MPT0B098

MPT0B098 is a microtubule inhibitor with a K_i of 0.8 μM and an IC₅₀ of 0.8 μM. MPT0B098 inhibits tubulin polymerization, blocks HuR nuclear-cytoplasmic translocation to decrease HIF-1α mRNA stability, suppresses HIF-1α, TGF-β/Smad, JAK2/STAT3 and FAK/actin cytoskeleton signaling pathways, upregulates SOCS3 to reinforce the inhibition of JAK2/STAT3 cascade, and induces apoptosis. MPT0B098 can be used for research on multiple malignancies including head and neck squamous cell carcinoma and human non-small cell lung cancer^[1][2][3]. In Vitro:MPT0B098 inhibits proliferation of multiple human cancer cell lines, including H460, A549, H1299, HONE-1, PC-3, KB, HT29 and MKN-45 cells, with IC₅₀ values of 78-150 nM, while HUVEC cells are less sensitive to MPT0B098 with an IC₅₀ of 510 nM^[1].
MPT0B098 inhibits tubulin polymerization with a K_i of 0.8 μM, and with an IC₅₀ of 0.8 μM^[1].
MPT0B098 (0-1000 nM; 24 h) induces G₂/M phase arrest and apoptosis in A549 cells by increasing cyclin B1 and MPM2, changing Cdc25C and Cdc2 phosphorylation, increasing TUNEL-positive cells, promoting Bcl-2 phosphorylation and inducing PARP cleavage^[1].
MPT0B098 (0.2-0.5 μM; 16 h) inhibits VEGF-induced capillary-like tube formation in HUVECs^[1].
MPT0B098 (0.25 μM; 24 h) inhibits VEGF-induced HUVEC migration without reducing HUVEC viability^[1].
MPT0B098 (0-2 μM; 18 h) concentration-dependently reduces intracellular VEGF protein and secreted VEGF level in HUVECs; 0-0.9 μM MPT0B098 (18 h) suppresses hypoxia-induced VEGF secretion from A549 cells^[1].
MPT0B098 (0-0.9 μM; 18 h) decreases HIF-1α protein and produced stronger growth inhibition and higher caspase-3 activity under hypoxia, destabilizes HIF-1α mRNA, and reduces HuR nuclear-to-cytoplasmic translocation in A549 cells^[1].
MPT0B098 (111-444 nM; 72 h) suppresses proliferation of OEC-M1 cells under normoxia and hypoxia, with IC₅₀ of 222 nM under normoxia and IC₅₀ of 265 nM under hypoxia^[2].
MPT0B098 (111-444 nM; 18 h) dose-dependently downregulates HIF-1α protein, blocks hypoxia-triggered F-actin cytoskeleton rearrangement and reduces hypoxia-induced FAK phosphorylation without changing total FAK protein in hypoxic OEC-M1 cells^[2].
MPT0B098 (111-444 nM; 18-36 h) suppresses EMT transcription factors Twist and SNAI2/Slug in hypoxic OEC-M1 cells^[2].
MPT0B098 (111-444 nM; 36 h) downregulates vimentin and N-cadherin while partially restoring E-cadherin, suppresses TGF-β protein expression and Smad2/3 phosphorylation, and reduces TGF-β1 and TGF-β2 mRNA levels in hypoxic OEC-M1 cells^[2].
MPT0B098 (111-444 nM; 18 h pretreatment + TGF-β 18 h co-stimulation) reverses TGF-β-triggered Smad2/3 phosphorylation in hypoxic OEC-M1 cells^[2].
MPT0B098 (111 nM; 48 h) reverses hypoxia-induced mesenchymal morphological transformation of OEC-M1 cells^[2].
MPT0B098 (111 nM; 4-18 h) inhibits hypoxia-induced OEC-M1 cell migration in a time-dependent manner without obvious cytotoxicity^[2].
MPT0B098 (0.12-0.5 μM; 72 h) concentration-dependently suppresses viability of multiple OSCC cell lines (OEC-M1, HSC-3, SCC-25, Tu183, DOK, YD-15) with IC₅₀ of 0.14-0.45 μM, while normal HOK cells exhibit weak sensitivity with IC₅₀ of 6.3 μM^[3].
MPT0B098 (0.25 μM; 0-60 min) induces time-dependent tubulin depolymerization in OEC-M1 and HSC-3 cells, and microtubule network can partially recover after drug washout for 60 min^[3].
MPT0B098 (0.25, 0.5 μM; 12 h) triggers dose-dependent G₂/M cell cycle arrest and Annexin V-positive early apoptosis in OEC-M1 cells^[3].
MPT0B098 (0.12-1 μM; 24 h) elevates cleaved caspase-3 and PARP, and downregulates anti-apoptotic proteins Bcl-2, Mcl-1, Pim-1, Survivin in OSCC cells^[3].
MPT0B098 (0.25 μM; 15-240 min) gradually reduces phosphorylation and total protein levels of JAK2, TYK2 and STAT3 without altering STAT3 mRNA expression^[3].
MPT0B098 (0.25 μM; 0-60 min) selectively upregulates SOCS2 and SOCS3 protein levels rather than PIAS1/3 and SOCS1 in OSCC cells^[3].
MPT0B098 (0.25 μM) combined with 5 μM Cisplatin (HY-17394) or 5 μM 5-FU (HY-90006) produces markedly stronger proliferation inhibition and caspase-3 activation effects in OEC-M1 cells compared with single drug treatment^[3].
In Vivo:MPT0B098 (25, 50 mg/kg; i.p.; once daily; for 5 consecutive days) suppresses tumor growth and reduces microvessel density in A549 human non-small cell lung cancer xenograft nude mouse model^[1].