Research on new synthetic routes about 1968-05-4

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Category: chlorides-buliding-blocks. So far, in addition to halogen atoms, other non-metallic atoms can become part of the aromatic heterocycle, and the target ring system is still aromatic. Compound: 3,3′-Diindolylmethane, is researched, Molecular C17H14N2, CAS is 1968-05-4, about Pharmacophore-inspired discovery of FLT3 inhibitor from kimchi.

Globally consumed kimchi is manufactured through fermenting cruciferous vegetables containing indole glucosinolates (IG). But few reports describe the IG metabolism during the fermentation Here, we show that indole-3-carbinol (I3C), a breakdown product of IG, is transformed during the kimchi fermentation into 3,3-diindolylmethane (DIM) and 2-(indol-3-ylmethyl)-3,3-diindolylmethane (LTr1). LTr1 was found to kill the acute myeloid leukemia (AML) cells with FMS-like tyrosine kinase 3 (FLT3) receptor mutations, by inhibiting the FLT3 phosphorylation and the expression of downstream proteins (STAT5, ERK, and AKT). In the immune-depleted mice xenografted with human MV4-11 cells, LTr1 was demonstrated to reduce the tumor growth and synergize with sorafenib, an anti-AML agent in clinic. The work updates the chem. and biol. knowledge about kimchi, and in particular establishes LTr1 as an FLT3 inhibitor that is effective and synergistic with sorafenib in treating AML.

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Discover the magic of the 1968-05-4

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In general, if the atoms that make up the ring contain heteroatoms, such rings become heterocycles, and organic compounds containing heterocycles are called heterocyclic compounds. An article called Combinatorial effect of chemotherapeutic drugs with natural products improves the combat against cancer cell drug resistance, published in 2021, which mentions a compound: 1968-05-4, Name is 3,3′-Diindolylmethane, Molecular C17H14N2, Name: 3,3′-Diindolylmethane.

A review. Cancer is one of the world’s leading causes of death making it an enticing condition to research and potentially develops prevention options. Sep. or in combination, Surgery, Radiation, Targeted treatments and Immunotherapy are widely used to treat cancer. These treatment strategies are becoming highly futile and tend to have achieved a clin. deficit due to massive side effects and multidrug resistance. Therefore, anti-cancer specific chemotherapy was needed to address and potentially solve this dilemma. The drawback of chemotherapy is the development of drug resistance. Naturally derived compounds were the cornerstone of chemotherapy for the last 40 years. Recent progress has allowed researchers to fully explore the possible use of effective, well suitable, sideeffect-free natural bio-active compounds along with well-proven chemotherapeutic drugs for treating or regulating cancer. However, merely a few substances were trialled in several cancer patients and there is only marginal knowledge of their therapeutic efficacy. Hereby, in this review, we discuss the efficacy of existing chemotherapy drugs such as Cisplatin, Doxorubicin, Paclitaxel, Methotrexate, 5-Fluorouracil and some natural compounds (Curcumin, Capsaicin, 3,3’Diindolylmethane (DIM), Lupeol, Diosgenin and Ellagic acid) and their beneficial effects on cancer. This systematic review strongly admits the use of these compounds in patients with advanced and/or metastatic cancers, along with chemotherapy drugs.

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Interesting scientific research on 1968-05-4

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Munakarmi, Suvesh; Shrestha, Juna; Shin, Hyun-Beak; Lee, Geum-Hwa; Jeong, Yeon-Jun published the article 《3,3′-diindolylmethane suppresses the growth of hepatocellular carcinoma by regulating its invasion, migration, and er stress-mediated mitochondrial apoptosis》. Keywords: DIM; EMT; ER stress; apoptosis; hepatocellular carcinoma; unfolded protein response.They researched the compound: 3,3′-Diindolylmethane( cas:1968-05-4 ).Category: chlorides-buliding-blocks. Aromatic heterocyclic compounds can be divided into two categories: single heterocyclic and fused heterocyclic. In addition, there is a lot of other information about this compound (cas:1968-05-4) here.

Hepatocellular carcinoma (HCC) is the leading cause of cancer-related death worldwide with limited treatment options. Biomarker-based active phenolic flavonoids isolated from medicinal plants might shed some light on potential therapeutics for treating HCC. 3,3′-diindolylmethane (DIM) is a unique biol. active dimer of indole-3-carbinol (I3C), a phytochem. compound derived from Brassica species of cruciferous vegetables-such as broccoli, kale, cabbage, and cauliflower. It has anti-cancer effects on various cancers such as breast cancer, prostate cancer, endometrial cancer, and colon cancer. However, the mol. mechanism of DIM involved in reducing cancer risk and/or enhancing therapy remains unknown. The aim of the present study was to evaluate anti-cancer and therapeutic effects of DIM in human hepatoma cell lines Hep3B and HuhCell proliferation was measured with MTT and trypan blue colony formation assays. Migration, invasion, and apoptosis were measured with Transwell assays and flow cytometry analyses. Reactive oxygen species (ROS) intensity and the loss in mitochondrial membrane potential of Hep3B and Huh7 cells were determined using dihydroethidium (DHE) staining and tetramethylrhodamine Et ester dye. Results showed that DIM significantly suppressed HCC cell growth, proliferation, migration, and invasion in a concentration-dependent manner. Furthermore, DIM treatment activated caspasedependent apoptotic pathway and suppressed epithelial-mesenchymal transition (EMT) via ER stress and unfolded protein response (UPR). Taken together, our results suggest that DIM is a potential anticancer drug for HCC therapy by targeting ER-stress/UPR.

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Some scientific research about 1968-05-4

If you want to learn more about this compound(3,3′-Diindolylmethane)Name: 3,3′-Diindolylmethane, you may wish to communicate with the author of the article,or consult the relevant literature related to this compound(1968-05-4).

The chemical properties of alicyclic heterocycles are similar to those of the corresponding chain compounds. Compound: 3,3′-Diindolylmethane, is researched, Molecular C17H14N2, CAS is 1968-05-4, about Tetrandrine attenuates intestinal epithelial barrier defects caused by colitis through promoting the expression of Occludin via the AhR-miR-429 pathway, the main research direction is tetrandrine intestinal epithelial colitis Occludin AhR miR 429; Occludin; aryl hydrocarbon receptor; colitis; intestinal epithelial barrier; tetrandrine.Name: 3,3′-Diindolylmethane.

The elevated intestinal permeability due to mucosal barrier defects is not only secondary to inflammatory bowel disease but also precedes enteritis. Tetrandrine, a bisbenzyl isoquinoline alkaloid isolated from the dried roots of Stephamis tetlandra S. Moor, was previously demonstrated to ameliorate colitis induced by dextran sulfate sodium (DSS) in mice. Here, we investigate whether and how tetrandrine protects against the disruption of the intestinal epithelial barrier under colitis condition. The data show that oral administration of tetrandrine significantly counteracted the increase of intestinal permeability in DSS-treated mice, enhanced the mRNA and protein expression of Occludin and Claudin1 in the colon, but hardly affected the expression of ZO-1 and Mucin2. In vitro, tetrandrine treatment rescued the decrease of monolayer transmembrane resistance and the increase of epithelial cell permeability induced by TNF-α, upregulated the expression of Occludin, and downregulated the expression of Claudin1 but did not affect the expression of ZO-1. The siRNA of Occludin largely weakened the protective effect of tetrandrine on the epithelial barrier function in Caco-2 cells. MiR-429 mimic obviously counteracted the upregulation of tetrandrine on the expression of Occludin and the amelioration on epithelial barrier defects, in contrast, miR-429 inhibitor showed the opposite effects. The antagonist (CH223191) and siAhR of aryl hydrocarbon receptor (AhR) nearly completely diminished the effects of tetrandrine, including inhibition of the miR429 expression, the upregulation of Occludin expression, and amelioration of intestinal epithelial barrier defects in Caco-2 cells. In colitis mice, CH223191 significantly weakened the protective effect of tetrandrine on colitis and intestinal mucosal barrier and diminished the downregulation on miR-429 expression and the promotion on Occludin expression in the colon. In summary, tetrandrine can attenuate the intestinal epithelial barrier defects in colitis through promoting Occludin expression via the AhR/miR-429 pathway, and it might be used to treat colitis as a barrier protector.

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Now Is The Time For You To Know The Truth About 1968-05-4

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The chemical properties of alicyclic heterocycles are similar to those of the corresponding chain compounds. Compound: 3,3′-Diindolylmethane, is researched, Molecular C17H14N2, CAS is 1968-05-4, about Indole treatment alleviates intestinal tissue damage induced by chicken coccidiosis through activation of the aryl hydrocarbon receptor, the main research direction is coccidiosis indole aryl hydrocarbon receptor; CD4+ T cells; Th17 cells; Treg cells; chicken; coccidiosis; indole.Application of 1968-05-4.

In the present study, we examined the effects of dietary indoles, 3,3′-diindolylmethane (DIM) and indole-3-carbinol (I3C), on CD4+T cell population and functions in chickens. Furthermore, the effects of dietary DIM treatment on chicken coccidiosis caused by an apicomplexan parasite were investigated. Dietary treatment of healthy chickens with DIM and I3C induced increased CD4+CD25+ (Treg) cells and the mRNA expression of IL-10, while decreasing number of CD4+IL-17A+ (Th17) cells and Th17-related cytokines transcripts expression in the intestine. In addition, we explored the role of AhR in indole-treated splenic lymphocytes by using AhR antagonist and our results suggested that DIM is a ligand for chicken AhR. In chicken coccidiosis, treatment of DIM increased the ratio of Treg/Th17 cells and significantly reduced intestinal lesion although no significant changes in body weight and fecal oocyst production were noted compared to non-treated control group. These results indicate that DIM is likely to affect the ratios of Treg/Th17 reducing the level of local inflammatory response induced by Eimeria or facilitate repairing process of inflamed gut following Eimeria infection. The results described herein are thus consistent with the concept that AhR ligand modulates the T cell immunity through the alteration of Treg/Th17 cells with Treg dominance. To our knowledge, present study is the first scientific report showing the effects of dietary indole on T cell immunity in poultry species.

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The Absolute Best Science Experiment for 1968-05-4

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Application In Synthesis of 3,3′-Diindolylmethane. Aromatic heterocyclic compounds can also be classified according to the number of heteroatoms contained in the heterocycle: single heteroatom, two heteroatoms, three heteroatoms and four heteroatoms. Compound: 3,3′-Diindolylmethane, is researched, Molecular C17H14N2, CAS is 1968-05-4, about Anticancer properties of a new non-oxido vanadium(IV) complex with a catechol-modified 3,3′-diindolylmethane ligand. Author is Dankhoff, Katja; Ahmad, Aamir; Weber, Birgit; Biersack, Bernhard; Schobert, Rainer.

In order to identify new active drug candidates against cancer diseases we investigated the tumor cell growth inhibition, formation of reactive oxygen species, mitochondrial membrane damage, cell cycle arrest and DNA binding activity of a new bis(triethylammonium) tris[1,1-bis(indol-3-yl)-1-(3,4-catecholate)methane]vanadate(IV) complex. It exhibited significant antiproliferative activity against various cancer cell lines, showed a stronger DNA binding than cisplatin and led to mitochondrial damage, a formation of reactive oxygen species, and a cell cycle arrest in the G2/M phase of cancer cells.

There is still a lot of research devoted to this compound(SMILES:C1(CC2=CNC3=C2C=CC=C3)=CNC4=C1C=CC=C4)Application In Synthesis of 3,3′-Diindolylmethane, and with the development of science, more effects of this compound(1968-05-4) can be discovered.

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Chemistry Milestones Of 1968-05-4

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In general, if the atoms that make up the ring contain heteroatoms, such rings become heterocycles, and organic compounds containing heterocycles are called heterocyclic compounds. An article called Incorporation of 3,3′-Diindolylmethane into Nanocapsules Improves Its Photostability, Radical Scavenging Capacity, and Cytotoxicity Against Glioma Cells, published in 2019-02-28, which mentions a compound: 1968-05-4, Name is 3,3′-Diindolylmethane, Molecular C17H14N2, Related Products of 1968-05-4.

3,3′-Diindolylmethane (DIM) is a phytochem. that presents health benefits (antitumor, antioxidant, and anti-inflammatory effects). However, it is water insoluble and thermo- and photolabile, restraining its pharmaceutical applications. As a strategy to overcome such limitations, this study aimed the development and characterization of DIM-loaded nanocapsules (NCs) prepared with different compositions as well as the in vitro assessment of scavenging activity and cytotoxicity. The formulations were obtained using the interfacial deposition of preformed polymer method and were composed by Eudragit RS100 or ethylcellulose as polymeric wall and primula or apricot oil as the core. All the formulations had adequate physicochem. characteristics: nanometric size (around 190 nm), low polydispersity index (< 0.2), pH value at acid range, high values of zeta potential, drug content, and encapsulation efficiency (∼ 100%). Besides, nanoencapsulation protected DIM against UVC-induced degradation and increased the scavenging activity assessed by the 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) and 1-1-diphenyl-2-picrylhydrazyl methods. The developed DIM-loaded nanocapsules were further evaluated regarding the in vitro release profile and cytotoxicity against a human glioblastoma cell line (U87 cells). The results demonstrated that the nanoencapsulation promoted a sustained release of the bioactive compound (in the range of 58-78% after 84 h) in comparison to its free form (86% after 12 h), as well as provided a superior cytotoxic effect against the U87 cells in the highest concentrations Therefore, our results suggest that nanoencapsulation could be a promising approach to overcome the DIM physicochem. limitations and potentialize its biol. properties. There is still a lot of research devoted to this compound(SMILES:C1(CC2=CNC3=C2C=CC=C3)=CNC4=C1C=CC=C4)Related Products of 1968-05-4, and with the development of science, more effects of this compound(1968-05-4) can be discovered.

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Little discovery in the laboratory: a new route for 1968-05-4

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Related Products of 1968-05-4. So far, in addition to halogen atoms, other non-metallic atoms can become part of the aromatic heterocycle, and the target ring system is still aromatic. Compound: 3,3′-Diindolylmethane, is researched, Molecular C17H14N2, CAS is 1968-05-4, about Indole-3-carbinol derivative DIM mitigates carbon tetrachloride-induced acute liver injury in mice by inhibiting inflammatory response, apoptosis and regulating oxidative stress.

3,3′-Diindolylmethane (DIM), a metabolic product of indole-3-carbinol extracted from cruciferous vegetables exhibits anti-inflammatory and anti-cancer properties. Earlier, the product has been demonstrated to possess anti-fibrotic properties; however, its protective effects on liver injury have not been clearly elucidated. In this study, we postulated the effects and mol. mechanisms of action of DIM on carbon tetrachloride (CCl4)-induced liver injury in mice. Acute liver injury was induced by a single i.p. administration of CCl4 (1 mL/kg) into mice. DIM was injected via s.c. route for three days at various doses (2.5, 5 and 10 mg/kg) before CCl4 injection. Mice were sacrificed and serum was collected for quantification of serum transaminases. The liver was collected and weighed. Treatment with DIM significantly reduced serum transaminases levels (AST and ALT), tumor necrosis factor-α (TNF-α) and reactive oxygen species (ROS). CCl4- induced apoptosis was inhibited by DIM treatment by the reduction in the levels of cleaved caspase-3 and Bcl2 associated X protein (Bax). DIM treated mice significantly restored Cytochrome P 450 2E1, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression in CCl4 treated mice. In addition, DIM downregulated overexpression of hepatic nuclear factor kappa B (NF-κB) and inhibited CCl4 mediated apoptosis. Our results suggest that the protective effects of DIM against CCl4- induced liver injury are due to the inhibition of ROS, reduction of pro-inflammatory mediators and apoptosis.

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Chemical Properties and Facts of 1968-05-4

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Computed Properties of C17H14N2. Aromatic heterocyclic compounds can also be classified according to the number of heteroatoms contained in the heterocycle: single heteroatom, two heteroatoms, three heteroatoms and four heteroatoms. Compound: 3,3′-Diindolylmethane, is researched, Molecular C17H14N2, CAS is 1968-05-4, about Pentafluorophenyl substitution of natural di(indol-3-yl)methane strongly enhances growth inhibition and apoptosis induction in various cancer cell lines. Author is Ahmad, Aamir; Dandawate, Prasad; Schruefer, Sebastian; Padhye, Subhash; Sarkar, Fazlul H.; Schobert, Rainer; Biersack, Bernhard.

Di(indol-3-yl)methane (=3,3′-methanediyldi(1H-indole), DIM, (1)) is a known weakly antitumoral compound formed by digestion of indole-3-carbinol (=1H-indol-3-ylmethanol), an ingredient of various Brassica vegetables. Out of a series of nine fluoroaryl derivatives of 1, three pentafluorophenyl derivatives 2c, 2h, and 2i were identified that exhibited a two to five times greater anti-proliferative effect and an increased apoptosis induction when compared with 1 in the following carcinoma cell lines: BxPC-3 pancreas, LNCaP prostate, C4-2B prostate, PC3 prostate and the triple-neg. MDA-MB-231 breast carcinoma. Compound 2h was particularly efficacious against androgen-refractory C4-2B prostate cancer cells (IC50=6.4 μM) and 2i against androgen-responsive LNCaP cells (IC50=6.2 μM). In addition, 2c and 2h exhibited distinct activity in three cancer cell lines resistant to 1.

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The preparation of ester heterocycles mostly uses heteroatoms as nucleophilic sites, which are achieved by intramolecular substitution or addition reactions. Compound: 3,3′-Diindolylmethane( cas:1968-05-4 ) is researched.Application In Synthesis of 3,3′-Diindolylmethane.Tsao, Chih-Wei; Li, Jia-Sin; Lin, Ya-Wen; Wu, Sheng-Tang; Cha, Tai-Lung; Liu, Chin-Yu published the article 《Regulation of carcinogenesis and mediation through Wnt/β-catenin signaling by 3,3-diindolylmethane in an enzalutamide-resistant prostate cancer cell line》 about this compound( cas:1968-05-4 ) in Scientific Reports. Keywords: enzalutamide Wnt diindolylmethane prostate cancer cell carcinogenesis. Let’s learn more about this compound (cas:1968-05-4).

Enzalutamide (ENZ) is an important drug used to treat castration-resistant prostate cancer (CRPC), which inhibits androgen receptor (AR) signaling. Previous study showed that 3,3-diindolylmethane (DIM) is an AR antagonist that also inhibits Wnt signaling and epithelial-mesenchymal transition (EMT). To investigate whether combined treatment with ENZ and DIM can overcome ENZ resistance by regulating Wnt signaling to inhibit AR signaling and EMT in ENZ-resistant prostate cancer cells, 22Rv1 cells were cultured in normal medium and treated with ENZ, DIM, and DIM with ENZ. Exposure of ENZ-resistant cells to both DIM and ENZ significantly inhibited cell proliferation without cytotoxicity and invasion in comparison with the control. DIM significantly increased the E-cadherin expression and inhibited the expressions of Vimentin and Fibronectin, subsequently inhibiting EMT. Co-treatment with ENZ and DIM significantly increased the expressions of GSK3β and APC and decreased the β-catenin protein expression, causing inhibition of Wnt signaling and AR expression, it also significantly decreased the AR-v7 expression and down-regulated AR signaling. Via suppression of Wnt and AR signaling, co-treatment increased the E-cadherin and decreased the Vimentin and Fibronectin RNA and protein expressions, then inhibited EMT. Co-treatment with DIM and ENZ regulated Wnt signaling to reduce not only the AR expression, but also the AR-v7 expression, indicating suppression of EMT that inhibits cancer cell proliferation, invasion and migration to ameliorate ENZ resistance.

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