TM-2-51

TM-2-51 (72 h) potently reduces the viability of U2OS and 143B osteosarcoma cells in a concentration-dependent manner^[1].
TM-2-51 (6 days) significantly inhibits the colony-forming ability of U2OS and 143B osteosarcoma cells^[1].
TM-2-51 (24 h) significantly reduces the proliferation rate of U2OS and 143B osteosarcoma cells^[1].
TM-2-51 (24 h) potently inhibits the migration and invasion abilities of U2OS and 143B osteosarcoma cells^[1].
TM-2-51 increases the expression levels of HDAC8 and TP53 proteins above the DMSO baseline in U2OS and 143B osteosarcoma cells, while reduces the expression levels of p-STAT3 and p-ERK proteins below the DMSO baseline, without altering the expression levels of total STAT3 and ERK^[1].
TM-2-51 (13-50 μM; 48-96 h) protects the human monocytic cell line THP-1 cells against LeTx-induced cytotoxicity, with its cytoprotective effect peaking at 25 μM and enabling continuous cell proliferation within 96 h^[2].
TM-2-51 (25 μM; 24-72 h) enhances the phosphorylation level of AKT at Ser-473 in LeTx-treated human monocytic THP-1 cells at a concentration of 25 μM^[2].
TM-2-51 (25 μM) increases the level of histone H3K27 trimethylation in LeTx-treated human monocytic THP-1 cells^[2].
TM-2-51 (10-80 μM; 24-72 h) selectively inhibits the proliferation of human neuroblastoma SH-SY5Y cells: at a concentration of 80 μM for 72 h, the proliferation inhibition rate is approximately 22%, while it exerts no effect on human neuroblastoma BE (2)-C cells^[4].
TM-2-51 (80 μM; 48 h) enhances the expression of p53 and p21 proteins in SH-SY5Y human neuroblastoma cells when treated at a concentration of 80 μM for 48 h, but exerts no effect on the expression of p53 and p21 in BE (2)-C human neuroblastoma cells^[4].
TM-2-51 (48 h) increases the proportion of U2OS and 143B osteosarcoma cells in the G₁ phase of the cell cycle and induces cell cycle arrest^[1].
TM-2-51 (25 μM; 48-72 h) inhibits LeTx-induced G₀-G₁ cell cycle arrest in the human monocytic cell line THP-1, and restores the cell cycle to a near-normal progression at 72 h^[2].
TM-2-51 potently inhibits α-glucosidase with an IC₅₀ of 171.21 μM^[3].
TM-2-51 exhibits no cytotoxicity against 3T3 mouse fibroblasts^[3].
TM-2-51 (2-20 μM) activates purified recombinant human HDAC8 by decreasing the Michaelis constant (K_m, from 650 μM to 184 μM) and increasing the catalytic constant (k_cat, from 0.0072 s^-1 to 0.035 s^-1; all these changes are measured at the highest tested concentration of 20 μM)^[4].
TM-2-51 activates purified recombinant human HDAC8 with positive cooperativity; at subsaturating substrate concentrations, its apparent activation constant is 6.1 μM and Hill coefficient is 1.7, whereas cooperativity decreases at saturating substrate concentrations^[4].
TM-2-51 (up to 1.8 μM) binds to purified recombinant human HDAC8, with an equilibrium dissociation constant of 0.28 μM and a stoichiometric ratio close to 1:1^[4].
TM-2-51 binds to two functional sites on purified recombinant human HDAC8, with negative cooperativity during the binding process; it exhibits the strongest binding affinity at the first site, with a binding constant of 2.09 × 10⁶ M^-1[4].
TM-2-51 (100 μM) increases the binding affinity of SAHA to purified recombinant human HDAC8 by approximately 2-fold, and alters the enthalpic and entropic contributions to the binding process^[4].
TM-2-51 (80 μM; 72 h) induces approximately 45% apoptosis in human neuroblastoma SH-SY5Y cells when treated at 80 μM for 72 h, but exerts no effect on human neuroblastoma BE (2)-C cells^[4].
TM-2-51 (10-48 μM; saturating concentration) potently and selectively activates recombinant human HDAC-8, reaching a maximum activation fold of 26.8 at saturating concentrations (apparent K_a = 12.4 μM), with no activating effect on other tested human HDAC isozymes^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.