MMP-9-IN-14
MMP-9-IN-14 is a MMP-9 inhibitor (IC50 = 34.46 μM). MMP-9-IN-14 induces G1-phase cell cycle arrest and caspase-dependent apoptosis in cancer cells. MMP-9-IN-14 promotes the accumulation of phosphorylated γH2AX. MMP-9-IN-14 inhibits the migration and invasion of cancer cells, and downregulates the expressions of MMP-2, MMP-9 and hTERT in cancer cells. MMP-9-IN-14 inhibits tumor growth and angiogenic spread in animal models. MMP-9-IN-14 can be used for the research of cancers such as lung adenocarcinoma, cervical cancer and colorectal cancer.
For research use only. We do not sell to patients.
- Formula: C25H18Cl2N2O2S
- Molecular Weight:481.39
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Caspase Isoforms
More
Biological Activity
|
MMP-9 34.46 μM (IC50) |
Caspase 3 |
Caspase-7 |
MMP-2 |
MMP-9-IN-14 (Compound 24) (0.39-100 μM; 30 min, 37°C) directly inhibits the enzymatic activity of recombinant human MMP-9, with an IC50 of 34.46 μM[1].
MMP-9-IN-14 (0-50 μM; 72 h) inhibits the viability of various cell lines (A-549, H-226, H-460, HCT-116, Hep G2, HeLa, HaCaT, MRC-5), with IC50 values of 2.23, 2.34, 5.49, 4.95, 51.41, 2.75, 8.89, and 18.47 μM, respectively[1].
MMP-9-IN-14 (2.23 μM; 24-72 h) induces G1-phase cell cycle arrest in A-549 cells[1].
MMP-9-IN-14 (2.23 μM; 24-72 h) induces caspase-dependent apoptosis in A-549 cells[1].
MMP-9-IN-14 (2.23 μM; 24-72 h) increases the number of γH2AX-positive cells and induces the accumulation of DNA damage in A-549 cells[1].
Compound 24 (5-30 μM; 0-24 h) inhibits the migration and invasion of A-549 cancer cells[1].
Compound 24 (15-30 μM; 48 h) downregulates the expression of metastasis-related genes (MMP-2, MMP-9) and hTERT in A-549 cells, and potently inhibits TGF-β1-induced MMP expression[1].
Compound 24 (10-50 μM; 72 h) inhibits the proliferation of A-549 3D spheroids and exhibits anti-metastatic activity in physiologically relevant 3D models[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:A-549 cells
-
Concentration:2.23 μM
-
Incubation Time:24 h, 48 h, 72 h
-
Result:Caused a significant decrease in the S-phase population after 24 h treatment. Induced cell accumulation in the G1 phase with a reduction in G2/M content by 48 h treatment.
Induced a marked G1-phase arrest, with ~65% of cells in G1 phase and concurrent reductions in S and G2/M fractions at 72 h treatment.
-
Cell Line:A-549,H-226,H-460,HCT-116,Hep G2,HeLa,HaCaT , MRC-5 cells
-
Concentration:0-50 μM
-
Incubation Time:72 h
-
Result:Inhibited the viability of various cell lines (A-549, H-226, H-460, HCT-116, Hep G2, HeLa, HaCaT, MRC-5), with IC50 values of 2.23, 2.34, 5.49, 4.95, 51.41, 2.75, 8.89, and 18.47, respectively.
-
Cell Line:A-549 cells
-
Concentration:2.23 μM
-
Incubation Time:24 h, 48 h, 72 h
-
Result:Caused a increase in apoptosis, with ~10% early apoptotic and ~8% late apoptotic cells after 24 h treatment.
Increased early apoptosis to ~11% and late apoptosis to ~15%, with ~70% cell viability remaining at 48 h treatment.
Increased caspase-3/7 activity by ~5-fold at 24 h, ~5-6-fold at 48 h, and ~7-fold at 72 h compared to controls.
-
Cell Line:A-549 cells
-
Concentration:5, 10, 15 μM
-
Incubation Time:0 h, 6 h, 12 h,
18 h, 24 h -
Result:Significantly and in a concentration-dependent manner inhibited cell migration and delayed wound closure.
-
Cell Line:A-549 cells
-
Concentration:15, 30 μM
-
Incubation Time:24 h
-
Result:Reduced the number of invading A-549 cells to ~65% of control levels at 15 μM. Reduced the number of invading cells to ~25% of control levelsat 30 μM.
-
Cell Line:A-549 cells (with or without TGF-β1 stimulation)
-
Concentration:15, 30 μM
-
Incubation Time:48 h
-
Result:Significantly suppressed TGF-β1-induced MMP-2 and MMP-9 mRNA expression: at 15 μM, MMP-2 expression was reduced by ~60% and MMP-9 by ~70% ; at 30 μM, both MMP-2 and MMP-9 mRNA levels were reduced to near baseline.
Downregulated hTERT expression: at 15 μM, hTERT expression was reduced by ~50%, and at 30 μM, was almost undetectable.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:A-549 Xenotransplantation chorioallantoic membrane (CAM) model[1]
-
Dosage:25 μM; 50 μM
-
Administration:topical; single administration
-
Result:Reduced median tumour area. Showed weaker, less homogeneous CellTracker Green signals in treated tumours, indicating reduced tumour cell viability/density.
Revealed a near-complete absence of disseminated fluorescent tumour cells in distal CAM regions, compared to frequent vasculotropic spread in vehicle controls.
Chemical Information
-
Molecular Weight 481.39
-
Formula C25H18Cl2N2O2S
-
SMILES
O=C(C1=CC=C(Cl)C=C1)CSC2=NC(C3=CC=C(Cl)C=C3)=CN2C4=CC=C(C(C)=O)C=C4
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)