Cat. No.: HY-101519

BETd-260

Name: BETd-260
Brand: MedChemExpress
SKU: HY-101519
Price: 400.00 USD
Availability: InStock
Rating: 5 (4 reviews)

(Synonyms: ZBC 260)

4 Cited Publications

Customer Review

Based on 4 publication(s) in Google Scholar

BETd-260 (ZBC 260) is a BET PROTAC degrader. BETd-260 recruits BRD2, BRD3, and BRD4 to the CUL4-RBX1-DDB1-CRBN E3 ubiquitin ligase complex, driving cereblon-, proteasome-, and NEDD8-activating enzyme-dependent ubiquitination and degradation, with a DC50 of approximately 30-100 pM in RS4;11 cells. BETd-260 induces cancer cell apoptosis via endogenous signaling pathways, regulates the expression of the Bcl-2 family, inhibits the oncogene c-Myc, and reduces cell viability. BETd-260 suppresses tumor growth in mouse xenograft models with good biosafety. BETd-260 can be used in research related to acute leukemia, hepatocellular carcinoma, osteosarcoma, and triple-negative breast cancer.
(Pink: BET ligand (HY-112429); Blue: Cereblon ligand (HY-43722); Black: linker).

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

Purity: 99.68%
CAS No.: 2093388-62-4
Formula: C₄₃H₄₆N₁₀O₆
Molecular Weight:798.89

Storage:

-80°C, protect from light, stored under nitrogen

BETd-260 Chemical Structure

CAS No.: 2093388-62-4

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Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (4)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

BETd-260 (ZBC 260) is a BET PROTAC degrader. BETd-260 recruits BRD2, BRD3, and BRD4 to the CUL4-RBX1-DDB1-CRBN E3 ubiquitin ligase complex, driving cereblon-, proteasome-, and NEDD8-activating enzyme-dependent ubiquitination and degradation, with a DC50 of approximately 30-100 pM in RS4;11 cells. BETd-260 induces cancer cell apoptosis via endogenous signaling pathways, regulates the expression of the Bcl-2 family, inhibits the oncogene c-Myc, and reduces cell viability. BETd-260 suppresses tumor growth in mouse xenograft models with good biosafety. BETd-260 can be used in research related to acute leukemia, hepatocellular carcinoma, osteosarcoma, and triple-negative breast cancer^[1]^[2]^[3]^[4]. (Pink: BET ligand (HY-112429); Blue: Cereblon ligand (HY-43722); Black: linker).

IC₅₀ & Target

^[1]^[2]^[3]

BRD4

<30 pM (DC₅₀)

BRD2

30-100 pM (DC₅₀)

BRD3

30-100 pM (DC₅₀)

All PROTACs Isoforms :

All Epigenetic Reader Domain Isoforms :

All Bcl-2 Family Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
RS4-11	IC50	0.051 nM	Cell growth inhibition against human RS4;11 acute leukemia cells assessed via lactate dehydrogenase-based WST-8 assay after 4 days of incubation. Cell growth inhibition against human RS4;11 acute leukemia cells assessed via lactate dehydrogenase-based WST-8 assay after 4 days of incubation.	28339196
MOLM-13	IC50	2.2 nM	Cell growth inhibition against human MOLM-13 acute leukemia cells assessed via lactate dehydrogenase-based WST-8 assay after 4 days of incubation. Cell growth inhibition against human MOLM-13 acute leukemia cells assessed via lactate dehydrogenase-based WST-8 assay after 4 days of incubation.	28339196
HepG2	EC50	10.3 nM	Inhibition of cell viability against human HepG2 cells assessed by CCK-8 assay after 72 hrs of treatment. Inhibition of cell viability against human HepG2 cells assessed by CCK-8 assay after 72 hrs of treatment.	31993368
Bel-7402	EC50	5.4 nM	Inhibition of cell viability against human BEL-7402 cells assessed by CCK-8 assay after 72 hrs of treatment. Inhibition of cell viability against human BEL-7402 cells assessed by CCK-8 assay after 72 hrs of treatment.	31993368
SK-HEP1	EC50	24.3 nM	Inhibition of cell viability against human SK-HEP-1 cells assessed by CCK-8 assay after 72 hrs of treatment. Inhibition of cell viability against human SK-HEP-1 cells assessed by CCK-8 assay after 72 hrs of treatment.	31993368
SMMC-7721	EC50	23.3 nM	Inhibition of cell viability against human SMMC-7721 cells assessed by CCK-8 assay after 72 hrs of treatment. Inhibition of cell viability against human SMMC-7721 cells assessed by CCK-8 assay after 72 hrs of treatment.	31993368
Huh-7	EC50	63.3 nM	Inhibition of cell viability against human HuH-7 cells assessed by CCK-8 assay after 72 hrs of treatment. Inhibition of cell viability against human HuH-7 cells assessed by CCK-8 assay after 72 hrs of treatment.	31993368
MHCC97H	EC50	64.9 nM	Inhibition of cell viability against human MHCC97H cells assessed by CCK-8 assay after 72 hrs of treatment. Inhibition of cell viability against human MHCC97H cells assessed by CCK-8 assay after 72 hrs of treatment.	31993368
SAOS-2	EC50	1.1 nM	Inhibition of cell viability against human Saos-2 osteosarcoma cells incubated for 72 h by CCK-8 assay. Inhibition of cell viability against human Saos-2 osteosarcoma cells incubated for 72 h by CCK-8 assay.	31653826
MG-63	EC50	7.2 nM	Inhibition of cell viability against human MG-63 osteosarcoma cells incubated for 72 h by CCK-8 assay. Inhibition of cell viability against human MG-63 osteosarcoma cells incubated for 72 h by CCK-8 assay.	31653826
SJSA-1	EC50	16.1 nM	Inhibition of cell viability against human SJSA-1 osteosarcoma cells incubated for 72 h by CCK-8 assay. Inhibition of cell viability against human SJSA-1 osteosarcoma cells incubated for 72 h by CCK-8 assay.	31653826

In Vitro

BETd-260 (for 4 days) potently inhibits the proliferation of RS4;11 human acute leukemia cells, with an IC₅₀ of 51 pM^[1].
BETd-260 (for 4 days) inhibits the proliferation of human acute leukemia cell line MOLM-13, with an IC₅₀ of 2.2 nM^[1].
BETd-260 (0.1-1 nM; 3 h) potently degrades BRD2, BRD3 and BRD4 proteins in the human acute leukemia cell line RS4;11^[1].
BETd-260 (0.03-10 nM; 24 h) degrades BRD2, BRD3 and BRD4 proteins in RS4;11 human acute leukemia cells and downregulates c-Myc^[1].
BETd-260 (1 nM; 3 h, preceded by 2 h pretreatment) induces the degradation of BRD2, BRD3 and BRD4 in human acute leukemia cell line RS4;11, and this process depends on binding to BET proteins, cereblon, the proteasome and NEDD8-activating enzyme^[1].
BETd-260 (10-100 nM; 1-48 h) rapidly and potently degrades BRD2, BRD3 and BRD4 proteins in human hepatocellular carcinoma HepG2 cells^[2].
BETd-260 (100 nM; 24 h) exhibits broad BET protein degradation activity in human hepatocellular carcinoma (HCC) cell lines, completely eliminating BRD2, BRD3 and BRD4 in BEL-7402, SK-HEP-1 and SMMC-7721 cells, and reducing the levels of these proteins to low levels in HuH-7 and MHCC97H cells^[2].
BETd-260 (72 h) potently inhibits the cell viability of MNNG/HOS, Saos-2, MG-63 and SJSA-1 osteosarcoma cell lines, with EC₅₀ values ranging from 1.1 nM to 16.1 nM^[3].
BETd-260 (3-30 nM; 1-24 h) potently degrades BRD2, BRD3 and BRD4 in MNNG/HOS, Saos-2, MG-63 and SJSA-1 osteosarcoma cell lines^[3].
BETd-260 (10 nM; 2 h, preceded by 1 h pre-treatment with inhibitors) induces the degradation of BRD2, BRD3 and BRD4 in MNNG/HOS osteosarcoma cells via a pathway mediated by the Cullin-dependent E3 ligase and ubiquitin-proteasome system, and this degradation process depends on specific binding to BET proteins^[3].
BETd-260 potently inhibits the growth of human triple-negative breast cancer (TNBC) cell lines^[4].
BETd-260 efficiently degrades BRD2, BRD3 and BRD4 proteins in human triple-negative breast cancer (TNBC) cell lines^[4].
BETd-260 (0.3-30 nM; 24 h) induces cell cycle arrest and significant apoptosis in RS4;11 and MOLM-13 human acute leukemia cells^[1].
BETd-260 (72 h) potently and dose-dependently inhibits the viability of human HepG2, BEL-7402, SK-HEP-1, SMMC-7721, HuH-7 and MHCC97H hepatocellular carcinoma cells, with EC₅₀ values ranging from 5.4 to 64.9 nM^[2].
BETd-260 (10-100 nM; 48 h) induces extensive apoptosis in human HepG2, BEL-7402, SK-HEP-1, SMMC-7721, HuH-7 and MHCC97H hepatocellular carcinoma cells^[2].
BETd-260 (10-100 nM; 24 h) activates the apoptotic signaling pathway in human HepG2, BEL-7402, SK-HEP-1, SMMC-7721, HuH-7 and MHCC97H hepatocellular carcinoma cells, and induces PARP cleavage and caspase-3 activation^[2].
BETd-260 (10-100 nM; 24 h) bidirectionally regulates the expression of apoptosis-related proteins, inhibits c-Myc expression, upregulates Bad expression, and downregulates the expressions of Mcl-1, Bcl-2, XIAP and c-Myc in human hepatocellular carcinoma cells^[2].
BETd-260 (100 nM; 48 h following 24 h siRNA transfection) induces cell death in human HepG2 and BEL-7402 hepatocellular carcinoma cells, and this process depends on the endogenous caspase-9-mediated apoptotic pathway rather than the exogenous caspase-8 pathway^[2].
BETd-260 (100 nM; 48 h after 24 h siRNA transfection) induces cell death in human HepG2 and BEL-7402 hepatocellular carcinoma cells in a Bad-dependent manner^[2].
BETd-260 (10-100 nM; 24 h) disrupts mitochondrial membrane integrity in human HepG2 and BEL-7402 hepatocellular carcinoma cells, and induces the release of cytochrome c from mitochondria into the cytosol^[2].
BETd-260 (10-100 nM; 4-24 h) upregulates the expression of Bad mRNA in human HepG2 and BEL-7402 hepatocellular carcinoma cells in a dose-dependent manner^[2].
BETd-260 (3-30 nM; 24 h) induces dose-dependent apoptosis in MNNG/HOS and Saos-2 osteosarcoma cells^[3].
BETd-260 (3-30 nM; 24 h) activates the mitochondrial apoptotic pathway in MNNG/HOS and Saos-2 osteosarcoma cells, which is evidenced by the cleavage of caspase-3, caspase-9 and PARP-1^[3].
BETd-260 (10 nM; 24-48 h, with 1 h pre-treatment with inhibitors) induces death and apoptosis in MNNG/HOS and Saos-2 osteosarcoma cells, a process that mainly relies on the endogenous pathway mediated by the caspase-9 and caspase-3 cascade^[3].
BETd-260 (3-30 nM; 1-24 h) regulates the expression of Bcl-2 family members in MNNG/HOS and Saos-2 osteosarcoma cells, and inhibits c-Myc (without affecting p53), specifically characterized by depletion of Mcl-1 and Bcl-xl, upregulation of Noxa levels, and reduction of c-Myc levels^[3].

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

Western Blot Analysis^[1]

Cell Line:

RS4;11 human acute leukemia cells
Concentration:

0.1, 0.3 and 1 nM
Incubation Time:

3 h
Result:

Decreased levels of BRD2 and BRD4 at concentrations as low as 0.3 nM.
Decreased BRD3 levels at 0.1 nM.

Western Blot Analysis^[1]

Cell Line:

RS4;11 human acute leukemia cells
Concentration:

0.03, 0.1, 0.3, 1, 3 and 10 nM
Incubation Time:

24 h
Result:

Decreased BRD4 levels at 0.03 nM.
Decreased BRD2 and BRD3 levels at 0.1 nM.
Decreased c-Myc levels at 0.1 nM.

Western Blot Analysis^[1]

Cell Line:

RS4;11 human acute leukemia cells
Concentration:

1 nM (this compound); 10-30 μM (Lenalidomide (HY-A0003)); 20 μM (MG-132 (HY-13259)); 1 μM (MLN4924 (HY-70062))
Incubation Time:

3 h (BETd-260); 2 h (pretreatment)
Result:

Completely blocked this compound-induced degradation of BRD2, BRD3, and BRD4 following pretreatment with 8, lenalidomide, MG-132, or MLN4924.

Cell Cycle Analysis^[1]

Cell Line:

RS4;11 human acute leukemia cells; MOLM-13 human acute leukemia cells
Concentration:

0.3, 1, 3, 10 and 30 nM
Incubation Time:

24 h
Result:

Induced strong cell cycle arrest at 0.3 nM.
Induced robust apoptosis at 3-10 nM.

Western Blot Analysis^[2]

Cell Line:

human HepG2 hepatocellular carcinoma (HCC) cells
Concentration:

10, 30 and 100 nM (24 h time point); 100 nM (time course)
Incubation Time:

24 h (10-100 nM); 1 h, 3 h, 12 h, 24 h, 48 h (100 nM time course)
Result:

Almost completely eliminated BRD2, BRD3, and BRD4 protein levels at 10-100 nM after 24 h.
Reduced BET protein levels within 1 h and achieved complete elimination by 12 h at 100 nM.

Western Blot Analysis^[2]

Cell Line:

human BEL-7402, SK-HEP-1, SMMC-7721, HuH-7, and MHCC97H HCC cells
Concentration:

100 nM
Incubation Time:

24 h
Result:

Completely degraded BRD2, BRD3, and BRD4 proteins in BEL-7402, SK-HEP-1, and SMMC-7721 cell lines.
Reduced BET protein levels to very low levels in HuH-7 and MHCC97H cell lines.

Apoptosis Analysis^[2]

Cell Line:

human HepG2, BEL-7402, SK-HEP-1, SMMC-7721, HuH-7, and MHCC97H HCC cells
Concentration:

10, 30 and 100 nM
Incubation Time:

48 h
Result:

Triggered apoptosis in HepG2 and BEL-7402 cells at 10 nM.
Induced 86% apoptosis in HepG2 cells and 77% apoptosis in BEL-7402 cells at 100 nM.
Induced 45-85% cell death in SK-HEP-1, SMMC-7721, HuH-7, and MHCC97H cells.

Western Blot Analysis^[2]

Cell Line:

human HepG2, BEL-7402, SK-HEP-1, SMMC-7721, HuH-7, and MHCC97H HCC cells
Concentration:

10, 30 and 100 nM
Incubation Time:

24 h
Result:

Caused extensive cleavage of PARP in all 6 HCC cell lines.
Induced robust activation of caspase-3 in all 6 HCC cell lines.\nIncreased Bad protein levels in HepG2 and BEL-7402 cells.
Reduced Mcl-1, Bcl-2, and XIAP protein levels in HepG2 and BEL-7402 cells.
Distinctly reduced c-Myc protein levels in 5 of the 6 HCC cell lines.

Cell Cytotoxicity Assay^[2]

Cell Line:

human HepG2 and BEL-7402 HCC cells
Concentration:

100 nM
Incubation Time:

48 h (after 24 h siRNA transfection)
Result:

Significantly attenuated triggered cell death when caspase-9 was knocked down.
Showed no effect on triggered cell death when caspase-8 was knocked down.\nSignificantly attenuated induced cell death in both HepG2 and BEL-7402 cell lines when Bad was knocked down.

Western Blot Analysis^[2]

Cell Line:

human HepG2 and BEL-7402 HCC cells
Concentration:

10, 30 and 100 nM
Incubation Time:

24 h
Result:

Increased cytochrome c levels in the cytosolic fraction.
Decreased cytochrome c levels in the mitochondria-enriched fraction.

Real Time qPCR^[2]

Cell Line:

human HepG2 and BEL-7402 HCC cells
Concentration:

10, 30 and 100 nM (4 h time point); 100 nM (4 h, 12 h, 24 h time course)
Incubation Time:

4 h (10-100 nM); 4 h, 12 h, 24 h (100 nM time course)
Result:

Increased Bad mRNA levels 3-fold at 4 h and 8-fold at 12 h in HepG2 cells at 100 nM.
Increased Bad mRNA levels 3-fold at 4 h, 7-fold at 12 h, and 2-fold at 24 h in BEL-7402 cells at 100 nM.
Dose-dependently upregulated Bad mRNA levels in both cell lines at 10-100 nM after 4 h.

Western Blot Analysis^[3]

Cell Line:

MNNG/HOS, Saos-2, MG-63, SJSA-1
Concentration:

3 nM, 10 nM, 30 nM
Incubation Time:

24 h (3 nM, 10 nM, 30 nM); 1 h, 4 h, 14 h, 24 h (30 nM)
Result:

Potently degraded BRD2, BRD3, and BRD4 in all four osteosarcoma cell lines.
Completely depleted BRD3 and BRD4, and largely suppressed BRD2 levels in MNNG/HOS and Saos-2 cells at 3 nM for 24 h.
Achieved maximum degradation of BET proteins within 1 h in MNNG/HOS cells at 30 nM, with the effect lasting up to 24 h.

Western Blot Analysis^[3]

Cell Line:

MNNG/HOS
Concentration:

10 nM
Incubation Time:

2 h (preceded by 1 h pre-treatment with inhibitors)
Result:

Largely had its BRD2, BRD3, and BRD4 degradation activity abrogated when cells were pre-treated with proteasome inhibitor MG-132, NEDD8-activating enzyme inhibitor MLN4924, or excess BET inhibitor HJB-97.

Apoptosis Analysis^[3]

Cell Line:

MNNG/HOS, Saos-2
Concentration:

3 nM, 10 nM, 30 nM
Incubation Time:

24 h
Result:

Induced apoptosis in 43%, 62%, and 84% of MNNG/HOS cells at 3 nM, 10 nM, and 30 nM respectively.
Induced apoptosis in 25%, 57%, and 75% of Saos-2 cells at 3 nM, 10 nM, and 30 nM respectively.

Western Blot Analysis^[3]

Cell Line:

MNNG/HOS, Saos-2
Concentration:

3 nM, 10 nM, 30 nM
Incubation Time:

24 h
Result:

Induced activation of caspase-3 and caspase-9, and cleavage of PARP-1 in both MNNG/HOS and Saos-2 cells.
Increased effects of caspase-3, caspase-9 activation, and PARP-1 cleavage with higher concentrations.

In Vivo

BETd-260 (compound 23) (5 mg/kg; intravenous injection; once every two days; for 3 consecutive weeks) induces regression of RS4;11 xenograft tumors in SCID mice, and triggers sustained degradation of BET proteins, downregulation of c-Myc expression, and apoptosis in tumor tissues^[1].
BETd-260 (5 mg/kg; intravenous injection; single administration / three times per week; for 3 consecutive weeks) exerts potent anti-hepatocellular carcinoma activity in vivo. It inhibits tumor growth in HepG2 and BEL-7402 xenograft models by degrading BET proteins, regulating apoptosis regulators, and inducing tumor cell apoptosis^[2].
BETd-260 (5 mg/kg; intravenous injection; three times per week; for 3 consecutive weeks) inhibits tumor growth in the MNNG/HOS osteosarcoma xenograft model of BALB/c mice, with durable efficacy and no observed toxicity^[3].
BETd-260 (5 mg/kg; intravenous injection; three times per week; for 4 consecutive weeks) inhibits tumor growth in an osteosarcoma PDX xenograft model in NOD SCID mice, with no observed toxicity^[3].
BETd-260 (5 mg/kg; intravenous injection; 3 times per week; for 3 consecutive weeks) inhibits the growth of MDA-MB-231 and MDA-MB-468 xenograft tumors, with activity comparable to or stronger than that of BETi-211 (HY-122703). It also depletes BET proteins, upregulates p21^WAF1 and downregulates MCL1 in tumors, without significant toxicity^[4].

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

Animal Model:

severe combined immunodeficient (SCID) mice^[1]
Dosage:

5 mg/kg (tumor regression); 5 mg/kg (pharmacodynamic analysis)
Administration:

i.v.; every other day, three times a week; 3 weeks (tumor regression); i.v.; single dose (pharmacodynamic analysis)
Result:

Achieved >90% tumor regression in RS4;11 xenografts, with no signs of toxicity or animal weight loss.
Induced near-complete degradation of BRD2, BRD3, and BRD4 proteins in tumor tissue starting at 1 hour, with effects persisting for >24 hours.
Caused strong down-regulation of c-Myc protein for at least 6 hours.
Detected robust cleavage of PARP and caspase-3 starting at 3 hours, peaking at 6 hours.
Reached tumor concentrations of 166.3 ng/g at 1 hour, 98.5 ng/g at 3 hours, and 35.8 ng/g at 6 hours after a single dose.

Animal Model:

Balb/c (6-week-old; subcutaneous xenograft model injected with HepG2 or BEL-7402 cells)^[2]
Dosage:

5 mg/kg (pharmacodynamic analysis); 5 mg/kg (efficacy analysis)
Administration:

i.v.; single dose (pharmacodynamic analysis); 3 times per week; 3 weeks (efficacy analysis)
Result:

Suppressed BRD2, BRD3, and BRD4 expression in HepG2 and BEL-7402 xenograft tumor tissues.
Reduced Mcl-1 expression, increased Bad expression, augmented cleaved PARP and activated caspase-3 levels in HepG2 and BEL-7402 xenograft tumor tissues.
Reduced Ki-67 expression by 57% (HepG2) and 71% (BEL-7402).
Achieved a tumor growth inhibition (TGI) of 49% in HepG2 xenografts and 78% in BEL-7402 xenografts.
Caused only slight effects on mouse body weight.

Animal Model:

BALB/c (6-week-old; subcutaneous xenograft induced by injecting 5 million MNNG/HOS cells suspended in Matrigel)^[3]
Dosage:

5 mg/kg
Administration:

i.v.; single dose (pharmacodynamic study); i.v.; three times per week; 3 weeks (efficacy study)
Result:

Completely depleted BRD2, BRD3, and BRD4 proteins in tumor tissue starting at 1 h post-treatment, with the effect lasting more than 24 h.
Triggered PARP-1 cleavage and reduced Ki67-positive cells, indicating massive apoptosis and inhibited tumor cell proliferation.
Achieved ~94% tumor growth inhibition (TGI).
Reduced tumor volume from 164 mm³ to 155 mm³ after 3 doses, with this partial reduction persisting for 69 days after treatment cessation.
Resulted in an average tumor volume of 246.9 mm³ at study termination (day 121), compared to 1540.1 mm³ in control mice, with 5 out of 7 treated tumors remaining smaller than their initial volume.
Caused no significant weight loss or other signs of toxicity.

Animal Model:

NOD SCID (6-week-old; subcutaneous patient-derived xenograft induced by implanting 300-1000 mg PDX tumor masses)^[3]
Dosage:

5 mg/kg (pharmacodynamic study); 5 mg/kg (efficacy study)
Administration:

i.v.; single dose (pharmacodynamic study); i.v.; three times per week; 4 weeks (efficacy study)
Result:

Markedly reduced BRD2, BRD3, and BRD4 protein levels, increased cleaved PARP-1-positive cells, and reduced Ki67-positive cells in PDX tumor tissue.
Achieved 57% tumor growth inhibition (TGI).
Resulted in an average tumor volume of 740.9 mm³ at study termination (day 39), compared to 1623.4 mm³ in control mice.
Caused no significant weight loss or apparent toxicity.

Animal Model:

SCID mice bearing subcutaneous xenograft tumors were established by injecting 5 million MDA-MB-231 cells or 5 million MDA-MB-468 cells, respectively^[4]
Dosage:

5 mg/kg
Administration:

i.v.; 3 times per week; 3 weeks
Result:

Exerted stronger antitumor activity than BETd-246 at 10 mg/kg with the same dosing schedule.
Reduced BET protein levels in tumors at 1-3 hours post-exposure.
Upregulated p21WAF1 in tumors at 1-3 hours post-exposure.
Downregulated MCL1 in tumors at 1-3 hours post-exposure.
Caused no significant weight loss or overt toxicity.\nExerted stronger antitumor activity than BETd-246 at 10 mg/kg with the same dosing schedule.
Reduced BET protein levels in tumors at 1-3 hours post-exposure.
Upregulated p21WAF1 in tumors at 1-3 hours post-exposure.
Downregulated MCL1 in tumors at 1-3 hours post-exposure.
Caused no significant weight loss or overt toxicity.

Chemical Information

CAS No. 2093388-62-4
Appearance Solid
Molecular Weight 798.89
Formula C₄₃H₄₆N₁₀O₆
Color Off-white to yellow
SMILES

CCN1N=C(C2CC2)C=C1NC3=NC(C(NCCCCCC4=CC=CC5=C4CN(C6C(NC(CC6)=O)=O)C5=O)=O)=NC7=C3C8=CC(OC)=C(C9=C(C)ON=C9C)C=C8N7
Synonyms

ZBC 260
Shipping

Shipping with dry ice.
Storage

-80°C, protect from light, stored under nitrogen

Publications (4)

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Journal Impact Factor

PLoS Biol

The cell cycle regulator PLK1 promotes murine melanoma progression by regulating the transcription factor BACH1. [Abstract]

2025 Nov 24;23(11):e3003490. PMID: 41284701
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
ACS Pharmacol Transl Sci

Developing MYC Degraders Bearing the Von Hippel-Lindau Ligand to Target the "Undruggable" MYC. [Abstract]

2024 Nov 15;7(12):3955-3968. PMID: 39698270
bioRxiv

2023: 2023 Feb 6.527237.

Solvent & Solubility

In Vitro:

DMSO : 25 mg/mL (31.29 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

1.2517 mL

6.2587 mL

12.5174 mL

5 mM

0.2503 mL

1.2517 mL

2.5035 mL

10 mM

0.1252 mL

0.6259 mL

1.2517 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 (protect from light, stored under nitrogen). When stored at -80°C, please use it within 6 months.

Molarity Calculator

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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 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 0.83 mg/mL (1.04 mM); Clear solution

This protocol yields a clear solution of ≥ 0.83 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (8.3 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: ≥ 0.83 mg/mL (1.04 mM); Clear solution

This protocol yields a clear solution of ≥ 0.83 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 (8.3 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

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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 (310 KB)
SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
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- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
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- Portuguese - PT (394 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]. Zhou B, et al. Discovery of a Small-Molecule Degrader of Bromodomain and Extra-Terminal (BET) Proteins with Picomolar Cellular Potencies and Capable of Achieving Tumor Regression. Journal of medicinal chemistry. 2018 Jan 25;61(2):462-481. [Content Brief]

[2]. Zhang H, et al. Targeting BET Proteins With a PROTAC Molecule Elicits Potent Anticancer Activity in HCC Cells. Frontiers in oncology. 2019;9:1471. [Content Brief]

[3]. Shi C, et al. PROTAC induced-BET protein degradation exhibits potent anti-osteosarcoma activity by triggering apoptosis. Cell death & disease. 2019 Oct 25;10(11):815.

[4]. Shi C, et al. Targeted Degradation of BET Proteins in Triple-Negative Breast Cancer. Cancer Res. 2017 May 1;77(9):2476-2487. [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

Storage method and period of stock solution: -80°C, 6 months (protect from light, stored under nitrogen). When stored at -80°C, please use it within 6 months.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.2517 mL	6.2587 mL	12.5174 mL	31.2934 mL
	5 mM	0.2503 mL	1.2517 mL	2.5035 mL	6.2587 mL
	10 mM	0.1252 mL	0.6259 mL	1.2517 mL	3.1293 mL
	15 mM	0.0834 mL	0.4172 mL	0.8345 mL	2.0862 mL
	20 mM	0.0626 mL	0.3129 mL	0.6259 mL	1.5647 mL
	25 mM	0.0501 mL	0.2503 mL	0.5007 mL	1.2517 mL
	30 mM	0.0417 mL	0.2086 mL	0.4172 mL	1.0431 mL

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BETd-260

Publications Citing Use of MedChemExpress (MCE) BETd-260

All PROTACs Isoforms

All Epigenetic Reader Domain Isoforms

All Bcl-2 Family Isoforms