Cat. No.: HY-16954

ARV-825

Name: ARV-825
Brand: MedChemExpress
SKU: HY-16954
Price: 180.00 USD
Availability: InStock
Rating: 5 (37 reviews)

37 Cited Publications

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Based on 37 publication(s) in Google Scholar

ARV-825 is a BET protein PROTAC degrader that recruits cereblon, and it targets BRD2, BRD3, and BRD4 for degradation via the ubiquitin-proteasome pathway. ARV-825 downregulates c-MYC, PLK1, MYCN, CDK4/6, JAK2, pSTAT3/5, PIM1, and Bcl-xL, upregulates p21 and p27, and modulates H3K27Ac-mediated transcription, the G2/M checkpoint, the Wnt/β-catenin pathway, and amino acid transport pathways. ARV-825 induces G1 phase cell cycle arrest, caspase 3/PARP-mediated apoptosis, DNA damage, and reactive oxygen species (ROS) production, reduces mitochondrial respiration, and simultaneously inhibits cell proliferation, clonogenic growth, and cell migration. ARV-825 is used in research on gastric cancer, leukemia, neuroblastoma, and cholangiocarcinoma.
(Pink: BRD4 ligand (HY-15743); Blue: E3 ligase ligand; Black: linker).

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

Purity: 99.21%
CAS No.: 1818885-28-7
Formula: C₄₆H₄₇ClN₈O₉S
Molecular Weight:923.43

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 1 year , -20°C, 6 months

ARV-825 Chemical Structure

CAS No.: 1818885-28-7

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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
Publications (37)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
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Biological Activity

Description

ARV-825 is a BET protein PROTAC degrader that recruits cereblon, and it targets BRD2, BRD3, and BRD4 for degradation via the ubiquitin-proteasome pathway. ARV-825 downregulates c-MYC, PLK1, MYCN, CDK4/6, JAK2, pSTAT3/5, PIM1, and Bcl-xL, upregulates p21 and p27, and modulates H3K27Ac-mediated transcription, the G2/M checkpoint, the Wnt/β-catenin pathway, and amino acid transport pathways. ARV-825 induces G1 phase cell cycle arrest, caspase 3/PARP-mediated apoptosis, DNA damage, and reactive oxygen species (ROS) production, reduces mitochondrial respiration, and simultaneously inhibits cell proliferation, clonogenic growth, and cell migration. ARV-825 is used in research on gastric cancer, leukemia, neuroblastoma, and cholangiocarcinoma^[1]^[2]^[3]^[4]^[5]^[6]. (Pink: BRD4 ligand (HY-15743); Blue: E3 ligase ligand; Black: linker).

IC₅₀ & Target

^[1]^[2]^[3]^[4]^[5]^[6]

BRD2

BRD3

BRD4

PLK1

c-Myc

MYCN

CDK4

CDK6

JAK2

p-STAT3

STAT5

PIM1

Bcl-xL

p21

P27

H3K27Ac

Wnt

β-catenin

Caspase 3

PARP

All PROTACs Isoforms :

All Epigenetic Reader Domain Isoforms :

All Polo-like Kinase (PLK) Isoforms :

All CDK Isoforms :

All JAK Isoforms :

All STAT Isoforms :

All Pim Isoforms :

All Bcl-2 Family Isoforms :

All PAK Isoforms :

All Wnt Isoforms :

All Caspase Isoforms :

All PARP Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
SK-N-SH	IC50	146.9 nM	Inhibition of cell viability in human SK-N-SH neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm. Inhibition of cell viability in human SK-N-SH neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm.	33324552
SH-SY5Y	IC50	53.71 nM	Inhibition of cell viability in human SH-SY5Y neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm. Inhibition of cell viability in human SH-SY5Y neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm.	33324552
IMR-32	IC50	7.024 nM	Inhibition of cell viability in human IMR-32 neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm. Inhibition of cell viability in human IMR-32 neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm.	33324552
SK-N-BE(2)	IC50	232.8 nM	Inhibition of cell viability in human SK-N-BE(2) neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm. Inhibition of cell viability in human SK-N-BE(2) neuroblastoma cells incubated for 72 h measured by CCK8 assay with absorbance read at 450 nm.	33324552
SET-2	IC50	14.5 nM	Apoptosis induction in post-MPN sAML SET2 cells assessed by annexin-V and TO-PRO-3 iodide staining and flow cytometry. Apoptosis induction in post-MPN sAML SET2 cells assessed by annexin-V and TO-PRO-3 iodide staining and flow cytometry.	28042144
MGC-803	IC50	91.4 nM	Inhibits MGC8003 cells viability. Inhibits MGC8003 cells viability.	34733788
SGC-7901	IC50	188.7 nM	Inhibits SGC7901 cells viability. Inhibits SGC7901 cells viability.	34733788
AGS	IC50	163.6 nM	Inhibits AGS cells viability. Inhibits AGS cells viability.	34733788
HGC-27	IC50	35.9 nM	Inhibits HGC27 cells viability. Inhibits HGC27 cells viability.	34733788
BGC-823	IC50	116.1 nM	Inhibits BGC823 cells viability. Inhibits BGC823 cells viability.	34733788
MOLT-4	IC50	0.534 μM	Inhibits MOLT-4 cells viability. Inhibits MOLT-4 cells viability.	33888130
Jurkat	IC50	0.254 μM	Inhibits Jurkat cells viability. Inhibits Jurkat cells viability.	33888130

In Vitro

ARV-825 (1-10000 nM; 72 h) potently suppresses viability of multiple human gastric cancer cell lines, with MGC803 and HGC27 cells showing higher sensitivity than AGS, SGC7901, BGC823, and SNU-216 cells^[1].
ARV-825 (62.5-1000 nM; 2 weeks) dose-dependently inhibits long-term clonogenic growth of MGC803, HGC27, AGS, and SGC7901 gastric cancer cells^[1].
ARV-825 (62.5-500 nM; 72 h) dose-dependently reduces c-Myc and PLK1 protein levels in MGC803, HGC27, AGS, and SGC7901 gastric cancer cells^[1].
ARV-825 (72 h) CRBN expression level modulates the antiproliferative potency of ARV-825 in gastric cancer cells, with CRBN knockdown decreasing and CRBN overexpression increasing ARV-825 sensitivity^[1].
ARV-825 (12.5-200 nM; 4-24 h) induces rapid, dose- and time-dependent, proteasome-mediated BRD4 degradation that persists for at least 24 h after compound removal in HuCCT1, HuH28, and OZ human cholangiocarcinoma cells^[4].
ARV-825 (25-100 nM; 96 h) reduces viability of HuCCT1 and HuH28 human cholangiocarcinoma cells in a dose-dependent manner following 96 h of treatment^[4].
ARV-825 (50 nM; 7 days) completely abolishes clonogenic growth of HuCCT1 human cholangiocarcinoma cells over 7 days^[4].
ARV-825 (12.5-200 nM; 4-24 h) causes sustained downregulation of c-Myc protein in high c-Myc-expressing HuCCT1 and OZ human cholangiocarcinoma cells but does not affect c-Myc protein levels in low c-Myc-expressing HuH28 cells^[4].
ARV-825 (100 nM; 6-24 h) downregulates c-Myc mRNA expression in HuCCT1 and OZ human cholangiocarcinoma cells in a dose-dependent manner^[4].
ARV-825 (12.5-200 nM; 24 h) upregulates p21 protein expression in HuCCT1, HuH28, and OZ human cholangiocarcinoma cells in a dose-dependent manner after 24 h of treatment^[4].
ARV-825 (62.5-1000 nM) induces G1 phase cell cycle arrest in MGC803, HGC27, AGS, and SGC7901 gastric cancer cells^[1].
ARV-825 (1 μM; 48 h) induces G1-phase cell cycle arrest in Jurkat, CCRF-CEM, Molt4, and 6T-CEM T-ALL cells after 48 h of treatment^[2].
ARV-825-induced growth inhibition in Jurkat, 6T-CEM, and Molt4 T-ALL cells is CRBN-mediated, as CRBN overexpression decreases and CRBN knockdown increases the IC₅₀ of ARV-825^[2].
ARV-825 (10-10000 nM; 72 h) potently suppresses proliferation of human cholangiocarcinoma cells in a dose-dependent manner^[4].
ARV-825 (25-100 nM; 24-72 h) induces G1 phase cell cycle arrest in HuCCT1, HuH28, and OZ human cholangiocarcinoma cells^[4].
ARV-825 (62.5-250 nM; 72 h) dose-dependently induces apoptosis in MGC803, HGC27, AGS, and SGC7901 gastric cancer cells after 72 h of treatment^[1].
ARV-825 (62.5-500 nM; 72 h) induces dose-dependent degradation of BRD2, BRD3, and BRD4 and activates apoptotic caspase 3 and PARP cleavage in MGC803, HGC27, AGS, and SGC7901 gastric cancer cells^[1].
ARV-825 (1 μM; 48 h) induces apoptosis in Jurkat, CCRF-CEM, Molt4, and 6T-CEM T-ALL cells after 48 h of treatment, as measured by Annexin V/PI flow cytometry^[2].
ARV-825 (0.5-4 μM; 48 h) potently degrades BRD2, BRD3, and BRD4 proteins in 6T-CEM, Molt4, Jurkat, and CCRF T-ALL cells in a concentration-dependent manner at 48 h, with DC₅₀ values in the low nanomolar range for most cell lines and BET isoforms, and concomitantly increases cleaved caspase 3 and PARP protein levels^[2].
ARV-825 (50-200 nM; 48 h) induces caspase 3/7 activation in HuCCT1 and HuH28 human cholangiocarcinoma cells after 48 h of treatment^[4].
ARV-825 (50-100 nM; 72 h) induces apoptosis in HuCCT1 human cholangiocarcinoma cells after 72 h of treatment, as measured by Annexin V positivity^[4].
ARV-825 (1.0 μM; 24 h treatment followed by 24 h drug-free washout) induces profound and sustained depletion of BRD4 and BRD2, including sustained nuclear depletion after drug washout, in post-MPN sAML SET2 cells^[6].
ARV-825 (20-500 nM; 48 h) dose-dependently induces apoptosis in post-MPN sAML SET2 cells (IC₅₀ 14.5 nM) and UKE1 cells (IC₅₀ 256 nM), with greater potency in SET2 cells^[6].
ARV-825 dose-dependently induces cell death in patient-derived CD34⁺ post-MPN sAML cells while relatively sparing normal CD34⁺ hematopoietic progenitor cells^[6].
Co-treatment with ARV-825 and Ruxolitinib (HY-50856) synergistically induces apoptosis in post-MPN sAML SET2 and HEL92.1.7 cells, associated with greater attenuation of p-STAT5, c-Myc, CDK4/6, PIM1, and Bcl-xL^[6].
ARV-825 (1 μM; 48 h-7 days) suppresses viability and proliferation of Jurkat, CCRF-CEM, Molt4, and 6T-CEM T-ALL cells in a dose- and time-dependent manner^[2].
ARV-825 (1-8 μM; 7 days) inhibits growth and downregulates BET proteins and c-Myc in primary pediatric T-ALL cells^[2].
ARV-825 (72 h) potently inhibits the viability of SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2) neuroblastoma cells with IC₅₀ values in the nanomolar range, with IMR-32 being the most sensitive and SK-N-BE(2) the least sensitive cell line^[3].
ARV-825 (0.01-1000 nM) suppresses long-term clonogenic proliferation of SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2) neuroblastoma cells in a dose-dependent manner^[3].
ARV-825 (1-500 nM) triggers G₂/M cell cycle arrest in SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2) neuroblastoma cells, accompanied by an increased G₁ phase proportion and decreased S and G₂ phase proportions^[3].
ARV-825 (5-1000 nM; 72 h) induces dose-dependent apoptosis in SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2) neuroblastoma cells after 72 h of treatment^[3].
ARV-825 (0.1-1000 nM) induces cleavage of PARP and Caspase-3 in SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2) neuroblastoma cells in a dose-dependent manner^[3].
ARV-825 (0.1-1000 nM) induces dose-dependent degradation of BRD2, BRD3, and BRD4 proteins in SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2) neuroblastoma cells^[3].
ARV-825 (0.1-1000 nM) downregulates protein levels of MYCN in MYCN-amplified IMR-32 and SK-N-BE(2) cells and c-Myc in MYCN non-amplified SK-N-SH and SH-SY5Y neuroblastoma cells in a dose- and time-dependent manner^[3].
ARV-825 downregulates mRNA levels of MYCN in MYCN-amplified SK-N-BE(2) cells and c-Myc in MYCN non-amplified SK-N-SH neuroblastoma cells^[3].
ARV-825 downregulates the expression of MYCN-associated super enhancer genes (ISL1, PHOX2B, HAND2, GATA3, TBX2) in both MYCN-amplified SK-N-BE(2) and MYCN non-amplified SK-N-SH neuroblastoma cells^[3].

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

Cell Viability Assay^[1]

Cell Line:

MGC803, HGC27, AGS, SGC7901, BGC823, SNU-216 human gastric cancer cell lines
Concentration:

1-10000 nM
Incubation Time:

72 h
Result:

Induced a dose-dependent decrease in cell viability across all gastric cancer cell lines.
Decreased cell number and cell shrinkage were observed after 500 nM ARV-825 relative to untreated control cells.

Cell Proliferation Assay^[1]

Cell Line:

MGC803, HGC27, AGS, SGC7901 human gastric cancer cell lines
Concentration:

62.5-1000 nM
Incubation Time:

2 weeks
Result:

Dose-dependently suppressed clonal formation in all four gastric cancer cell lines.
Markedly reduced the number of clones compared with untreated control groups.

Apoptosis Analysis^[1]

Cell Line:

MGC803, HGC27, AGS, SGC7901 human gastric cancer cell lines
Concentration:

62.5-1000 nM
Incubation Time:

72 h
Result:

Increased the percentage of apoptotic cells in a dose-dependent manner compared with control groups.

Western Blot Analysis^[1]

Cell Line:

MGC803, HGC27, AGS, SGC7901 human gastric cancer cell lines
Concentration:

62.5-500nM
Incubation Time:

72 h
Result:

Efficiently degraded BRD4 protein in all four gastric cancer cell lines.
Reduced BRD2 and BRD3 protein levels in parallel with BRD4.
Increased cleavage of caspase 3 and PARP, consistent with the induction of apoptosis.\nDecreased c-Myc and PLK1 protein levels in a dose-dependent manner in all four gastric cancer cell lines.

Apoptosis Analysis^[2]

Cell Line:

Jurkat, CCRF-CEM, Molt4, 6T-CEM human T-ALL cell lines
Concentration:

1 μM
Incubation Time:

48 h
Result:

Increased the apoptotic rates of T-ALL cell lines, especially CCRF, Jurkat, and Molt4 cells, after 48 h of treatment.

Western Blot Analysis^[2]

Cell Line:

Jurkat, CCRF-CEM, Molt4, 6T-CEM human T-ALL cell lines
Concentration:

0.5 μM; 1 μM; 2 μM; 4 μM
Incubation Time:

48 h
Result:

Induced almost complete BRD4 protein degradation in T-ALL cell lines.
Reduced BRD2 and BRD3 protein expression levels.
Was more potent in degrading BRD2 than BRD4 in Jurkat and CCRF cells.
Exhibited DC₅₀ values at 48 h as follows: 6T-CEM - BRD2: 23.12 nM, BRD3: 16.41 nM, BRD4: 25.64 nM; Molt4 - BRD2: 13.55 nM, BRD3: 5.38 nM, BRD4: 4.75 nM; Jurkat - all three BET proteins around 5 nM; CCRF - BRD2: 34.28 nM, BRD3: 29.72 nM, BRD4: 225.42 nM.
Decreased CRBN protein levels with increasing concentration.
Increased PARP and cleaved caspase 3 levels in a concentration-dependent manner in most cell lines.
Markedly upregulated cleaved caspase 3 in all treated cells.
Increased PARP in most treated T-ALL cells, except CCRF.

Apoptosis Analysis^[3]

Cell Line:

SK-N-SH, SH-SY5Y, IMR-32, SK-N-BE(2)
Concentration:

IMR-32: 5-10 nM; SH-SY5Y: 5-50 nM; SK-N-BE(2): 100-1000 nM
Incubation Time:

72 h
Result:

Robustly elicited apoptosis in all four NB cell lines in a dose-dependent manner.
Substantially increased the proportion of apoptotic cells compared with DMSO-treated controls.

Western Blot Analysis^[4]

Cell Line:

HuCCT1, HuH28, OZ human cholangiocarcinoma cell lines
Concentration:

12.5-200 nM (dose-response); 100 nM (time-course); 100 nM (proteasome inhibition); 100 nM (washout/recovery)
Incubation Time:

24 h (dose-response); 4-24 h (time-course); 12 h (proteasome inhibition); 24 h pre-treatment, 6-24 h post-washout (washout/recovery)
Result:

Downregulated BRD4 protein levels in a dose- and time-dependent manner across all three CCA cell lines.
Induced BRD4 degradation that was completely blocked by co-treatment with the proteasome inhibitor MG132 (HY-13259).
Suppressed BRD4 protein expression for up to 24 h after compound removal and washout in HuCCT1, OZ, and HuH28 cells.

ELISA Assay^[4]

Cell Line:

human cholangiocarcinoma cell lines
Concentration:

10-10000 nM
Incubation Time:

72 h
Result:

Potently inhibited CCA cell proliferation in a dose-dependent manner across all tested cell lines.
Exhibited significantly lower IC₅₀ values compared to the BET inhibitors OTX-015 and JQ1.

Cell Viability Assay^[4]

Cell Line:

HuCCT1, HuH28 human cholangiocarcinoma cell lines
Concentration:

25 nM; 50 nM; 100 nM
Incubation Time:

96 h
Result:

Dose-dependently inhibited cell viability of HuCCT1 and HuH28 cells after 96 h of treatment.

Apoptosis Analysis^[4]

Cell Line:

HuCCT1 human cholangiocarcinoma cell line
Concentration:

50 nM; 100 nM
Incubation Time:

72 h
Result:

Caused a significant increase in the percentage of Annexin V-positive HuCCT1 cells after 72 h of treatment.

Western Blot Analysis^[4]

Cell Line:

HuCCT1, OZ, HuH28 human cholangiocarcinoma cell lines
Concentration:

12.5-200 nM
Incubation Time:

4-24 h
Result:

Markedly downregulated c-Myc protein levels in HuCCT1 and OZ cells in a dose- and time-dependent manner.

Real Time qPCR^[4]

Cell Line:

HuCCT1, OZ human cholangiocarcinoma cell lines
Concentration:

100 nM
Incubation Time:

6 h; 24 h
Result:

Led to marked downregulation of c-Myc mRNA levels in HuCCT1 and OZ cells in a dose-dependent manner.

Western Blot Analysis^[4]

Cell Line:

HuCCT1, HuH28, OZ human cholangiocarcinoma cell lines
Concentration:

12.5-200 nM
Incubation Time:

24 h
Result:

Induced a dose-dependent increase in p21 protein expression across all tested CCA cell lines.

Cell Cycle Analysis^[4]

Cell Line:

HuCCT1, HuH28, OZ human cholangiocarcinoma cell lines
Concentration:

25 nM; 50 nM; 100 nM; 100 nM
Incubation Time:

24 h; 48 h; 72 h
Result:

Suppressed G1/S transition, causing cell cycle arrest at the G1 phase in all tested CCA cell lines.

Western Blot Analysis^[6]

Cell Line:

post-MPN sAML SET2 cells
Concentration:

1.0 μM
Incubation Time:

24 h treatment; followed by 24 h drug-free washout
Result:

Caused marked depletion of BRD4 and BRD2 protein levels in SET2 cells.
Significantly depleted nuclear expression of BRD4 in sAML cells as confirmed by confocal immunofluorescence microscopy.
Induced sustained depletion of BRD4 and BRD2 levels following 24-hour washout after 24-hour treatment.

In Vivo

ARV-825 (10 mg/kg; i.p.; daily) suppresses gastric cancer xenograft tumor growth, reduces Ki67-positive cell ratio, and downregulates BRD4 protein expression in vivo without obvious body weight loss or toxic side effects^[1].
ARV-825 reduces leukemia burden and prolongs survival in a mouse model of disseminated human acute myeloid leukemia^[5].
ARV-825 (10 mg/kg; i.p.; daily) effectively suppresses T-ALL xenograft tumor growth by depleting BET and c-Myc proteins, reducing proliferation, and inducing apoptosis^[2].
ARV-825 (5 mg/kg; i.p.; daily) effectively suppresses tumor growth, reduces proliferation, and downregulates BRD4 and MYCN protein expression in a MYCN-amplified neuroblastoma subcutaneous xenograft mouse model^[3].

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

Animal Model:

Nude mice (four-week-old male; Lingchang BioTech; n=6 per group)^[1]
Dosage:

10 mg/kg
Administration:

i.p.; daily
Result:

Reduced tumor burden compared with the control group.
Lowered the ratio of Ki67-positive cells in treated tumors.
Significantly downregulated BRD4 protein levels in vivo.
Caused no remarkable difference in mouse body weight compared with the control group, and no obvious toxic side effects were detected.

Animal Model:

Nude mice (female, 4 weeks old, from Lingchang BioTech Co., Ltd.)^[2]
Dosage:

10 mg/kg
Administration:

i.p.; daily
Result:

Significantly reduced tumor burden and xenograft tumor weight compared with control.
Downregulated BRD4 and c-Myc protein expression in xenograft tumors.
Reduced Ki67 positive cells in tumors.
Increased the proportion of cleaved-caspase 3 positive cells in tumors.
Showed no significant difference in mouse body weight compared with control group.

Animal Model:

Nude mice (athymic nude, male, 5 weeks old)^[3]
Dosage:

5 mg/kg
Administration:

i.p.; daily; until tumors exceeded 1,000 mm³
Result:

Significantly reduced tumor burden and tumor weight in the SK-N-BE(2) xenograft model compared to vehicle control.
Showed no significant difference in mouse body weight compared to the control group.
Substantially lowered the proportion of Ki-67 positive cells in tumors, indicating reduced tumor proliferative activity.
Downregulated BRD4 and MYCN protein expression in the xenograft tumor tissue.

Chemical Information

CAS No. 1818885-28-7
Appearance Solid
Molecular Weight 923.43
Formula C₄₆H₄₇ClN₈O₉S
Color Light yellow to yellow
SMILES

CC1=NN=C2N1C(SC(C)=C3C)=C3C(C4=CC=C(Cl)C=C4)=N[C@H]2CC(NC5=CC=C(OCCOCCOCCOCCNC6=C(C(N(C7CCC(NC7=O)=O)C8=O)=O)C8=CC=C6)C=C5)=O
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	1 year
	-20°C	6 months

Publications (37)

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Nat Aging

Comparative analysis of senolytic drugs reveals mitochondrial determinants of efficacy and resistance. [Abstract]

2026 Feb;6(2):316-328. PMID: 41611832
Nat Aging

SARS-CoV-2 infection triggers paracrine senescence and leads to a sustained senescence-associated inflammatory response. [Abstract]

2022 Feb;2(2):115-124. PMID: 37117754
Nat Commun

Hepatocyte growth factor derived from senescent cells attenuates cell competition-induced apical elimination of oncogenic cells. [Abstract]

2022 Jul 18;13(1):4157. PMID: 35851277
Nat Commun

A proximity biotinylation-based approach to identify protein-E3 ligase interactions induced by PROTACs and molecular glues. [Abstract]

2022 Jan 10;13(1):183. PMID: 35013300
Nat Commun

BRD4 prevents the accumulation of R-loops and protects against transcription-replication collision events and DNA damage. [Abstract]

2020 Aug 14;11(1):4083. PMID: 32796829

ARV-825 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2020 Aug 14;11(1):4083. [Abstract]

Representative IF images and quantification of nuclear S9.6 intensity, γH2AX foci, and RNase H1 in HeLa cells in the absence (−DOX) or presence (+DOX) of doxycycline-induced FLAG-tagged RNase H1 expression for 24 h, followed by treatment with 100 nM ARV-825 for 6 h.

ARV-825 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2020 Aug 14;11(1):4083. [Abstract]

Cells treated with ARV-825 shows marked degradation of BRD4 protein and significantly reduces levels of MYC protein, demonstrating reduced levels of BRD4-driven MYC transcription.
Nat Commun

A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells. [Abstract]

2020 Apr 22;11(1):1935. PMID: 32321921
J Adv Res

Redistribution of super-enhancers promotes malignancy in human hepatocellular carcinoma. [Abstract]

2025 Jul 4:S2090-1232(25)00504-1. PMID: 40617410
Acta Pharm Sin B

2026 May 19.
Biomaterials

Tumor microenvironment responsive nano-PROTAC for BRD4 degradation enhanced cancer photo-immunotherapy. [Abstract]

2025 Nov:322:123387. PMID: 40344878
Cell Commun Signal

Inhibition of bromodomain and extra-terminal proteins targets constitutively active NFκB and STAT signaling in lymphoma and influences the expression of the antiapoptotic proteins BCL2A1 and c-MYC. [Abstract]

2024 Aug 27;22(1):415. PMID: 39192247
Cell Commun Signal

BRD4/nuclear PD-L1/RelB circuit is involved in the stemness of breast cancer cells. [Abstract]

2023 Nov 3;21(1):315. PMID: 37924094
Mater Today Bio

A pH-responsive PROTAC-based nanosystem triggers tumor-specific ferroptosis to construct in situ tumor vaccines. [Abstract]

2025 Jan 24:31:101523. PMID: 39935894
Clin Cancer Res

Overcoming BET Inhibitor Resistance in Malignant Peripheral Nerve Sheath Tumors. [Abstract]

2019 Jun 1;25(11):3404-3416. PMID: 30796033
J Med Chem

Alkyne Two-Phase Strategy: Rapid Generation of TK-285-Derived PROTACs as BRD4 Degraders. [Abstract]

2026 Mar 19. PMID: 41852276
Anal Chem

Hydrogen/Deuterium Exchange for Chiral Stability Assessment in Acidic Methine-Containing Compounds. [Abstract]

2025 Dec 2;97(47):26097-26107. PMID: 41243541
Mol Cancer Ther

Harnessing senolytics and PARP inhibition to expand the antitumor activity of CDK4/6 inhibitors in prostate cancer. [Abstract]

2025 Jul 2. PMID: 40601842
JCI Insight

Inhibition of bromodomain extraterminal histone readers alleviates skin fibrosis in experimental models of scleroderma. [Abstract]

2022 May 9;7(9):e150871. PMID: 35349485
Biochem Pharmacol

Discovery of a potent BRD4 PROTAC and evaluation of its bioactivity in breast cancer cell lines. [Abstract]

2025 Nov:241:117159. PMID: 40659131
Int J Mol Sci

BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells. [Abstract]

2025 Aug 21;26(16):8074. PMID: 40869394
Cancer Sci

MYC Addiction as a Targetable Vulnerability in Nelarabine-Resistant T-Cell Acute Lymphoblastic Leukemia. [Abstract]

2026 Jun;117(6):1608-1622. PMID: 41947770
Sci Rep

Interplay between interferon regulatory factor 1 and BRD4 in the regulation of PD-L1 in pancreatic stellate cells. [Abstract]

2018 Sep 5;8(1):13225. PMID: 30185888

ARV-825 purchased from MedChemExpress. Usage Cited in: Sci Rep. 2018 Sep 5;8(1):13225. [Abstract]

ARV-825 decreases IFN-γ-induced PD-L1 mRNA and protein expression in primary PSCs and in the stellate cell line.
Cancers (Basel)

BRD4 Inhibition as a Strategy to Prolong the Response to Standard of Care in Estrogen Receptor-Positive Breast Cancer. [Abstract]

2023 Aug 11;15(16):4066. PMID: 37627092
J Cell Mol Med

Inactivation of CDK12 Enhances Mitochondrial Efficiency to Suppress DNA Damage. [Abstract]

2026 Apr;30(7):e71101. PMID: 41896195
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
Hum Gene Ther

HIV Tat- conjugated Histone H3 peptides induce tumor cell death via cellular stress responses. [Abstract]

2023 Jan;34(1-2):42-55. PMID: 36373826
J Biol Chem

Degradation and inhibition of epigenetic regulatory protein BRD4 exacerbate Alzheimer's disease-related neuropathology in cell models. [Abstract]

2022 Apr;298(4):101794. PMID: 35248531
Invest New Drugs

Targeting Myc through BET-PROTAC elicits potent anti-lymphoma activity in diffuse large B cell lymphoma. [Abstract]

2025 Jun;43(3):621-633. PMID: 40307411
J Pharm Biomed Anal

Development and optimization of a high-throughput LC-MS/MS method for the simultaneous determination of Exatecan and its Cathepsin B-sensitive prodrug, and ARV-825 in rat plasma: Application to pharmacokinetic study. [Abstract]

2025 Jun 15:258:116746. PMID: 39955884
bioRxiv

2025 Sep 7.
Indiana University Indianapolis

2025.
bioRxiv

2025 April 30.
bioRxiv

2024 Mar 21.
Environ Toxicol

Transcriptional factor BRD4 promotes the stemness of esophageal cancer by activating the nuclear PD-L1/RelB axis. [Abstract]

2024 Feb;39(2):669-679. PMID: 37615218
University of Texas

2023 Jun 13.
Research Square Print

November 18th, 2022
Martin-Luther-Universität Halle-Wittenberg

2020 Dec.
Aging

ARV-825-induced BRD4 protein degradation as a therapy for thyroid carcinoma. [Abstract]

2020 Mar 12;12(5):4547-4557. PMID: 32163373

Solvent & Solubility

In Vitro:

DMSO : ≥ 50 mg/mL (54.15 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

* "≥" means soluble, but saturation unknown.

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

1.0829 mL

5.4146 mL

10.8292 mL

5 mM

0.2166 mL

1.0829 mL

2.1658 mL

10 mM

0.1083 mL

0.5415 mL

1.0829 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, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Molarity Calculator

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

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

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

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

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 (2.71 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 (2.71 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:

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 (305 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 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]. Liao X, et al. ARV-825 Demonstrates Antitumor Activity in Gastric Cancer MYC-Targets and G2M-Checkpoint Signaling Pathways. Frontiers in oncology. 2021;11:753119.

[2]. Wu S, et al. BRD4 PROTAC degrader ARV-825 inhibits T-cell acute lymphoblastic leukemia by targeting 'Undruggable' Myc-pathway genes. Cancer cell international. 2021 Apr 22;21(1):230.

[3]. Li Z, et al. PROTAC Bromodomain Inhibitor ARV-825 Displays Anti-Tumor Activity in Neuroblastoma by Repressing Expression of or . Frontiers in oncology. 2020;10:574525.

[4]. Lu Q, et al. BRD4 degrader ARV-825 produces long-lasting loss of BRD4 protein and exhibits potent efficacy against cholangiocarcinoma cells. American journal of translational research. 2019;11(9):5728-5739.

[5]. Piya S, et al. BRD4 Proteolysis Targeting Chimera (PROTAC) ARV‑825, Causes Sustained Degradation of BRD4 and Modulation of Chemokine Receptors, Cell Adhesion and Metabolic Targets in Leukemia Resulting in Profound Anti‑Leukemic Effects. Blood. 2016 Dec 2;128(22):748.

[6]. Saenz DT, et al. Novel BET protein proteolysis-targeting chimera exerts superior lethal activity than bromodomain inhibitor (BETi) against post-myeloproliferative neoplasm secondary (s) AML cells. Leukemia. 2017 Sep;31(9):1951-1961.

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

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.0829 mL	5.4146 mL	10.8292 mL	27.0730 mL
	5 mM	0.2166 mL	1.0829 mL	2.1658 mL	5.4146 mL
	10 mM	0.1083 mL	0.5415 mL	1.0829 mL	2.7073 mL
	15 mM	0.0722 mL	0.3610 mL	0.7219 mL	1.8049 mL
	20 mM	0.0541 mL	0.2707 mL	0.5415 mL	1.3536 mL
	25 mM	0.0433 mL	0.2166 mL	0.4332 mL	1.0829 mL
	30 mM	0.0361 mL	0.1805 mL	0.3610 mL	0.9024 mL
	40 mM	0.0271 mL	0.1354 mL	0.2707 mL	0.6768 mL
	50 mM	0.0217 mL	0.1083 mL	0.2166 mL	0.5415 mL

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Cat. No.:
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MCE Japan Authorized Agent:

Product Name:
CAS No.:
Species:
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ARV-825

Publications Citing Use of MedChemExpress (MCE) ARV-825

All PROTACs Isoforms

All Epigenetic Reader Domain Isoforms

All Polo-like Kinase (PLK) Isoforms

All CDK Isoforms

All JAK Isoforms

All STAT Isoforms

All Pim Isoforms

All Bcl-2 Family Isoforms

All PAK Isoforms

All Wnt Isoforms

All Caspase Isoforms

All PARP Isoforms