Cat. No.: HY-183377

DMBT

DMBT is an orally effective anti-tumor metastasis and anti-angiogenesis agent. DMBT downregulates key molecules such as EGFR/p-Akt/HIF-1α/VEGF/MMP-9, inhibits the HIF-1α/VE-cadherin (cadherin)/MMPs and Nrf2/HO-1 signaling pathways, and reduces hypoxia-induced ROS levels as well as the secretion and activity of MMP-9. DMBT inhibits hypoxia-induced vasculogenic mimicry, cancer cell migration, invasion and metastasis, and exhibits no obvious cytotoxicity to normal cells. DMBT reduces the area of laser-induced choroidal neovascularization lesions. DMBT can be used in studies related to breast cancer, melanoma and macular degeneration.

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CAS No.: 1260071-76-8
Formule: C₃₀H₃₈O₁₇
Masse moléculaire:670.61

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

DMBT Chemical Structure

CAS No.: 1260071-76-8

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Activité biologique
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
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Activité biologique

Description

IC₅₀ & Target^[1]^[2]

MMP-9

HIF-1α

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In Vitro

DMBT (1-16 μM; 6-24 h) reverses hypoxia-induced migration of MDA-MB-231 and MCF-7 human mammary adenocarcinoma cells^[1]^[3].
DMBT (16 μM; 24 h) inhibits hypoxia-induced migration of human mammary adenocarcinoma cell lines MDA-MB-231 and MCF-7^[1].
DMBT (16 μM; 24 h) inhibits hypoxia-induced invasion of human breast adenocarcinoma cell lines MDA-MB-231 and MCF-7^[1].
DMBT (16 μM; 12-24 h for MDA-MB-231, 5-9 h for MCF-7) inhibits hypoxia-induced vasculogenic mimicry (VM) formation in human breast cancer cell lines MDA-MB-231 and MCF-7^[1].
DMBT (16 μM; 24 h) inhibits hypoxia-induced upregulation of HIF-1α, VE-cadherin, MMP-9, MMP-2, Rac1, Cdc42 and p-Akt in MDA-MB-231 human breast adenocarcinoma cells^[1].
DMBT (16 μM; 24 h) inhibits hypoxia-induced upregulation of MMP-9, Rac1, Cdc42 and Beclin1, reverses hypoxia-induced downregulation of p-mTOR, and exerts no effect on the expression of HIF-1α and VE-cadherin in MCF-7 human breast adenocarcinoma cells^[1].
DMBT (1-80 μM; 48 h) exerts no significant antiproliferative or cytotoxic effects on B16BL6 cells^[2].
DMBT (2-8 μM; 48-72 h) significantly inhibits the migration of B16BL6 cells in scratch wound healing assays^[2].
DMBT (2-8 μM; 24 h) potently inhibits the invasive ability of B16BL6 cells to penetrate Matrigel-coated Transwell chambers^[2].
DMBT (2-8 μM; 24 h) regulates gene expression in B16BL6 cells by downregulating the mRNAs of VEGFA, Akt1 and PIK3r1 and upregulating the mRNA of GSK-3β^[2].
DMBT (1-8 μM; 48 h) inhibits the protein expression of VEGF and MMP-9 in B16BL6 cells, while reducing the levels of phosphorylated Akt, GSK-3β, mTOR and total β-catenin^[2].
DMBT (2-8 μM; 48 h) reduces the levels of β-catenin in both the cytoplasm and nucleus of B16BL6 cells and inhibits the nuclear translocation of β-catenin^[2].
DMBT (0.5-8 μM; 24 h) dose-dependently inhibits the Matrigel invasion of human breast adenocarcinoma MDA-MB-231 cells^[3].
DMBT (1-8 μM; 24 h) significantly inhibits the activity and expression of MMP-9 in MDA-MB-231 human breast adenocarcinoma cells, while exerting only weak inhibitory effects on MMP-2^[3].
DMBT (2-8 μM; 24 h) dose-dependently inhibits capillary tube formation of HUVEC on Matrigel^[3].
DMBT (4-8 μM; 24 h) significantly downregulates the expression of VEGF, p-VEGFR-2, VEGFR-2, p-EGFR, EGFR, and p-Akt in MDA-MB-231 human breast adenocarcinoma cells, but exerts no effect on p-ERK1/2^[3].
At high concentrations, DMBT (2-128 μM; 24-72 h) does not significantly reduce the viability of MDA-MB-231 human breast adenocarcinoma cells^[3].
DMBT (2-64 μM; 24 h) exhibits no cytotoxicity against MDA-MB-231 human mammary adenocarcinoma cells^[3].
DMBT (2-128 µM; 24-72 h) exerts weak inhibitory effects on the viability of ARPE-19 and RF/6A cells^[4].
DMBT (32 µM; pre-treated with CoCl₂ for 30 min, followed by 24 h incubation) significantly inhibits hypoxia-induced activation of the ERK/Nrf2/HO-1/HIF-1α and Akt/NF-κB/HIF-1α pathways in ARPE-19 cells, with inhibition rates of target proteins ranging from 29.5% to 55.9%^[4].
Treatment of hypoxia-induced ARPE-19 cells with DMBT (8-32 µM; 6-24 h) inhibits the migratory capacity of RF/6A choroidal endothelial cells^[4].
Treatment with hypoxic conditioned medium from ARPE-19 cells exposed to DMBT (8-32 µM; 6 h) significantly inhibits tube formation in RF/6A choroidal endothelial cells^[4].
DMBT (8-32 µM; 30 min pre-incubation, 24 h hypoxic incubation) significantly inhibits hypoxia-induced VEGF secretion by ARPE-19 cells^[4].
DMBT (8-32 µM; pre-incubated for 30 minutes followed by hypoxic incubation) reduces hypoxia-induced ROS levels in ARPE-19 cells in a concentration-dependent manner^[4].

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

Cell Migration Assay ^[1]

Cell Line:

human breast adenocarcinoma MDA-MB-231, MCF-7 cells
Concentration:

16 μM
Incubation Time:

6, 12, 24 h
Result:

Reversed hypoxia-induced acceleration of migration distance in both cell lines at 6, 12, and 24 h post-scratch.

Cell Migration Assay ^[1]

Cell Line:

human breast adenocarcinoma MDA-MB-231, MCF-7 cells
Concentration:

16 μM
Incubation Time:

24 h
Result:

Reduced the number of migrated cells in both cell lines to levels lower than the hypoxic group.

Cell Invasion Assay^[1]

Cell Line:

human breast adenocarcinoma MDA-MB-231, MCF-7 cells
Concentration:

16 μM
Incubation Time:

24 h
Result:

Reduced the number of invaded cells in both cell lines to levels lower than the hypoxic group.

Western Blot Analysis^[1]

Cell Line:

human breast adenocarcinoma MDA-MB-231 cells
Concentration:

16 μM
Incubation Time:

24 h
Result:

Significantly reduced the expression of HIF-1α, VE-cadherin, MMP-9, MMP-2, Rac1, Cdc42, and p-Akt, with no effect on VEGF expression.

Western Blot Analysis^[1]

Cell Line:

human breast adenocarcinoma MCF-7 cells
Concentration:

16 μM
Incubation Time:

24 h
Result:

Significantly reduced the expression of MMP-9, Rac1, Cdc42, and Beclin1, while increasing p-mTOR expression, with no effect on HIF-1α, VE-cadherin, or VEGF expression.

Cell Proliferation Assay^[2]

Cell Line:

mouse melanoma B16BL6 cells
Concentration:

1 μM, 2 μM, 4 μM, 8 μM, 16 μM, 20 μM, 40 μM, 80 μM
Incubation Time:

48 h
Result:

Does not significantly decrease cellular viability at any tested concentration.
Shows only 15% inhibition even at the highest concentration of 80 μM.
Exhibits no evident cytotoxicity as verified by trypan blue staining.

Cell Migration Assay ^[2]

Cell Line:

mouse melanoma B16BL6 cells
Concentration:

2 μM, 4 μM, 8 μM
Incubation Time:

48 h, 72 h
Result:

Reduces B16BL6 cell migration in a concentration-dependent manner compared to untreated controls.
Shows statistically significant inhibition at all tested concentrations.

Cell Invasion Assay^[2]

Cell Line:

mouse melanoma B16BL6 cells
Concentration:

2 μM, 4 μM, 8 μM
Incubation Time:

24 h
Result:

Markedly suppresses the invasive capability of B16BL6 cells.
Significantly reduces the number of cells penetrating the Matrigel-coated filters at all tested concentrations compared to controls (P < 0.01).
Shows greater inhibitory activity than brartemicin at equivalent concentrations (P < 0.05).

Real Time qPCR^[2]

Cell Line:

mouse melanoma B16BL6 cells
Concentration:

2 μM, 4 μM, 8 μM
Incubation Time:

24 h
Result:

Down-regulates mRNA expression of VEGFA, Akt1, and PIK3r1 in a concentration-dependent manner (P < 0.01 for all tested concentrations).
Up-regulates GSK-3β mRNA expression at 8 μM (P < 0.05).

Western Blot Analysis^[2]

Cell Line:

mouse melanoma B16BL6 cells
Concentration:

1 μM, 2 μM, 4 μM, 8 μM
Incubation Time:

48 h
Result:

Reduces protein levels of VEGF (8.4% to 32.4% inhibition) and MMP-9 (25.6% to 68.4% inhibition) in a concentration-dependent manner (P < 0.05 at 4 and 8 μM).
Decreases phosphorylated levels of Akt (9.3% to 32.0% reduction), GSK-3β (29.9% to 54.7% reduction), and mTOR.
Reduces total β-catenin protein levels (P < 0.05 at 4 and 8 μM).
Has no significant effect on total GSK-3β protein levels.

Western Blot Analysis^[2]

Cell Line:

mouse melanoma B16BL6 cells
Concentration:

2 μM, 4 μM, 8 μM
Incubation Time:

48 h
Result:

Decreases cytoplasmic β-catenin levels (P < 0.05 at 4 and 8 μM) in a concentration-dependent manner.
Decreases nuclear β-catenin levels (P < 0.05 at 4 μM, P < 0.01 at 8 μM) in a concentration-dependent manner.

Cell Viability Assay^[3]

Cell Line:

MDA-MB-231 human breast adenocarcinoma cells
Concentration:

2, 4, 8, 16, 32, 64 and 128 μM
Incubation Time:

24 h; 48 h; 72 h
Result:

Did not significantly decrease cellular viability at any tested concentration or incubation time.
Reduced viability by only 27% at 128 μM for 72 h, with no significant anti-proliferative, cytostatic, or cytotoxic effects observed.

Cell Cytotoxicity Assay^[3]

Cell Line:

MDA-MB-231 human breast adenocarcinoma cells
Concentration:

2, 4, 8, 16, 32 and 64 μM
Incubation Time:

24 h
Result:

Showed no evident cytotoxicity at any tested concentration.
Exhibited no significant difference in viable cell counts compared to untreated controls.

Cell Invasion Assay^[3]

Cell Line:

MDA-MB-231 human breast adenocarcinoma cells
Concentration:

0.5, 1, 2, 4 and 8 μM
Incubation Time:

24 h
Result:

Dose-dependently reduced the number of invaded cells compared to untreated controls.
Showed statistically significant inhibition at concentrations of 1 μM (P < 0.05) and 2, 4, 8 μM (P < 0.01).

Western Blot Analysis^[3]

Cell Line:

MDA-MB-231 human breast adenocarcinoma cells
Concentration:

1, 2, 4 and 8 μM
Incubation Time:

24 h
Result:

Dose-dependently suppressed the expression of VEGF, p-VEGFR-2, VEGFR-2, p-EGFR, and EGFR, with statistically significant reductions at 4 and 8 μM (P < 0.05 or P < 0.01).
Significantly inhibited p-Akt expression at 4 and 8 μM (P < 0.05 or P < 0.01), while total Akt expression was unchanged.
Had no significant effect on p-ERK1/2 expression.

Cell Viability Assay^[4]

Cell Line:

ARPE-19 human retinal pigment epithelial cells, RF/6A choroidal endothelial cells
Concentration:

2, 4, 8, 16, 32, 64 and 128 µM
Incubation Time:

24 h; 48 h; 72 h
Result:

Reduced cell viability in a dose-dependent manner in both cell lines, but was non-cytotoxic at concentrations ≤32 µmol/L.
Inhibited viability by 13.2% in ARPE-19 cells and 17.6% in RF/6A cells at the highest concentration of 128 µmol/L for 72 h.

Cell Migration Assay^[4]

Cell Line:

RF/6A choroidal endothelial cells treated with ARPE-19 cell hypoxia-conditioned medium
Concentration:

8 and 32 µM
Incubation Time:

6 h; 12 h; 24 h
Result:

Had no significant effect on RF/6A cell migration under direct hypoxia.
Significantly restricted migration by 29.82% after 24 h of incubation with hypoxia-conditioned medium from ARPE-19 cells treated with DMBT.

ELISA Assay^[4]

Cell Line:

Hypoxic ARPE-19 human retinal pigment epithelial cells
Concentration:

8 and 32 µM
Incubation Time:

30 min pre-incubation; 24 h hypoxic incubation
Result:

Significantly inhibited CoCl₂-induced VEGF secretion, which increased VEGF levels to 1.7-fold of the control level.
Suppressed VEGF secretion more potently at 32 µmol/L than the ROS inhibitor NAC (5 mmol/L).

Western Blot Analysis^[4]

Cell Line:

Hypoxic ARPE-19 human retinal pigment epithelial cells
Concentration:

8 and 32 µM
Incubation Time:

30 min CoCl₂ pre-treatment; 24 h incubation
Result:

Significantly inhibited CoCl₂-stimulated activation of p-ERK1/2 (53.6% inhibition), intranuclear Nrf2 (50.2% inhibition), HO-1 (29.5% inhibition), and HIF-1α (55.9% inhibition) at 32 µmol/L.
Reduced accumulation of hypoxia-induced p-Akt, p-NF-κB, and HIF-1α at 32 µmol/L.

In Vivo

DMBT (1-10 mg/kg; p.o.; daily; 14 days) inhibits vasculogenic mimicry formation in MDA-MB-231 breast cancer xenografts in nude mice, resulting in smaller, thinner blood vessels compared to controls^[1].
DMBT (1-10 mg/kg; p.o.; daily; 14 days) significantly reduces lung metastasis of B16BL6 melanoma cells in C57BL/6J mice by approximately 55% and 57%, respectively^[2].
DMBT (1-10 mg/kg; p.o.; daily; 14 days) significantly inhibits lung metastasis of luciferase-expressing B16-F10 melanoma cells in Balb/c-nu mice, as measured by bioluminescence imaging and histology^[2].
DMBT (0.2-1 mmol/L; intravitreal; twice over 3 days) significantly reduces laser-induced choroidal neovascularization lesion area and retinal VEGF protein levels in male C57BL/6 mice^[4].

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

Animal Model:

Balb/c-nu (female, 6 weeks of age, tail vein injection of MDA-MB-231-luc-D3L2HN human breast adenocarcinoma cells)^[1]
Dosage:

1 mg/kg; 10 mg/kg
Administration:

p.o.; daily; 14 days
Result:

Inhibited vasculogenic mimicry formation, resulting in small, thin blood vessels compared to controls with thick, dense blood vessels including VM, mosaic vessels, and endothelial-dependent vessels.

Animal Model:

C57BL/6J mice (female, 4-6 weeks of age, syngeneic melanoma lung metastasis model via tail vein injection of 1.5×10⁵ B16BL6 melanoma cells)^[2]
Dosage:

1 mg/kg; 10 mg/kg
Administration:

p.o.; daily; 14 days
Result:

Reduced the number of lung nodules to 72.7, compared to the control group's 162.1 nodules.
Reduced the number of lung nodules to 69.3, compared to the control group's 162.1 nodules.
Achieved statistically significant inhibition relative to controls (P < 0.01).

Animal Model:

Balb/c-nu mice (female, 6 weeks of age, melanoma lung metastasis model via tail vein injection of 2×10⁵ B16-F10-luc-G5 luciferase-expressing melanoma cells)^[2]
Dosage:

1 mg/kg; 10 mg/kg
Administration:

p.o.; daily; 14 days
Result:

Significantly reduced bioluminescent signal intensity in mice on days 11 and 14 post-inoculation (P < 0.05).
Reduced lung-infiltrating tumor cells relative to controls, confirmed by H&E staining.

Animal Model:

C57BL/6 (male, 6 weeks of age, laser-induced choroidal neovascularization model)^[4]
Dosage:

0.2 mmol/L; 1 mmol/L
Administration:

intravitreal; twice over 3 days
Result:

Significantly reduced laser-induced CNV lesion area at 7 days compared to saline controls.
Reduced lesion area to a similar extent as the positive control 1 µmol/L Endostar (1 mmol/L dose).
Significantly reduced retinal VEGF protein levels relative to untreated CNV controls at 5 days post-photocoagulation (both doses).

Chemical Information

CAS No. 1260071-76-8
Masse moléculaire 670.61
Formule C₃₀H₃₈O₁₇
SMILES

O=C(C1=C(C(OC)=CC=C1)OC)OC[C@H]([C@H]([C@@H]([C@H]2O)O)O)O[C@@H]2O[C@H]3O[C@@H]([C@H]([C@@H]([C@H]3O)O)O)COC(C4=C(C(OC)=CC=C4)OC)=O
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

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

Pureté et documentation

Instruction de manipulation (2659 KB)

Références

[1]. Li S, et al. Inhibitory effects of compound DMBT on hypoxia-induced vasculogenic mimicry in human breast cancer. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2017 Dec;96:982-992. [Content Brief]

[2]. Tang L, et al. Inhibition of invasion and metastasis by DMBT, a novel trehalose derivative, through Akt/GSK-3β/β-catenin pathway in B16BL6 cells. Chem Biol Interact. 2014 Oct 5;222:7-17. [Content Brief]

[3]. Tang L, et al. Inhibition of angiogenesis and invasion by DMBT is mediated by downregulation of VEGF and MMP-9 through Akt pathway in MDA-MB-231 breast cancer cells. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2013 Jun;56:204-13. [Content Brief]

[4]. Chen S, et al. Anti-neovascularization effects of DMBT in age-related macular degeneration by inhibition of VEGF secretion through ROS-dependent signaling pathway. Molecular and cellular biochemistry. 2018 Nov;448(1-2):225-235. [Content Brief]

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DMBT

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Chemical Information

Pureté et documentation

Références

Calculators

Help & FAQs

DMBT Related Classifications

HY-183377 Related Classifications

Bioz