Molecular Weight(MW): 331.41
Marimastat (BB-2516) is a broad spectrum matrix metalloprotease (MMP) inhibitor for MMP-9, MMP-1, MMP-2, MMP-14 and MMP-7 with IC50 of 3 nM, 5 nM, 6 nM, 9 nM and 13 nM, respectively. Phase 3.
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(E, F) Uev1A mediates negative feedback of NF-κB signaling pathway is dependent on TACE activity. Forty-eight hours after transfection, the cells were pre-treated with BB-2516 (20 μM) for 1 h, followed by TNFα (40 ng/ml) treatment for 2 h. Cell was fixed and stained with antibodies against HA and p65. The same cells were also stained with DAPI to reveal nuclei. White arrows indicate UEV1A-overexpressed cells. (F) Quantitative analysis of the experiments shown in (E). Percentage of cells displaying nuclear p65 is shown for UEV1A- overexpressed or vector-transfected cells. Each sample contains about 1000 cells. The significance of differences was assessed by two-tailed Student's test (***P < 0.001).
Cell Signal, 2018, 42:155-164. Marimastat (BB-2516) purchased from Selleck.
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|Description||Marimastat (BB-2516) is a broad spectrum matrix metalloprotease (MMP) inhibitor for MMP-9, MMP-1, MMP-2, MMP-14 and MMP-7 with IC50 of 3 nM, 5 nM, 6 nM, 9 nM and 13 nM, respectively. Phase 3.|
Marimastat (100 nM) signiﬁcantly inhibits the expression of MMP14 in U251, U87, GBM39, and GBM43 tumor cells. Marimastat speciﬁcally inhibits the growth of glioma cells and has no effect on normal human astrocytes (NHA). Marimastat early down-regulates the expression of Notch target genes, such as Hes1 and Hes5.
|In vivo||In an orthotopic oral squamous cell carcinoma implantation model, marimastat (150 mg/kg/day, p.o.) administered by an osmotic pump significantly suppresses the cervical lymph node metastasis and activation of MMP-2, and has a significantly better survival than control group. Marimastat reduces MMP hyperactivity of polycystic human and rat cholangiocytes and blocks the cystic expansion of PCK cholangiocytes. Chronic treatment of 8-week-old PCK rats with marimastat inhibits hepatic cystogenesis and ﬁbrosis.|
Inhibitor kinetics:Recombinant human MMP2 is activated with 1 mM of 4-aminophenylmercuric acetate for 1 hour at 37°C. Rates of cleavage of 1 μM of the quenched fluorescent MMP substrate (7-methoxycoumarin-4-yl)acetyl-Pro-Leu-Gly-Leu-[3-(2,4-dinitrophenyl)-L-2,3-diaminoproprionyl]-Ala-Arg-NH2 are measured in 96-well fluorimetry plates at 37°C 100 mM Tris-HCl (pH 7.5), 100 mM NaCl, 10 mM CaCl2, 0.05% Brij 35 using a 320 nm excitation filter and a 405 nm emission filter in the presence of increasing inhibitor concentrations. Curve-fitting and IC50 calculations are done using GraphPad Prism 5.0 Software.
-  Rasmussen HS, et al. Pharmacol Ther. 1997, 75(1), 69-75.
-  auf dem Keller U, et al. Cancer Res. 2010, 70(19), 7562-7569.
-  Ulasov I, et al. Cancer Med.?013, 2(4), 457-467.
|In vitro||DMSO||54 mg/mL (162.94 mM)|
|Ethanol||7 mg/mL warmed (21.12 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
For best results, use promptly after mixing.
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