MMB-DTCs-1,3-diaminopropane-DTCs-MMB
MMB-DTCs-1,3-diaminopropane-DTCs-MMB is a Cuproptosis/Ferroptosis/Apoptosis inducer, and serves as the active metabolite of DMAPT-DTCs-1,3-diaminopropane-DTCs-DMAPT dimethanesulfonate (HY-182918). MMB-DTCs-1,3-diaminopropane-DTCs-MMB induces mitochondrial dysfunction, promotes reactive oxygen species (ROS) production, disrupts redox homeostasis, and triggers apoptosis, ferroptosis and cuproptosis in lung cancer cells. MMB-DTCs-1,3-diaminopropane-DTCs-MMB can be used in the research of lung cancer.
For research use only. We do not sell to patients.
- Formula: C35H46N2O6S4
- Molecular Weight:719.01
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (Compound 86) (72 h) potently inhibits the viability of NCI-H820 human lung adenocarcinoma cells, with an IC50 value of 0.46 μM[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (72 h) inhibits the viability of mouse embryonic fibroblast 3T3 cells with an IC50 of 1.70 μM, and exhibits selective cytotoxicity against lung cancer cells[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.2-1 μM; 7−10 days) inhibits colony formation of human lung adenocarcinoma cells NCI-H820 and A549 in a dose-dependent manner, and exhibits significantly stronger activity than MMB and CDDP at the concentration of 1 μM[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.2-1 μM; 24 h) dose-dependently inhibits the migration of human lung adenocarcinoma cells NCI-H820 and A549, and its activity at the concentration of 1 μM is significantly stronger than that of MMB and CDDP[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5 μM; 72 h) induces apoptosis, ferroptosis and cuproptosis in human lung adenocarcinoma cells NCI-H820 and A549 via reactive oxygen species generation, independent of autophagy or necrosis[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5-2 μM; 4-48 h) dose-dependently increases the levels of total reactive oxygen species, cytosolic reactive oxygen species, lipid reactive oxygen species, and mitochondrial reactive oxygen species in human lung adenocarcinoma cell lines NCI-H820 and A549[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5 μM; 48 h) exerts inhibitory effects on human lung adenocarcinoma cells NCI-H820 and A549 mainly by inducing mitochondrial reactive oxygen species[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5 μM; 48 h) increases mitochondrial reactive oxygen species levels, thereby promoting the production of cytoplasmic and lipid reactive oxygen species in human lung adenocarcinoma cells NCI-H820 and A549[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5-2 μM; 48 h) induces apoptosis in human lung adenocarcinoma cell lines NCI-H820 and A549 in a dose-dependent manner after 48 h of treatment[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5-2 μM; 48 h) dose-dependently regulates the expression of apoptosis-related proteins (upregulates Bax, downregulates Bcl-2 and Mcl-1) in human lung adenocarcinoma cell lines NCI-H820 and A549 after a 48 h treatment[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5-2 μM; 48 h) dose-dependently regulates the expression of ferroptosis-related proteins in human lung adenocarcinoma cells NCI-H820 and A549 (downregulates GPX4 and SLC7A11, upregulates ACSL4) with a treatment duration of 48 h[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5-2 μM; 48 h) downregulates the expression of cuproptosis-related FDX1 and DLAT proteins in human lung adenocarcinoma cell lines NCI-H820 and A549 in a dose-dependent manner after 48 h of treatment[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5 μM; 48 h, 72 h) induces ferroptosis in human lung adenocarcinoma cells NCI-H820 and A549, which is evidenced by lipid ROS accumulation and its synergistic activity with ferroptosis inducers[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5-2 μM; 48 h) induces mitochondrial membrane depolarization and dysfunction in a dose-dependent manner in human lung adenocarcinoma cell lines NCI-H820 and A549[1].
MMB-DTCs-1,3-diaminopropane-DTCs-MMB (0.5 μM; 72 h) exhibits synergistic antiproliferative effects with the cuproptosis inducer BSO in NCI-H820 and A549 human lung adenocarcinoma cells after 72 h of treatment[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:human lung adenocarcinoma NCI-H820 and A549 cells
-
Concentration:0.2, 0.5 and 1 μM
-
Incubation Time:24 h
-
Result:Inhibited migration capacity in both NCI-H820 and A549 cells in a dose-dependent manner.
At 1 μM, exhibited a more pronounced inhibitory effect on cell migration than the parent compound MMB and positive control CDDP.
-
Cell Line:human lung adenocarcinoma NCI-H820 and A549 cells
-
Concentration:0.5 μM
-
Incubation Time:72 h
-
Result:The inhibitory effect was partially rescued by apoptosis inhibitor Z-VAD-FMK, ferroptosis inhibitors Liproxstatin-1 and Ferrostatin-1, and cuproptosis inhibitor TTM.
The effect was unaffected by autophagy inhibitor 3-methyladenine or necrosis inhibitor Necrostatin-1.
The effect was completely rescued by ROS inhibitor NAC.
-
Cell Line:human lung adenocarcinoma NCI-H820 and A549 cells
-
Concentration:0.5, 1 and 2 μM
-
Incubation Time:48 h
-
Result:Increased the percentage of apoptotic cells in a dose-dependent manner in both NCI-H820 and A549 cells.
-
Cell Line:human lung adenocarcinoma NCI-H820 and A549 cells
-
Concentration:0.5, 1 and 2 μM
-
Incubation Time:48 h
-
Result:Upregulated pro-apoptotic Bax protein levels in both cell lines.
Significantly downregulated anti-apoptotic Bcl-2 and Mcl-1 protein levels in both cell lines.\nSignificantly suppressed GPX4 and SLC7A11 protein expression in both cell lines.
Upregulated ACSL4 protein expression in both cell lines.\nSignificantly decreased FDX1 and DLAT protein levels in a dose-dependent manner in both cell lines.
Chemical Information
-
Molecular Weight 719.01
-
Formula C35H46N2O6S4
-
SMILES
O=C1O[C@@H]2[C@H]3[C@@](C)(CC/C=C(CC[C@H]2C1=C)/CSC(NCCCNC(SC/C4=C/CC[C@@]5(C)O[C@H]5[C@H]([C@H]6CC4)OC(C6=C)=O)=S)=S)O3
-
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)