^[3].
A1874 (8-2000 nM; 18 h) does not induce BRD4 degradation or alter MDM2 protein levels in UC3 (p53^F113C) or UC3-p53KO cells following 18 h of treatment^[3].
A1874 (25-500 nM; 24 h-72 h) induces caspase-dependent mitochondrial apoptosis in primary human colon cancer cells (pCan1, pCan2, pCan3, pCan4) and established HCT116 colon cancer cells^[2].
A1874 (100 nM; 8 h-72 h) induces BRD4 degradation and downregulates BRD4-dependent genes (c-Myc, Bcl-2, cyclin D1) in primary human colon cancer cells (pCan1, pCan2)^[2].
A1874 (100 nM; 8 h-72 h) induces p53 protein stabilization and oxidative damage (ROS production, decreased GSH/GSSG ratio, DNA strand breaks) in primary human colon cancer cells (pCan1, pCan2) via a BRD4-independent mechanism^[2].

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

Western Blot Analysis^[1]

Cell Line:

HCT116 colon cancer cells (wild-type p53)
Concentration:

25 nM, 100 nM, 250 nM, 1 μM, 2.5 μM, 10 μM
Incubation Time:

24 h
Result:

Induced dose-dependent degradation of BRD4, reaching a maximum degradation (D_max) of 98% relative to vehicle-treated cells, with a DC₅₀ of 32 nM.
Reduced c-Myc expression by 85% relative to control cells, which was greater than the suppression caused by JQ1 alone.
Caused dose-dependent stabilization of p53 (up to 5.9-fold over steady-state levels) and upregulation of p21CIP1/WAF1, with significant p21 induction detected at 250 nM.

Cell Viability Assay^[1]

Cell Line:

HCT116 colon cancer cells (wild-type p53)
Concentration:

10 nM, 25 nM, 100 nM, 250 nM, 1 μM, 2.5 μM, 10 μM
Incubation Time:

48 h
Result:

Reduced HCT116 cell viability by 97% relative to vehicle-treated cells, which was greater than the effects of bromodomain and extra-terminal motif inhibitor JQ1 (25% viability loss) or MDM2 inhibitor idasanutlin (62% viability loss) alone, and slightly more effective than combined treatment with bromodomain and extra-terminal motif inhibitor JQ1 and MDM2 inhibitor idasanutlin.
Showed synergistic antiproliferative effects at concentrations of 100 nM or greater (CI values < 1).

Cell Viability Assay^[1]

Cell Line:

A375 melanoma cells (wild-type p53)
Concentration:

10 nM, 25 nM, 100 nM, 250 nM, 1 μM, 2.5 μM, 10 μM
Incubation Time:

48 h
Result:

Reduced A375 cell viability by 98% relative to vehicle-treated cells, which was greater than the effects of JQ1 (15% viability loss) or idasanutlin (64% viability loss) alone.
Showed synergistic antiproliferative effects at concentrations of 250 nM or greater.

Cell Viability Assay^[1]

Cell Line:

p53-mutant NCI-H2030 lung cancer cells, p53-mutant HT29 colon cancer cells, p53-deficient isogenic HCT116 colon cancer cells
Concentration:

10 nM, 25 nM, 100 nM, 250 nM, 1 μM, 2.5 μM, 10 μM
Incubation Time:

48 h
Result:

Reduced NCI-H2030 cell viability by only 22.4% at 10 μM, with nominal loss at lower concentrations.
Caused no reduction in HT29 cell viability even at 10 μM.
Reduced p53-deficient HCT116 cell viability to a similar extent as JQ1, with diminished effectiveness relative to wild-type p53 HCT116 cells.

Cell Viability Assay^[1]

Cell Line:

Daudi lymphoma cells (mutant p53), MOLM-13 myeloid leukemia cells (wild-type p53), SJSA1 osteosarcoma cells (wild-type p53, MDM2-overexpressing)
Concentration:

10 nM, 25 nM, 100 nM, 250 nM, 1 μM, 2.5 μM, 10 μM
Incubation Time:

48 h
Result:

Reduced Daudi cell viability by 70%, MOLM-13 cell viability by 95%, and SJSA1 cell viability by 97.5% relative to vehicle-treated cells.
Had an IC₅₀ of 46.5 nM in SJSA1 cells, compared with 86.3 nM in HCT116 cells and 236 nM in A375 cells.

Western Blot Analysis^[3]

Cell Line:

JAR-E6, JAR, CCF-STTG1-E6, CCF-STTG1
Concentration:

8, 25, 74, 222, 666, 2000 nM
Incubation Time:

18 h
Result:

Induced BRD4 degradation, MDM2 induction, and p53 expression in parental JAR cells (functional p53).
Eliminated BRD4 degradation, and failed to induce MDM2 or p53 in JAR-E6 cells (non-functional p53).
Induced BRD4 degradation and robust MDM2 induction, and reduced p53 expression in parental CCF-STTG1 cells (functional p53).
Diminished BRD4 degradation, failed to induce MDM2, and showed absent p53 expression in CCF-STTG1-E6 cells (non-functional p53) compared to parental cells.

Western Blot Analysis^[4]

Cell Line:

MCF7 (p53 wt) cells, HT1080 (p53 wt) cells, LNCAP (p53 wt) cells, HFF (normal fibroblast, p53 wt) cells
Concentration:

8, 25, 74, 222, 666, 2000 nM
Incubation Time:

18 h
Result:

Reduced BRD4 protein levels in a concentration-dependent manner in MCF7 cells, while increased MDM2, p21, and p53 protein levels.
Reduced BRD4 protein levels in a concentration-dependent manner in HT1080 cells, with increases in MDM2, p21, and p53 protein levels.
Reduced BRD4 protein levels in a concentration-dependent manner in LNCAP cells, while increased MDM2, p21, and p53 protein levels.
Reduced BRD4 protein levels in a concentration-dependent manner in HFF cells, with increases in MDM2, p21, and p53 protein levels.

Western Blot Analysis^[4]

Cell Line:

UC3 (p53-F113C, mutant p53) cells, UC3-p53KO (p53 knockout) cells
Concentration:

8, 25, 74, 222, 666, 2000 nM
Incubation Time:

18 h
Result:

Did not reduce BRD4 protein levels across tested concentrations in UC3 (p53-F113C) cells, and MDM2 protein levels remained largely unchanged.
Did not reduce BRD4 protein levels across tested concentrations in UC3-p53KO cells, with no consistent change in MDM2 protein levels.

Western Blot Analysis^[4]

Cell Line:

HT1376 (p53-P250L, temperature-sensitive mutant p53) cells, H441 (p53-R158L, temperature-sensitive mutant p53) cells
Concentration:

8, 25, 74, 222, 666, 2000 nM
Incubation Time:

18 h (37°C or 32°C)
Result:

Did not reduce BRD4 protein levels across tested concentrations in HT1376 cells at 37°C, with minimal change to MDM2 and p53 protein levels.
Reduced BRD4 protein levels in a concentration-dependent manner in HT1376 cells at 32°C, while increased MDM2 and p53 protein levels.
Did not reduce BRD4 protein levels across tested concentrations in H441 cells at 37°C, with minimal change to MDM2 and p53 protein levels.
Reduced BRD4 protein levels in a concentration-dependent manner in H441 cells at 32°C, while increased MDM2 protein levels.

Western Blot Analysis^[4]

Cell Line:

HCT116 cells
Concentration:

500 nM (A1874); 1.1, 3.3, 10 μM (doxorubicin, camptothecin, etoposide, mitomycin)
Incubation Time:

18 h
Result:

Reduced BRD4 protein levels and increased MDM2 and p53 protein levels in HCT116 cells when used alone.
Dose-dependently reduced MDM2 protein levels while maintaining p53 protein levels, and diminished the BRD4-degrading activity of A1874 when co-treated with doxorubicin, camptothecin, or mitomycin.
Did not reduce MDM2 protein levels, and A1874 maintained its BRD4-degrading activity when co-treated with etoposide.

Western Blot Analysis^[4]

Cell Line:

A549, U2OS, SJSA (MDM2 amplified), JAR (MDM2 amplified), A875, JEG3, CCF-STTG1 (MDM2 amplified) cells
Concentration:

666 nM
Incubation Time:

18 h
Result:

Induced BRD4 degradation in A549, U2OS, SJSA, JAR, and A875 cells, with the most pronounced degradation observed in cells with higher MDM2 expression levels (SJSA, JAR).
Did not induce BRD4 degradation in CCF-STTG1 or JEG3 cells despite CCF-STTG1 having the highest measured MDM2 expression level.

Western Blot Analysis^[4]

Cell Line:

JAR-E6 (HPV E6-expressing, p53-inactivated) cells, JAR (parental, p53-functional) cells, CCF-STTG1-E6 (HPV E6-expressing, p53-inactivated) cells, CCF-STTG1 (parental, p53-functional) cells
Concentration:

8, 25, 74, 222, 666, 2000 nM (JAR-E6, CCF-STTG1-E6); 666, 2000 nM (JAR, CCF-STTG1)
Incubation Time:

18 h
Result:

Did not induce MDM2 expression and only minimally reduced BRD4 protein levels across tested concentrations in JAR-E6 cells.
Induced MDM2 expression and reduced BRD4 protein levels at 666 and 2000 nM in parental JAR cells.
Did not induce MDM2 expression and only minimally reduced BRD4 protein levels across tested concentrations in CCF-STTG1-E6 cells.
Induced MDM2 expression and reduced BRD4 protein levels at 666 and 2000 nM in parental CCF-STTG1 cells.

Western Blot Analysis^[6]

Cell Line:

U-87 MG, U-87 MG TR glioblastoma cells
Concentration:

200 nM
Incubation Time:

24 h
Result:

Analyzed protein levels of BRD4, TP53, MDM2, and C-Myc, with GAPDH used as a loading control.

In Vivo

A1874 (20 mg/kg; p.o.; once daily for 21 days) potently inhibits colon cancer xenograft growth in SCID mice, associated with BRD4 degradation, apoptosis activation, p53 elevation, and oxidative stress in tumor tissues analyzed at Day 7^[2].

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

Animal Model:

SCID mice (female, 5-6 week old, 18-19 g, subcutaneous colon cancer xenograft model)^[2]
Dosage:

20 mg/kg
Administration:

p.o.; once daily for 21 days
Result:

Reduced estimated daily tumor growth relative to vehicle control.
Decreased xenograft tumor weight significantly at Day 42 relative to vehicle control.
Showed no significant difference in mouse body weights relative to vehicle control, with no noticeable toxicity observed.
Decreased BRD4, c-Myc, Bcl-2, and cyclin D1 protein expression significantly in tumor tissues at Day 7.
Detected cleavage of caspase-3 and PARP in tumor tissues at Day 7.
Elevated p53 protein levels in tumor tissues at Day 7.
Reduced GSH/GSSG ratio in tumor tissues at Day 7, indicating oxidative stress.

Chemical Information

CAS No. 2064292-12-0
Appearance Solid
Molecular Weight 1173.59
Formula C₅₈H₆₂Cl₃F₂N₉O₇S
Color White to off-white
SMILES

ClC(C=C1)=CC=C1C2=N[C@H](C3=NN=C(C)N3C4=C2C(C)=C(C)S4)CC(NCCOCCOCCOCCNC(C5=CC(OC)=C(NC([C@H]6[C@H](C7=C(F)C(Cl)=CC=C7)[C@](C8=CC=C(Cl)C=C8F)(C#N)[C@H](CC(C)(C)C)N6)=O)C=C5)=O)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, stored under nitrogen

* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

Publications (3)

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Structure

PROTAC-mediated activation, rather than degradation, of a nuclear receptor reveals complex ligand-receptor interaction network. [Abstract]

2024 Dec 5;32(12):2352-2363.e8. PMID: 39389062
Pharm Res

2026 Jul 1. PMID: 42387117
bioRxiv

2026 Jan 13.

Solvent & Solubility

In Vitro:

DMSO : 150 mg/mL (127.81 mM; Need ultrasonic; 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

0.8521 mL

4.2604 mL

8.5209 mL

5 mM

0.1704 mL

0.8521 mL

1.7042 mL

10 mM

0.0852 mL

0.4260 mL

0.8521 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 (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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

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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 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (2.13 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

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

Solubility: ≥ 2.5 mg/mL (2.13 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 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 (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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

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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 (305 KB)
SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
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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]. Hines J, et al. MDM2-Recruiting PROTAC Offers Superior, Synergistic Antiproliferative Activity via Simultaneous Degradation of BRD4 and Stabilization of p53. Cancer research. 2019 Jan 01;79(1):251-262. [Content Brief]

[2]. Qin AC, et al. The therapeutic effect of the BRD4-degrading PROTAC A1874 in human colon cancer cells. Cell death & disease. 2020 Sep 25;11(9):805.

[3]. Fatima Z, et al. MDM2 Amplification Enables Selective PROTAC Targeting of Tumor Cells. Molecular cancer therapeutics. 2026 Jun 01;25(6):948-956.

[4]. Patel H, et al. Leveraging Carnitine-functionalized Lipid Nanocarrier based Targeted Delivery of A1874 PROTAC for Glioblastoma. Pharmaceutical research. 2026 Jul 01.

[5]. Marvalim C, et al. Abstract P49: PROTAC A1874: A Potential Targeted Therapy for Breast Cancer[J]. Cancer Research, 2024, 84(8_Supplement): P49-P49.

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	0.8521 mL	4.2604 mL	8.5209 mL	21.3022 mL
	5 mM	0.1704 mL	0.8521 mL	1.7042 mL	4.2604 mL
	10 mM	0.0852 mL	0.4260 mL	0.8521 mL	2.1302 mL
	15 mM	0.0568 mL	0.2840 mL	0.5681 mL	1.4201 mL
	20 mM	0.0426 mL	0.2130 mL	0.4260 mL	1.0651 mL
	25 mM	0.0341 mL	0.1704 mL	0.3408 mL	0.8521 mL
	30 mM	0.0284 mL	0.1420 mL	0.2840 mL	0.7101 mL
	40 mM	0.0213 mL	0.1065 mL	0.2130 mL	0.5326 mL
	50 mM	0.0170 mL	0.0852 mL	0.1704 mL	0.4260 mL
	60 mM	0.0142 mL	0.0710 mL	0.1420 mL	0.3550 mL
	80 mM	0.0107 mL	0.0533 mL	0.1065 mL	0.2663 mL
	100 mM	0.0085 mL	0.0426 mL	0.0852 mL	0.2130 mL

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Quantity:

A1874

Publications Citing Use of MedChemExpress (MCE) A1874

All PROTACs Isoforms

All Epigenetic Reader Domain Isoforms