Iron transport and heme synthesis are essential processes in human metabolism, and any dysregulation in these mechanisms, such as inflammation, can have deleterious effects. Lipopolysaccharide (LPS)‑induced inflammatory responses can result in a number of adverse effects, including cancer. Natural mineral sulfur, methylsulfonylmethane (MSM) and nontoxic sulfur (NTS) suppress inflammatory responses. The present study hypothesized that MSM and NTS may inhibit LPS‑induced inflammatory responses in THP‑1 human monocytes. Reverse transcription‑quantitative PCR and western blotting assays were performed to analyze the molecular signaling pathways associated with sulfur‑treated and untreated cells. A comet assay was used to evaluate DNA damage, flow cytometry was performed to analyze cell surface receptors and chromatin immunoprecipitation was used to examine molecular interactions. Notably, LPS‑induced inflammation increased iron/heme metabolism, whereas MSM and NTS inhibited this effect. Furthermore, LPS treatment activated the Toll‑like receptor 4/NF‑κB signaling axis, which was downregulated by NTS and MSM. These sulfur compounds also suppressed the nuclear accumulation of LPS‑induced NF‑κB, which could induce the production of proinflammatory cytokines, such as TNF‑α, IL‑1β and IL‑6. Finally, MSM and NTS inhibited LPS‑induced reactive oxygen species generation and DNA damage in THP‑1 monocytic leukemia cells. These results suggested that natural sulfur molecules may be considered promising candidates for anti‑inflammation studies.

Embryonic cancer stem cells (CSCs), referred to as self‑renewable cells, are commonly found in liquid and solid cancers and can also be attributed to tumor onset, resistance, expansion, recurrence and metastasis following treatment. Cancer therapy targeting CSCs using natural bioactive products is an optimal option for inhibiting cancer recurrence, thereby improving prognosis. Several natural compounds and extracts have been used to identify direct or indirect therapy effects that reduce the pathological activities of CSCs. Natural gallic acid (GA) is noted to have anticancer properties for oncogene expression, cycle arrest, apoptosis, angiogenesis, migration and metastasis in various cancers. The present study demonstrated that GA has various anticancer activities in NTERA‑2 and NCCIT human embryonic carcinoma cells. In two types of embryonic CSCs, GA effectively induced cell death via late apoptosis. Furthermore, GA showed the G0/G1 cell cycle arrest activity in embryonic CSCs by inducing the increase of p21, p27 and p53 expression and the decrease of CDK4, cyclin E and cyclin D1 expression. The present study showed that GA inhibited the expression levels of mRNA and protein for stem cell markers, such as SOX2, NANOG and OCT4, in NTERA‑2 and NCCIT cells. The induction of cellular and mitochondrial reactive oxygen species by GA also activated the cellular DNA damage response pathway by raising the phosphorylated‑BRCA1, ATM, Chk1, Chk2 and histone. Finally, GA inhibited CSCs invasion and migration by inhibiting the expression of matrix metalloproteinase by the downregulation of EGFR/JAK2/STAT5 signaling pathway. Thus, it is hypothesized that GA could be a potential inhibitor of cancer emergence by suppressing CSC properties.

The skin plays a vital role in host defense against microorganisms, viruses, and environmental agents. Inflammatory skin conditions are initiated by increased expression of cytokines, interferons, and interleukins, which activate immune responses. TNF-α and lipopolysaccharide (LPS) are key inducers of skin inflammation, contributing to diseases, including psoriasis, ichthyosis, atopic dermatitis, and potentially melanoma. Protocatechuic acid (PCA), a natural anthocyanin with anticancer and anti-inflammatory properties, was chemically modified to synthesize PCA alkyl ester (PAE) derivatives to improve its anti-inflammatory efficacy. This study aimed to investigate whether PAE derivatives more effectively inhibit TNF-α-induced inflammation in HaCaT keratinocyte cells compared to unmodified PCA. The expression levels of key downstream molecules in the Akt signaling pathway were assessed by western blotting, and the relative mRNA expression of muscle atrophy-related genes was analyzed using real-time PCR. We evaluated cytokine expression using ELISA, and MTT assays were performed to assess cytotoxicity. The PAE derivatives, particularly PAE-5, 6, and 7, significantly reduced IL-8 production at lower concentrations than PCA while maintaining low cytotoxicity. In contrast, PAE-12 exhibited reduced efficacy despite higher hydrophobicity, suggesting that excessive hydrophobicity may hinder biological activity. Moreover, PAE-5 and PAE-6 markedly suppressed LPS-induced expression of IL-6, IL-1β, and TNF-α, underscoring the importance of optimal alkyl chain length. Our results provides that PCA alkyl ester derivatives are promising anti-inflammatory agents with low toxicity, offering potential applications in cosmeceutical formulations for treating inflammatory skin conditions.

The skin is the most voluminous organ of the human body and is exposed to the outer environment. Such exposed skin suffers from the effects of various intrinsic and extrinsic aging factors. Skin aging is characterized by features such as wrinkling, loss of elasticity, and skin pigmentation. Skin pigmentation occurs in skin aging and is caused by hyper-melanogenesis and oxidative stress. Protocatechuic acid (PCA) is a natural secondary metabolite from a plant-based source widely used as a cosmetic ingredient. We chemically designed and synthesized PCA derivatives conjugated with alkyl esters to develop effective chemicals that have skin-whitening and antioxidant effects and enhance the pharmacological activities of PCA. We identified that melanin biosynthesis in B16 melanoma cells treated with alpha-melanocyte-stimulating hormone (α-MSH) is decreased by PCA derivatives. We also found that PCA derivatives effectively have antioxidant effects in HS68 fibroblast cells. In this study, we suggest that our PCA derivatives are potent ingredients for developing cosmetics with skin-whitening and antioxidant effects.

The detecting and screening of explosives has become a global consideration in dealing with potential terrorism threats and the misuse of high explosives. Several detection techniques have been developed, but their disadvantages include the requirement of expensive equipment, complicated pre-treatment, and prolonged testing. So far, fluorescence-based sensors have been of great interest as they overcome the limitations of other techniques. BODIPY, which is a fluorophore, shows excellent fluorescence features, and it can be used as a sensor material for explosives detection. However, to date, BODIPY-based explosive sensors have not been explored in detail. This work reviews the recent developments on explosive sensors based on BODIPY and its analogs.

Iron homeostasis is considered a key factor in human metabolism, and abrogation in the system could create adverse effects, including cancer. Moreover, 6-gingerol is a widely used bioactive phenolic compound with anticancer activity, and studies on its exact mechanisms on non-small cell lung cancer (NSCLC) cells are still undergoing. This study aimed to find the mechanism of cell death induction by 6-gingerol in NSCLC cells. Western blotting, real-time polymerase chain reaction, and flow cytometry were used for molecular signaling studies, and invasion and tumorsphere formation assay were also used with comet assay for cellular processes. Our results show that 6-gingerol inhibited cancer cell proliferation and induced DNA damage response, cell cycle arrest, and apoptosis in NSCLC cells, and cell death induction was found to be the mitochondrial-dependent intrinsic apoptosis pathway. The role of iron homeostasis in the cell death induction of 6-gingerol was also investigated, and iron metabolism played a vital role in the anticancer ability of 6-gingerol by downregulating EGFR/JAK2/STAT5b signaling or upregulating p53 and downregulating PD-L1 expression. Also, 6-gingerol induced miR-34a and miR-200c expression, which may indicate regulation of PD-L1 expression by 6-gingerol. These results suggest that 6-gingerol could be a candidate drug against NSCLC cells and that 6-gingerol could play a vital role in cancer immunotherapy.

In order to investigate the changes in the spectroscopic properties of dimeric boron-dipyrromethenes (BODIPYs), four BODIPY derivatives are synthesized, including a monomer BODIPY in which a furyl group is substituted at the meso position and a dimer BODIPY with a furan group as a bridge. The four synthesized BODIPY derivatives are characterized through nuclear magnetic resonance and mass spectrometry. Photophysical properties such as ultraviolet–visible absorbance and the fluorescence emission of monomers (mT1 and mT2) and dimers (biT1 and biT2) are studied in eight different solvents. In addition, the relationship of their structural properties and optical properties are also considered through density functional theory calculations. The covalent link between the two BODIPY units using a furan group has a profound effect on the optical properties of the dimeric BODIPYs. We believe that an understanding of the synthesis and physical properties of dimeric BODIPYs will have a promising perspective in designing new BODIPY derivatives and predicting their spectroscopic characteristics in the future.

Embryonic cancer cells (CSCs) could cause different types of cancer, a skill that makes them even more dangerous than other cancer cells. Identifying CSCs using natural products is a good option as it inhibits the recurrence of cancer with moderate various effects. Ursolic acid (UA) is a pentacyclic triterpenoid extracted from fruit and herbal remedies and has known anticancer functions against various cancer cells. However, its potential against CSCs remains uncertain. This study was planned to examine the induction of cell apoptosis by the UA. For cell signaling studies, we performed experiments, which are real-time qPCR and immunoblotting. Also, various cellular processes were analyzed using flow cytometry. The results raised a barrier to cell proliferation by the UA in NTERA-2 and NCCIT cells. Morphological studies also confirmed the UA's ability to cause cell death in embryonic CSCs. Examination of cell death importation showed that the UA formed the expression of the iNOS and thus the cell generation and mitochondrial reactive oxygen generation, which created a reaction to cellular DNA damage by raising the protein levels of phospho-histone ATR and ATM. In addition, the UA created the binding of the G0/G1 cell cycle to NTERA-2 and NCCIT cells, improved the expression levels of p21 and p27, and reduced the expression levels of CDK4, cyclin D1, and cyclin E, confirming the UA's ability to initiate cell cycle arrest. Finally, the UA created an internal mechanism of apoptosis in the embryonic CSC using BAX and cytochrome c regulation as well as the regulation of BCL-xL and BCL-2 proteins. Therefore, UA could be the best candidate for targeting CSCs and thus suppressing the emergence of cancer.

Aims: In biology and medicine, hypoxia refers to reduced oxygen tension or oxygen starvation resulting from various environmental or pathological conditions. Prolonged hypoxia may lead to an imbalance in protein production and a loss of muscle mass in animals. The physiological response to hypoxia includes oxidative stress induced activation of complex cell-signaling networks such as hypoxia-inducible factor (HIF), phosphoinositide 3-kinase (PI3K), and Janus kinase/signal transducer and activator of transcription (JAK-STAT). Methylsulfonylmethane (MSM) is a natural sulfur compound that regulates HIF-1 alpha expression and provides cytoprotection from oxidative stress. In this study, we explored the anti-hypoxic activity and cytoprotective effect of MSM in cobalt chloride (CoCl2)-induced hypoxic C2C12 mouse myoblast culture. Materials and methods: We used western blotting, real time PCR, flow cytometry for molecular signaling studies and we also used MTT assay and ChIP assay along with comet assay for cellular processes. Key findings: MSM prevented the CoCl2 induced cytotoxicity. Molecular markers of hypoxia, induced by CoCl2, were normalized or reduced by MSM, which also inhibited the effect of CoCl2-induced JAK2/STAT5b/Cyclin D1 and PI3K/AKT signaling. CoCl2-induced oxidative stress results in activation of the NRF2/HO-1-mediated cell survival pathway and inhibition of DNA repair, both of which were prevented by MSM. Significance: We suggest MSM can be considered as a candidate drug for reducing the effects of hypoxia in both animals and humans.

Lipopolysaccharide (LPS)-induced inflammatory response leads to serious damage, up to and including tumorigenesis. Natural mineral sulfur, non-toxic sulfur (NTS), and methylsulfonylmethane (MSM) have anti-inflammatory activity that may inhibit LPS-induced inflammation. We hypothesized that sulfur compounds could inhibit LPS-induced inflammatory responses in CCD-986Sk skin fibroblasts. We used Western blotting and real-time PCR to analyze molecular signaling in treated and untreated cultures. We also used flow cytometry for cell surface receptor analysis, comet assays to evaluate DNA damage, and ELISA-based cytokine detection. LPS induced TLR4 activation and NF-κB signaling via canonical and protein kinase C (PKC)-dependent pathways, while NTS and MSM downregulated that response. NTS and MSM also inhibited LPS-induced nuclear accumulation and binding of NF-κB to proinflammatory cytokines COX-2, IL-1β, and IL-6. Finally, the sulfur compounds suppressed LPS-induced ROS accumulation and DNA damage in CCD-986Sk cells. These results suggest that natural sulfur compounds could be used to treat inflammation and may be useful in the development of cosmetics.

A ratiometric and colorimetric probe (FD) for the sensitive detection of fluoride ions are reported. Only fluoride anions can induce a red-shift (116 nm) in the maximum absorption wavelength and its dynamic detection range is determined as 60-250 mu M. Moreover, FD is applied to a paper-based sensing system for convenient "naked-eye" measurement.dagger dagger

Janus kinase 2 (JAK2) and STAT3 signaling is considered a major pathway in lipopolysaccharide (LPS)-induced inflammation. Toll-like receptor 4 (TLR-4) is an inflammatory response receptor that activates JAK2 during inflammation. STAT3 is a transcription factor for the pro-inflammatory cytokine IL-6 in inflammation. Sulfur is an essential element in the amino acids and is required for growth and development. Non-toxic sulfur (NTS) can be used in livestock feeds as it lacks toxicity. The present study aimed to inhibit LPS-induced inflammation in C2C12 myoblasts using NTS by regulating TLR-4 and JAK2/STAT3 signaling via the modulation of IL-6. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was conducted to analyze cell viability and reverse transcription polymerase chain reaction and western blotting performed to measure mRNA and protein expression levels. Chromatin immunoprecipitation and enzyme-linked immunosorbent assays were used to determine the binding activity of proteins. The results indicated that NTS demonstrated a protective effect against LPS-induced cell death and inhibited LPS-induced expression of TLR-4, JAK2, STAT3 and IL-6. In addition, NTS inhibited the expression of nuclear phosphorylated-STAT3 and its binding to the IL-6 promoter. Therefore, NTS may be a potential candidate drug for the treatment of inflammation.

Sulfur is an essential nutrient—along with nitrogen, phosphorus, and potassium—for plant growth and development. Sulfur is mostly supplied to crops through soil fertilizers. However, chemical fertilizers are overused to increase crop yields despite environmental threats. The proper use of chemical fertilizers positively affects crop growth and yield increase. Regardless, residues from misuse threaten not only the soil ecosystem, but also the marine ecosystem. Therefore, the need to minimize chemical fertilizer abuse is imperative. This article reports that sulfur can be applied to crop leaves as nontoxic sulfur (NTS) in trace amounts to positively affect plant hormones, chloroplast content, and ROS scavenging system, thereby promoting growth, and increasing crop yields. Furthermore, NTS and microelements, the micronutrients calcium and magnesium, produced a synergistic effect when applied together, and NTS enhanced the expression of auxin and gibberellin-related genes. Additionally, chlorophyll content was increased, and ROS scavenging ability was greatly improved. Therefore, NTS can effectively deliver potent growth-promoting functions of plants faster and safer than did soil fertilizers and consequently increase crop yield. This finding is a new strategy to replace soil chemical fertilizers in supplying sulfur. It is potentially valuable for increasing crop yields and can be applied to other crops.

Hormone-specific anticancer drugs for breast cancer treatment can cause serious side effects. Thus, treatment with natural compounds has been considered a better approach as this minimizes side effects and has multiple targets. 6-Gingerol is an active polyphenol in ginger with various modalities, including anticancer activity, although its mechanism of action remains unknown. Increases in the level of reactive oxygen species (ROS) can lead to DNA damage and the induction of DNA damage response (DDR) mechanism, leading to cell cycle arrest apoptosis and tumorsphere suppression. Epidermal growth factor receptor (EGFR) promotes tumor growth by stimulating signaling of downstream targets that in turn activates tumor protein 53 (p53) to promote apoptosis. Here we assessed the effect of 6-gingerol treatment on MDA-MB-231 and MCF-7 breast cancer cell lines. 6-Gingerol induced cellular and mitochondrial ROS that elevated DDR through ataxia-telangiectasia mutated and p53 activation. 6-Gingerol also induced G0/G1 cell cycle arrest and mitochondrial apoptosis by mediating the BAX/BCL-2 ratio and release of cytochrome c. It also exhibited a suppression ability of tumorsphere formation in breast cancer cells. EGFR/Src/STAT3 signaling was also determined to be responsible for p53 activation and that 6-gingerol induced p53-dependent intrinsic apoptosis in breast cancer cells. Therefore, 6-gingerol may be used as a candidate drug against hormone-dependent breast cancer cells.

Embryonic cancer stem cells (CSCs) can differentiate into any cancer type. Targeting CSCs with natural compounds is a promising approach as it suppresses cancer recurrence with fewer adverse effects. 6-Gingerol is an active component of ginger, which exhibits well-known anti-cancer activities. This study determined the mechanistic aspects of cell death induction by 6-gingerol. To analyze cellular processes, we used Western blot and real-time qPCR for molecular signaling studies and conducted flow cytometry. Our results suggested an inhibition of CSC marker expression and Wnt/β-catenin signaling by 6-gingerol in NCCIT and NTERA-2 cells. 6-Gingerol induced reactive oxygen species generation, the DNA damage response, cell cycle arrest, and the intrinsic pathway of apoptosis in embryonic CSCs. Furthermore, 6-gingerol inhibited iron metabolism and induced PTEN, which both played vital roles in the induction of cell death. The activation of PTEN resulted in the inhibition of PD-L1 expression through PI3K/AKT/p53 signaling. The induction of PTEN also mediated the downregulation of microRNAs miR-20b, miR-21, and miR-130b to result in PD-L1 suppression by 6-gingerol. Hence, 6-gingerol may be a promising candidate to target CSCs by regulating PTEN-mediated PD-L1 expression.

Recently, natural compounds have been used globally for cancer treatment studies. Silibinin is a natural compound extracted from Silybum marianum (milk thistle), which has been suggested as an anticancer drug through various studies. Studies on its activity in various cancers are undergoing. This study demonstrated the molecular signaling behind the anticancer activity of silibinin in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction and Western blotting analysis were performed for molecular signaling analysis. Wound healing assay, invasion assay, and in vitro angiogenesis were performed for the anticancer activity of silibinin. The results indicated that silibinin inhibited A549, H292, and H460 cell proliferation in a concentration-dependent manner, as confirmed by the induction of G0/G1 cell cycle arrest and apoptosis and the inhibition of tumor angiogenesis, migration, and invasion. This study also assessed the role of silibinin in suppressing tumorsphere formation using the tumorsphere formation assay. By binding to the epidermal growth factor receptor (EGFR), silibinin downregulated phosphorylated EGFR expression, which then inhibited its downstream targets, the JAK2/STAT5 and PI3K/AKT pathways, and thereby reduced matrix metalloproteinase, PD-L1, and vascular endothelial growth factor expression. Binding analysis demonstrated that STAT5 binds to the PD-L1 promoter region in the nucleus and silibinin inhibited the STAT5/PD-L1 complex. Altogether, silibinin could be considered as a candidate for tumor immunotherapy and cancer stem cell-targeted therapy.

The use of tetrahydrofuran for a matrix-dissolving solvent highly improved the SAMDI MS efficiency for the analysis of SAMs on gold. Appendix S1. Supporting Information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Cyclic adenosine monophosphate (cAMP) plays a key role in signal transduction pathways as a second messenger. Studies on the cAMP dynamics provided useful scientific insights for drug development and treatment of cAMP-related diseases such as some cancers and prefrontal cortex disorders. For example, modulation of cAMP-mediated intracellular signaling pathways by anti-tumor drugs could reduce tumor growth. However, most early stage tools used for measuring the cAMP level in living organisms require cell disruption, which is not appropriate for live cell imaging or animal imaging. Thus, in the last decades, tools were developed for real-time monitoring of cAMP distribution or signaling dynamics in a non-invasive manner. Genetically-encoded sensors based on fluorescent proteins and luciferases could be powerful tools to overcome these drawbacks. In this review, we discuss the recent genetically-encoded cAMP sensors advances, based on single fluorescent protein (FP), Föster resonance energy transfer (FRET), single luciferase, and bioluminescence resonance energy transfer (BRET) for real-time non-invasive imaging.

High glucose-induced inflammation leads to atherosclerosis, which is considered a major cause of death in type 1 and type 2 diabetic patients. Nuclear factor-kappa B (NF-κB) plays a central role in high glucose-induced inflammation and is activated through toll-like receptors (TLRs) as well as canonical and protein kinase C-dependent (PKC) pathways. Non-toxic sulfur (NTS) and methylsulfonylmethane (MSM) are two sulfur-containing natural compounds that can induce anti-inflammation. Using Western blotting, real-time polymerase chain reaction, and flow cytometry, we found that high glucose-induced inflammation occurs through activation of TLRs. An effect of NTS and MSM on canonical and PKC-dependent NF-κB pathways was also demonstrated by western blotting. The effects of proinflammatory cytokines were investigated using a chromatin immunoprecipitation assay and enzyme-linked immunosorbent assay. Our results showed inhibition of the glucose-induced expression of TLR2 and TLR4 by NTS and MSM. These sulfur compounds also inhibited NF-κB activity through reactive oxygen species (ROS)-mediated canonical and PKC-dependent pathways. Finally, NTS and MSM inhibited the high glucose-induced expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and binding of NF-κB protein to the DNA of proinflammatory cytokines. Together, these results suggest that NTS and MSM may be potential drug candidates for anti-inflammation therapy.

Bulletin of the Korean Chemical SocietyVolume 41, Issue 2 p. 220-222 Note Efficient and Safe Synthesis of 1-Methyl-3,5-Dinitro-1,2,4-Triazole Using Continuous Flow Chemistry Yun Seon Choi, Yun Seon Choi Green Chemistry and Materials Group, Korea Institute of Industrial Technology (KITECH), Cheonan, 31056 South KoreaSearch for more papers by this authorSejin Lee, Sejin Lee The 4th R&D Institute, Agency for Defense Development (ADD), Daejeon, 34186 South KoreaSearch for more papers by this authorSe Won Bae, Corresponding Author Se Won Bae [email protected] Green Chemistry and Materials Group, Korea Institute of Industrial Technology (KITECH), Cheonan, 31056 South KoreaSearch for more papers by this author Yun Seon Choi, Yun Seon Choi Green Chemistry and Materials Group, Korea Institute of Industrial Technology (KITECH), Cheonan, 31056 South KoreaSearch for more papers by this authorSejin Lee, Sejin Lee The 4th R&D Institute, Agency for Defense Development (ADD), Daejeon, 34186 South KoreaSearch for more papers by this authorSe Won Bae, Corresponding Author Se Won Bae [email protected] Green Chemistry and Materials Group, Korea Institute of Industrial Technology (KITECH), Cheonan, 31056 South KoreaSearch for more papers by this author First published: 20 December 2019 https://doi.org/10.1002/bkcs.11938Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Graphical Abstract Supporting Information Filename Description bkcs11938-sup-0001-Supinfo.docWord document, 915.5 KB Appendix S1: Supporting information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. References 1T. M. Klapötke, Chemistry of High-Energy Materials, 3rd ed., de Gruyter, Berlin, 2015. 2J. P. Agrawal, High Energy Materials, Wiley-VCH, Weinheim, 2010. 3J. Akhavan, The Chemistry of Explosives, 2nd ed., The Royal Society of Chemistry, Cambridge, 2004. 4P. Ravi, D. M. Badgujar, G. M. Gore, S. P. Tewari, A. K. Sikder, Propellants Explos. Pyrotech. 2011, 36, 393. 5 R. Surapaneni Ed., 7th International High Energy Materials Conference & Exhibit (HEMCE-2009), Pune, MoD, Pune, 2009, p. 7. 6M. B. Frankel, E. A. Burns, J. C. Butler, E. R. Wilson, J. Org. Chem. 1963, 28, 2428. 7A. R. Katritzky, A. V. Vakulenko, J. Sivapackiam, B. Draghici, R. Damavarapu, Synthesis 2008, 2008, 699. 8N. R. Smith, R. H. Wiley, Preparation of 1-Alkyl-3,5-dinitro-1,2,4-triazoles, US Patent 3,165,753, 1965. 9J. J. Roemer, D. W. Kaiser, Preparation of guanazole, US Patent 2,648,671, 1953. 10 D. V. Price, A. R. Stasio, In 2010 Insensitive Munitions and Energetic Materials Technology Symposium " International Progress in Insensitive Munitions and Energetic Materials", 11–14 October, 2010, Munich, BAE Systems, Kingsport, TN, 2010. URL https://imemg.org/wp-content/uploads/IMEMTS%202010/papers/Price-10503_Synthesis%20of%20DNMT-A%20New%20Energetic-Insensitive%20Melt-pour%20Ingredient_IMEMTS2010-Paper.pdf. 11T. F. Jamison, G. Koch, Flow Chemistry in Organic Synthesis, Thieme, Stuttgart, 2019. 12M. B. Plutschack, B. Pieber, K. Gilmore, P. H. Seeberger, Chem. Rev. 2017, 117, 11796. 13N. Oger, E. L. Grogneca, F.-X. Felpin, Org. Chem. Front. 2015, 2, 590. 14R. Porta, M. Benaglia, A. Puglisi, Org. Process. Res. Dev. 2016, 20, 2. 15B. J. Deadman, S. G. Collins, A. R. Maguire, Chem. Eur. J. 2015, 21, 2298. 16K. F. Jensen, B. J. Reizman, S. G. Newman, Lab Chip 2014, 14, 3206. 17T. N. Glasnov, C. O. Kappe, Chem. Eur. J. 2011, 17, 11956. 18R. L. Hartman, J. P. McMullen, K. F. Jensen, Angew. Chem. Int. Ed. 2011, 50, 7502. 19G. Panke, T. Schwalbe, W. Stirner, S. Taghavi-Moghadamand, G. Wille, Synthesis 2003, 18, 2827. 20J. Pelleterand, F. Renaud, Org. Process. Res. Dev. 2009, 13, 698. Citing Literature Volume41, Issue2February 2020Pages 220-222 ReferencesRelatedInformation