MMI-166
MMI-166 is an orally active selective matrix metalloproteinase (MMP) inhibitor (MMP-2 (IC50 = 2 nM), MMP-9 (IC50 = 53 nM)). MMI-166 can prevent tumor invasion, metastasis and angiogenic, and promotes apoptosis. MMI-166 dose not only directly inhibits the enzymatic activity of MMP-2 and MMP-9 but also downregulates their protein synthesis and expression levels at the post-transcriptional level. MMI-166 can be used in research on colon cancer, head and neck squamous cell carcinoma, microglioma, lung cancer, and pancreatic cancer.
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- No. CAS: 193809-84-6
- Fòrmula: C24H20N6O4S
- Peso molecular:488.52
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Actividad biológica
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Chemical Information
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Help & FAQs
Actividad biológica
Descripciòn
IC50 & Target
[1]|
MMP-2 2 nM (IC50) |
MMP-9 53 nM (IC50) |
In Vitro
MMI-166 (0-100 μM; 3 days) exhibits no significant cytotoxicity in YCU-MS861 and YCU-H891 cells[2].
MMI-166 (0-100 μM; 24 h) reduces MMP-2 and MMP-9 gelatinase activity in a dose-dependent manner in YCU-MS861 and YCU-H891 cells[2].
MMI-166 (0-10 μM; 24 h) significantly reduces MMP-2 and MMP-9 protein expression levels but does not affect mRNA levels in YCU-MS861 and YCU-H891 cells[2].
MMI-166 (1-100 μM; 24 h) inhibits cell invasion activity in a dose-dependent manner in YCU-MS861 and YCU-H891 cells[2].
MMI-166 (0.1-100 μM; 24 h) reduces MMP-2 and MMP-9 gelatinase activity in a dose-dependent manner in T98G, U87MG, and ONS12 glioma cells[3].
MMI-166 (0.1-100 μM; 23 h) significantly inhibits the invasive ability of tumor cells in T98G, U87MG, and ONS12 glioma cells[3].
MMI-166 (0.1-100 μM; 10 days) significantly inhibits glioma cell-induced angiogenesis in human umbilical vein endothelial cells (HUVECs) co-cultured with T98G, U87MG, and ONS12 cells[3].
MMI-166 (0.1-100 μM; 24-48 h) does not affect the proliferation of T98G, U87MG, and ONS12 glioma cells[3].
MMI-166 (4-16 μM; 18 h) inhibits cell invasion in a dose-dependent manner in Ma44-3 human lung cancer cells[4].
MMI-166 (50-100 μg/mL; 24 h) alters cell morphology in human pancreatic cancer SW1990 cells; it induces apoptosis and inhibits MMP-2 and MMP-9 activities in a dose-dependent manner, and downregulates the mRNA and protein expression levels of MMP-2, MMP-9, and c-myc, but has no significant effect on survivin mRNA and protein expression[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:T98G, U87MG, ONS12
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Concentration:0.1 μM, 1 μM, 10 μM, 100 μM
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Incubation Time:23 h
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Result:Significantly suppressed tumor cell invasion.
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Cell Line:T98G, U87MG, ONS12
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Concentration:0.1 μM, 1 μM, 10 μM, 100 μM
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Incubation Time:24 h, 48 h
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Result:Did not affect the proliferative capacity of tumor cells.
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Cell Line:Ma44-3
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Concentration:4 μM, 16 μM
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Incubation Time:18 h
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Result:Dose-dependently inhibited invasion through Matrigel.
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Cell Line:SW1990
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Concentration:50 μg/mL, 100 μg/mL
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Incubation Time:24 h
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Result:Significantly increased the number of apoptotic cells and the apoptotic rate in a dose-dependent manner.
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Cell Line:SW1990
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Concentration:50 μg/mL, 100 μg/mL
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Incubation Time:24 h
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Result:Significantly downregulated the relative mRNA expressions of MMP-2, MMP-9, and c-myc in the treated groups, while the relative mRNA expression of survivin did not differ significantly.
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Cell Line:SW1990
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Concentration:50 μg/mL, 100 μg/mL
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Incubation Time:24 h
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Result:Significantly downregulated the relative protein expressions of MMP-2, MMP-9, and c-myc in the treated groups, while the relative protein expression of survivin did not differ significantly.
In Vivo
MMI-166 (100 mg/kg; p.o.; 5 times/week; 27-day treatment) significantly inhibited local tumor growth and volume and reduced MMP-2 and MMP-9 protein expression in vivo in a female athymic nude mouse subcutaneous xenograft model. MMI-166 inhibited angiogenesis and promoted apoptosis in tumor tissues[2].
MMI-166 (100 mg/kg; p.o.; 5 times/week; 21-day treatment) significantly inhibited intracranial tumor growth and volume and reduced the number of tumor-induced microvessels in a female athymic mouse orthotopic glioma model[3].
MMI-166 (100 mg/kg and 200 mg/kg; i.g.; 5 times/week; 21-day treatment) significantly inhibited subcutaneous tumor growth in a dose-dependent manner in a male SCID mouse subcutaneous xenograft model, with no apparent toxicity observed[4].
MMI-166 (200 mg/kg; p.o.; 5 times/week; treatment for 13 days or until death) significantly inhibited lymph node metastasis and in situ MMP activity within metastatic foci, and significantly prolonged the median survival time of mice in a male SCID mouse orthotopic lung cancer model[4].
MMI-166 (200 mg/kg; p.o.; once daily; 28-day treatment) inhibits tumor growth in a human pancreatic cancer SW1990 nude mouse xenograft model. MMI-166 increases apoptosis in tumor tissues. MMI-166 downregulates the expression of MMP-2, MMP-9, c-myc, and survivin in tumor tissues[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nu/nu mice (male, 5 weeks old) were orthotopically implanted with human colon cancer TK-4 tissue (200 mg) sutured on the cecal surface[1]
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Dosage:200 mg/kg
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Administration:p.o.; 6 days/week; 5 weeks
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Result:Decreased the expression levels of active MMP-2 in tumors.
Suppressed the incidence of liver metastasis and reduced the number of metastatic foci.
Reduced the invasive growth features of cancer cells.
Significantly decreased tumor microvessel density (MVD).
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Animal Model:BALB/c nu/nu mice (female, 5 weeks old) were subcutaneously injected with 5 × 105 YCU-MS861 or YCU-H891 cells into the left flanks[2]
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Dosage:100 mg/kg
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Administration:p.o.; 5 times/week; 27 days
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Result:Significantly inhibited in vivo tumor growth and volume increase.
Lowered the protein expression levels of MMP-2 and MMP-9 in xenografts.
Reduced tumor microvessel density (CD34-positive).
Decreased the cell proliferation index (Ki-67-positive).
Increased tumor cell apoptosis (more TUNEL-positive cells).
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Animal Model:BALB/c nu/nu mice (female, 6-8 weeks old) were intracerebrally injected with 1 × 105 T98G cells for orthotopic implantation[3]
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Dosage:100 mg/kg
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Administration:p.o.; 5 times/week; 21 days
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Result:Significantly suppressed tumor growth in the brain and reduced tumor volume.
Inhibited tumor-induced angiogenesis and reduced the number of microvessels (decreased VWF expression).
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Animal Model:SCID mice (male, 8 weeks old) were subcutaneously injected with 2 × 105 Ma44-3 cells into the right groin[4]
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Dosage:100 mg/kg, 200 mg/kg
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Administration:i.g.; 5 times/week; 21 days
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Result:Significantly suppressed the growth of subcutaneous tumors in a dose-dependent manner.
Caused no obvious body weight loss or toxicity.
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Animal Model:SCID mice (male, 6-8 weeks old) were orthotopically injected with 5 × 104 Ma44-3 cells and Matrigel into the left lung[4]
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Dosage:200 mg/kg
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Administration:p.o.; 5 times/week; treatment for 13 days or until death
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Result:Significantly inhibited the weight and total metastatic area of mediastinal lymph node metastasis.
Inhibited in situ MMP gelatinolytic activity in mediastinal metastatic lesions.
Did not significantly suppress the volume of the primary implanted lung tumor.
Significantly prolonged the median survival time of the mice.
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Animal Model:BALB/c nude mice (male, 4-5-week-old, 18-22 g) were subcutaneously inoculated into the back with 1 × 107 SW1990 cells to establish the xenograft model[5]
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Dosage:200 mg/kg
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Administration:p.o.; daily; for 28 days
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Result:Inhibited tumor growth.
Induced apoptosis in tumor tissue cells.
Downregulated the expression of MMP-2, MMP-9, c-myc, and survivin, but had no significant effect on the expression of p53, bax, bcl-2, caspase-1, and Fas.
Chemical Information
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No. CAS 193809-84-6
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Peso molecular 488.52
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Fòrmula C24H20N6O4S
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SMILES
O=S(N[C@@H](C(O)=O)CC1=CNC2=CC=CC=C12)(C3=CC=C(C4=NN(C5=CC=CC=C5)N=N4)C=C3)=O
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. Oba K, et al. Prevention of liver metastasis of human colon cancer by selective matrix metalloproteinase inhibitor MMI-166. Cancer Lett. 2002 Jan 10;175(1):45-51. [Content Brief]
[2]. Katori H,et al. Reduction of in vivo tumor growth by MMI-166, a selective matrix metalloproteinase inhibitor, through inhibition of tumor angiogenesis in squamous cell carcinoma cell lines of head and neck. Cancer Lett. 2002 Apr 25;178(2):151-9. [Content Brief]
[3]. Nakabayashi H, et al. Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells. BMC Cancer. 2010 Jun 29;10:339. [Content Brief]
[4]. Fujino H, et al. Matrix metalloproteinase inhibitor MMI-166 inhibits lymphogenous metastasis in an orthotopically implanted model of lung cancer. Mol Cancer Ther. 2005 Sep;4(9):1409-16. [Content Brief]
[5]. Gao CC, et al. MMI-166, a selective matrix metalloproteinase inhibitor, promotes apoptosis in human pancreatic cancer. Med Oncol. 2015 Jan;32(1):418. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MMI-166 Related Classifications
HY-183408 Related Classifications
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