Homoharringtonine is a cytotoxic alkaloid from the evergreen tree.
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Homoharringtonine effectively suppresses IL-6-induced STAT3 phosphorylation in a dose- and time-dependent manner. Moreover, it impedes cellular growth, viability, and colony formation while promoting apoptosis via the mitochondrial pathway. We evaluate its cytotoxicity on human NSCLC cell lines A549 (wild type EGFR) and NCI-H1975 (H1975, mutant EGFR with L858R and T790M), using Gefitinib as a control. Through MTT assays, we find that Homoharringtonine demonstrates moderate cytotoxicity towards A549 cells, with an IC50 of 3.7 μM, while H1975 cells exhibit heightened sensitivity, with an IC50 of 0.7 μM. Furthermore, Homoharringtonine suppresses the proliferation and growth of both A549 and H1975 cells in a dose- and time-dependent manner, as confirmed by MTT assays. Additionally, using trypan blue exclusion assays, we observe a rapid reduction in viable A549 and H1975 cells in response to Homoharringtonine treatment, again in a dose- and time-dependent manner. Notably, Homoharringtonine significantly curtails the clonogenic potential of both A549 and H1975 cells[1].
体内研究
Homoharringtonine (10 mg/kg) significantly suppresses tumor growth compared to the vehicle control or Gefitinib (P<0.05). Furthermore, Homoharringtonine (HHT) administration does not lead to a reduction in mice body weight, suggesting its lack of apparent side effects. After euthanizing all the mice, tumors are isolated, imaged, and tumor sample cells are collected to extract protein for evaluating whether Homoharringtonine inhibits STAT3 phosphorylation via western blot analysis. The level of STAT3 phosphorylation and MCL1 in the Homoharringtonine treatment group are notably decreased compared to the vehicle control or Gefitinib treatment. Moreover, consistent with the aforementioned results, the phosphorylation of AKT1/2/3 and ERK1/2 is not inhibited by Homoharringtonine treatment. To further investigate STAT3 phosphorylation in the xenograft tumor samples subjected to different treatments, the tumor samples are frozen and sectioned into 10 μm sections for fluorescent immunohistochemistry. Homoharringtonine treatment effectively inhibits STAT3 phosphorylation compared to the vehicle control or Gefitinib treatment[1].
体外研究
Homoharringtonine effectively suppresses IL-6-induced STAT3 phosphorylation in a dose- and time-dependent manner. Moreover, it impedes cellular growth, viability, and colony formation while promoting apoptosis via the mitochondrial pathway. We evaluate its cytotoxicity on human NSCLC cell lines A549 (wild type EGFR) and NCI-H1975 (H1975, mutant EGFR with L858R and T790M), using Gefitinib as a control. Through MTT assays, we find that Homoharringtonine demonstrates moderate cytotoxicity towards A549 cells, with an IC50 of 3.7 μM, while H1975 cells exhibit heightened sensitivity, with an IC50 of 0.7 μM. Furthermore, Homoharringtonine suppresses the proliferation and growth of both A549 and H1975 cells in a dose- and time-dependent manner, as confirmed by MTT assays. Additionally, using trypan blue exclusion assays, we observe a rapid reduction in viable A549 and H1975 cells in response to Homoharringtonine treatment, again in a dose- and time-dependent manner. Notably, Homoharringtonine significantly curtails the clonogenic potential of both A549 and H1975 cells[1].
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