MMPP

MMPP is an orally active inhibitor of STAT3 and VEGFR2, as well as an activator of PPARγ. MMPP blocks the VEGFR2/AKT/ERK/NF-κB signaling pathway to inhibit angiogenesis. MMPP inhibits ferroptosis and inflammation, and alleviates sepsis-induced myocardial injury. MMPP induces G1-phase cell cycle arrest and apoptosis, and inhibits the growth of non-small cell lung cancer (NSCLC) and solid tumors. MMPP promotes adipogenesis and glucose uptake. MMPP can be used in research related to NSCLC, type 2 diabetes and myocardial injury^[1][2][3][4]. In Vitro:MMPP inhibits the viability of NCI-H460 non-small cell lung cancer cells, with an IC₅₀ value of 12.3 μg/mL^[1].
MMPP (5-20 μg/mL; 24 h) inhibits the viability of various cancer cell lines, including the NCI-H460 non-small cell lung cancer cell line, in a concentration-dependent manner (IC₅₀ = 11.99 μg/mL), but exerts no effect on the viability of non-cancerous LL-24 lung epithelial cells^[1].
MMPP (5-15 μg/mL; 24 h) induces apoptosis and G1-phase cell cycle arrest in NCI-H460 and A549 non-small cell lung cancer cells in a concentration-dependent manner^[1].
MMPP (10 μg/mL; 24 h) significantly inhibits VEGFA-induced migration of human umbilical vein endothelial cells (HUVECs) in scratch wound healing assays^[2].
MMPP (10 μg/mL) significantly inhibits VEGFA-induced invasion of HUVECs in Transwell assays^[2].
MMPP (10 μg/mL; 16 h) significantly inhibits VEGFA-induced angiogenesis in HUVECs^[2].
MMPP (10 μg/mL; 1.5 h) inhibits the VEGFR2/AKT/ERK signaling pathway in HUVECs by reducing the phosphorylation levels of VEGFR2, AKT and ERK^[2].
MMPP (10 μg/mL; 2 h) inhibits VEGFA-induced nuclear translocation of NF-κB p65 in HUVECs^[2].
MMPP (10 μg/mL; 25 h) significantly downregulates the mRNA expression of VEGFA, VEGFR2, MMP2 and MMP9 in HUVECs^[2].
MMPP (15 μg/mL; 24 h) upregulates the transcriptional activity of PPARγ in HEK 293T cells, and synergistically enhances this activity with Rosiglitazone (HY-17386)^[3].
MMPP (7.5-15 μg/mL; 2-8 days) dose-dependently promotes lipid accumulation in differentiated 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) increases glucose uptake in mature 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) enhances the expression of adipogenesis-related genes and reduces Il6 mRNA levels in mature 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) enhances the expression of adipogenesis-related proteins in fully differentiated 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) upregulates the expression of C/ebpb mRNA in early-stage (day 2) 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) upregulates the expression of C/EBPβ protein in early-stage (day 2) 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 1 h) enhances the phosphorylation levels of AKT, GSK3 and AMPKα in 3T3-L1 MBX cells co-treated with MDI for 1 h^[3].
MMPP (5-100 mg/L; 10 min) potently scavenges ABTS•⁺ in a cell-free system, and achieves nearly complete inhibition at a concentration of 100 mg/L^[4].
MMPP (40-200 mg/L) scavenges •OH in a cell-free system, with a scavenging rate of 48.14% at 200 mg/L^[4].
MMPP (100-1000 mg/L) scavenges O₂•^- in a cell-free system, with a scavenging rate of 61.24% at 1000 mg/L^[4].
MMPP (100-500 mg/L; 1 h) chelates Fe²⁺ in a cell-free system, with a chelating efficiency of up to 51.0% at the concentration of 500 mg/L^[4].
MMPP (100 μg/mL; 12.5 h) restores the viability of H9c2 cells treated with LPS (HY-D1056) after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces LDH release in LPS-treated neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces the Ptgs2 mRNA expression level in neonatal rat ventricular myocytes treated with LPS after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces the PTGS2 protein expression level in LPS-treated neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) inhibits LPS-induced release of cytochrome c (Cyt c) from mitochondria to cytoplasm in neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces the MDA level in neonatal rat ventricular myocytes treated with LPS after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) restores SOD levels in LPS-treated neonatal rat ventricular myocytes after 12 hours of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces intracellular ROS accumulation in lipopolysaccharide-treated neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces lipid ROS accumulation in neonatal rat ventricular myocytes treated with LPS after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) maintains the mitochondrial membrane potential of lipopolysaccharide-treated neonatal rat ventricular cardiomyocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) maintains mitochondrial function in LPS-treated neonatal rat ventricular cardiomyocytes after 12 h of incubation^[4]. In Vivo:MMPP (2.5-5 mg/kg; i.p., p.o.; 2-3 times per week; for 3 consecutive weeks) dose-dependently inhibits the growth of NCI-H460 xenograft tumors in BALB/c nude mice^[1].
MMPP (5 mg/kg; p.o.; three times per week; for 1 month) significantly inhibits tumor growth in patient-derived NSCLC xenograft models in immunodeficient mice by suppressing STAT3 activity, with no observed toxicity^[1].
MMPP (5 mg/kg; i.p.; twice weekly; for 3 consecutive weeks) inhibits tumor growth and STAT3 activity in BALB/c nude mice bearing A549 non-small cell lung cancer xenografts^[1].
MMPP (5 mg/kg; i.p.; twice weekly; for 3 consecutive weeks) inhibits tumor growth and STAT3 activity in BALB/c nude mice bearing HCT116 colon cancer xenografts^[1].
MMPP (5 mg/kg; i.p.; twice a week; for 3 consecutive weeks) inhibits tumor growth and STAT3 activity in BALB/c nude mice bearing PA-1 ovarian cancer xenografts^[1].
MMPP (1 mg; intravenous injection; single dose) inhibits ferroptosis via iron chelation, alleviates oxidative stress, reduces the production of pro-inflammatory cytokines, attenuates sepsis-induced myocardial injury, improves the 14-day survival rate of C57BL/6J mice, and restores key cardiac function parameters including ejection fraction and fractional shortening^[4].