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https://www.selleckchem.com/products/iacs-13909.html 12, 6.58, and 6.38 μM, respectively. Further mechanistic studies revealed that 23g inhibited microtubule polymerization by binding to the colchicine site of tubulin, arrested the cell cycle at the G2/M phase, induced cell apoptosis, and exhibited potent in vitro anti-metastasis activity. Finally, molecular docking, molecular dynamics, and free energy analyses were employed to explore the detailed binding interaction between 23g and tubulin. Collectively, these findings indicated that 23g should be further investigated as a potential novel potent antitumor agent targeting tubulin. Various genetic and environmental factors or their interactions may result in the failure of folic acid therapy for hyperhomocysteinemia (HHcy). We hypothesized that an optimal predictive model of gene-environment interactions could be constructed to predict the efficacy of folic acid therapy in HHcy. A prospective cohort study of 638 HHcy patients was performed. The patients were treated with oral folic acid (5 mg/d) for 90 days. We used conditional inference tree model to stratify the failure risk of folic acid therapy synthesizing information from a weighted genetic risk score (wGRS) and environmental exposures, simultaneously interpreting the gene-environment interaction network in predicting the efficacy of HHcy. We detected high-order interactions between medical history of stroke, coronary heart disease (CHD), wGRS, and baseline total homocysteine (tHcy) on the failure risk of folic acid therapy. The wGRS in fourth quartile had 3.73-fold increased failure risk of folic acid treatment (odds ratio = 3.73, 95% confidence interval 1.47-9.45). Stroke was identified as the key discriminator among the variables examined. A total of 3.3% of participants in failure group were at the lowest failure risk of folic acid therapy (nonstroke, non-CHD, baseline tHcy ≤ 31.1 μmol/L, wGRS ≤ 1.05). Individuals with stroke but with wGRS > 1.05 were at t
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