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High-Performance Liquid Chromatography
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Joel J. Kirschbaum, Adorjan Aszalos
The anticoccidial drug halofuginone was analyzed in animal feed and tissues using an octadecylsilane column with a mobile phase of acetonitrile-0.25 M acetate buffer-water (5:3:12) adjusted to an apparent pH of 4.3. The eluate flowing at 2 ml/min was monitored at 243 nm [483]. The limit of detection in feed is 1 μg/mg and in tissues is 1 ng/g. Respective recoveries averaged 93 and 84%.
Selected Antimalarial Plants
Published in Woon-Chien Teng, Ho Han Kiat, Rossarin Suwanarusk, Hwee-Ling Koh, Medicinal Plants and Malaria, 2016
Woon-Chien Teng, Ho Han Kiat, Rossarin Suwanarusk, Hwee-Ling Koh
Besides malaria, febrifugine derivatives are used in cancer, fibrosis, and inflammatory diseases. Halofuginone is in Phase II clinical trials for cancer and fibrosis. The inhibition of prolyl-tRNA synthetase and consequent activation of the amino acid response pathway by halofuginone may explain its role in immune regulation (Keller et al. 2012). It disrupted proline incorporation or uptake, leading to apoptosis from amino acid starvation response in T cells (Chu et al. 2013). Oral administration of halofuginone reduced concanavalin A–induced liver fibrosis possibly via inhibition of collagen I synthesis and inflammatory processes (Liang et al. 2013). It also showed proapoptotic activity on breast cancer cells and downregulated matrix metalloproteinase-9, which is involved in cancer metastasis (Jin et al. 2014).
Dietary Therapy for Psoriasis: Protein-Restricted Diets
Published in John Y. M. Koo, Ethan C. Levin, Argentina Leon, Jashin J. Wu, Mark G. Lebwohl, Mild to Moderate Psoriasis, 2014
Whitney A. Fisk, Ethan C. Levin, Judith Hong, John Y. M. Koo
Given that the AAR appears to specifically affect the Th17 pathway, triggering this response with a pharmacologic agent could be therapeutic for psoriasis patients. A molecule called halofuginone has been developed that induces a state of altered gene expression characteristic of amino acid depletion [53,54]. In animal models, this molecule improves autoimmune disease [50], but it has not yet been studied in human subjects.
Halofuginone inhibits cell proliferation and AKT/mTORC1 signaling in uterine leiomyoma cells
Published in Growth Factors, 2022
In the recent two decades, halofuginone, a natural quinazolinone alkaloid, has shown extensive antifibrotic efficacy in a variety of fibrotic diseases, such as cardiac fibrosis, pulmonary fibrosis and liver fibrosis (Wu et al. 2020; Luo et al. 2017; Jain et al. 2021; Bruck et al. 2001). Halofuginone also exhibits powerful anticarcinogenic effects on malignant lung cancer cells, colorectal cancer cells, as well as breast cancer cells (Demiroglu-Zergeroglu et al. 2020; Wang et al. 2020; Juarez et al. 2017). ULs possesses the feature of fibrosis meanwhile the tumor behavior and the therapeutic purpose should take the two features into consideration. Thus, halofuginone seems to be a good choice. Grudzien et al. (2010) demonstrated that halofuginone reduced collagen type I, collagen type III as well as TGFβI expression in primarily cultured leiomyoma cells paralleled with inhibition of cell proliferation dose-dependently. Koohestani et al. (2016) found the inhibitory effects of this drug in xenograft animal model loaded with primary leiomyomas smooth muscle cells isolated from patients. Consistently, we also found the inhibitory effect of halofuginone on proliferation of ULs cells in vitro and in vivo. Besides, Grudzien et al. (2010) reported halofuginone inhibited the proliferation of primary human myometrial smooth muscle cells which is in contrast with our finding that halofuginone did not affect the proliferation of UtSMC cells. The reasons might be we challenged smooth muscle cell strain using relative low doses of halofuginone (≤20 nM).
Therapy for prevention and treatment of skin ionizing radiation damage: a review
Published in International Journal of Radiation Biology, 2019
José L. Soriano, Ana C. Calpena, Eliana B. Souto, Beatriz Clares
Another approach for cutaneous radiation-induced fibrosis treatment is the administration of anti-transforming growth factor beta 1 (TGF-b1), because a number of cytokines, including TGF-b1, are increased within irradiated tissue (Muller and Meineke 2007). Conversely, halofuginone has been used as an inhibitor of TGF-b1, with positive effects on radiation-induced fibrosis noted in an animal model (Xavier et al. 2004). Another study demonstrated that halofuginone inhibits collagen gene expression in mice, reducing fibrosis (Nagler et al. 2007). Other chemicals such as phenylbutyrate and valproic acid, which are histone deacetylase inhibitors, have also been reported to reduce the generation of radiation-induced cytokines such as TGF-b1, TGF-b2 and tumor necrosis factor alpha (TNF-a), with potential use for fibrosis (Chung et al. 2004). In this context, inhibitors of the Smad3 protein involved in the regulation of TGF-b signaling have also been evaluated (Lee et al. 2010), although further studies need to be conducted (Segaert and Van Cutsem 2005).
Novel pharmacotherapy for burn wounds: what are the advancements
Published in Expert Opinion on Pharmacotherapy, 2019
Phosphorylation of Smad3 and not Smad2 primarily mediates the pro-fibrotic effect of TGF-ß [184]. This is because Smad2 and Smad 3 show non-overlapping target gene binding specificity and differential transcriptional activity [185]. Samd3 is more likely to regulate genes implicated in tissue fibrosis [186]. Furthermore, it has been reported that RNAi-mediated knockdown of Smad3 expression decreased collagen production in keloid fibroblasts [187]. A range of different inhibitors could be candidates for this goal including TRAP-1-like protein (TLP), which in turn co-activates Smad2, halofuginone, quercetin, P144, trichostatin A (TSA) and paclitaxel, among others [188]. Halofuginone is a selective inhibitor of type-1 collagen synthesis and blocks TGF-ß-mediated Smad3 activation in fibroblasts, suppressing dermal fibrosis in vivo [189]. Halofuginone reduced fibrosis in a murine model of sclerodermatous graft versus host disease [190].