Category: 41270-96-6

De Bie, Dick A. published the artcilePhotoreactivity of diazines. III. Pyrimidines. XXXVIII. Photoamination of halopyrimidines, Quality Control of 41270-96-6, the publication is Journal of the Chemical Society, Perkin Transactions 1: Organic and Bio-Organic Chemistry (1972-1999) (1974), 1363-5, database is CAplus.

4-Amino-6-phenylpyrimidine was prepared by uv-induced amination of 4-halo-6-phenylpyrimidines in liquid NH3. A pyrimidinyl radical was formed by cleavage of C-halogen bonds. The order of reactivity was I > Br > Cl. 4-Phenylpyrimidine was also formed from the iodo and bromo compounds

Journal of the Chemical Society, Perkin Transactions 1: Organic and Bio-Organic Chemistry (1972-1999) published new progress about 41270-96-6. 41270-96-6 belongs to iodides-buliding-blocks, auxiliary class Pyrimidine,Iodide,Benzene,Immunology/Inflammation,MIF, name is 4-Iodo-6-phenylpyrimidine, and the molecular formula is C10H7IN2, Quality Control of 41270-96-6.

Referemce:
https://en.wikipedia.org/wiki/Iodide,
Iodide – an overview | ScienceDirect Topics – ScienceDirect.com

Bozzi, Fabio published the artcileMIF/CD74 axis is a target for novel therapies in colon carcinomatosis, HPLC of Formula: 41270-96-6, the publication is Journal of Experimental & Clinical Cancer Research (2017), 16/1-16/15, database is CAplus and MEDLINE.

Background: Strategies aimed at obtaining a complete cytoredn. are needed to improve long-term survival for patients with colorectal cancer peritoneal carcinomatosis (CRC-pc). Methods: We established organoid models from peritoneal metastases of two naïve CRC patients. A standard paraffin inclusion was conducted to compare their 3D structure and immunohistochem. profile with that of the corresponding surgical samples. RNA expression levels of the CRC stem cell marker LGR5 was measured by in situ hybridization. The secretome of organoids was profiled by mass spectrometry. Energy homeostasis of organoids was interfered with 4-IPP and metformin. Biochem. and metabolic changes after drug treatments were investigated by western blot and mass spectrometry. Mitochondria impairment was evaluated by electron microscopy and mitotraker staining. Results: The two organoids recapitulated their corresponding clin. samples in terms of 3D structure and immmunoistochem. profile and were pos. for the cancer stem cells marker LGR5. Proteomic analyses of organoids highlighted their strong dependence on energy producing pathways, which suggest that their targeting could be an effective therapeutic approach. To test this hypothesis, we treated organoids with two drugs that target metabolism acting on AMP-activated protein kinase (AMPK), the main regulator of cellular energy homeostasis, which may act as metabolic tumor suppressor in CRC. Organoids were treated with 4-IPP, an inhibitor of MIF/CD74 signalling axis which activates AMPK function, or metformin that inhibits mitochondrial respiratory chain complex I. As a new finding we observed that treatment with 4-IPP downregulated AMPK signalling activity, reduced AKT phosphorylation and activated a JNK-mediated stress-signalling response, thus generating mitochondrial impairment and cell death. Metformin treatment enhanced AMPK activation, decreasing the activity of the anabolic factors ribosomal protein S6 and p4EBP-1 and inducing mitochondrial depolarization. Conclusions: We provide evidence that the modulation of AMPK activity may be a strategy for targeting metabolism of CRC-pc organoids.

Journal of Experimental & Clinical Cancer Research published new progress about 41270-96-6. 41270-96-6 belongs to iodides-buliding-blocks, auxiliary class Pyrimidine,Iodide,Benzene,Immunology/Inflammation,MIF, name is 4-Iodo-6-phenylpyrimidine, and the molecular formula is C10H7IN2, HPLC of Formula: 41270-96-6.

Referemce:
https://en.wikipedia.org/wiki/Iodide,
Iodide – an overview | ScienceDirect Topics – ScienceDirect.com

Kindt, Nadege published the artcilePharmacological inhibition of macrophage migration inhibitory factor interferes with the proliferation and invasiveness of squamous carcinoma cells, HPLC of Formula: 41270-96-6, the publication is International Journal of Oncology (2013), 43(1), 185-193, database is CAplus and MEDLINE.

Recent clin. observations and exptl. studies of our group indicate that macrophage migration inhibitory factor (MIF) may contribute to tumor progression in head and neck squamous cell carcinomas (HNSCC). The present study was undertaken to examine the effects of the irreversible MIF inhibitor 4-iodo-6-phenylpyrimidine (4-IPP) on proliferation and invasiveness of the squamous carcinoma cell line SCCVII. Cell counting, crystal violet assay and flow cytometry were used to analyze the effects of 4-IPP on SCCVII cell growth. The impact of 4-IPP on cell invasiveness was assessed by Boyden chamber assay. Knockdown of the MIF receptor CD74 was achieved by transduction with lentiviral vectors encoding anti-CD74 shRNAs. As shown by immunofluorescence staining, SCCVII cells express both MIF and CD74. Decreased MIF immunoreactivity as a result of exposure to 4-IPP suggested a covalent modification of the cytokine. 4-IPP inhibited SCCVII cell proliferation and invasiveness. Moreover, the cytostatic effect of 4-IPP was enhanced by CD74 knockdown. The inhibitory effects of 4-IPP on cell proliferation and invasiveness strongly suggest that MIF is involved in proliferative activity and invasive properties of squamous carcinoma cells. In conclusion, MIF inhibition may open possibilities for target-directed treatment of head and neck squamous cell carcinoma.

International Journal of Oncology published new progress about 41270-96-6. 41270-96-6 belongs to iodides-buliding-blocks, auxiliary class Pyrimidine,Iodide,Benzene,Immunology/Inflammation,MIF, name is 4-Iodo-6-phenylpyrimidine, and the molecular formula is C10H7IN2, HPLC of Formula: 41270-96-6.

Referemce:
https://en.wikipedia.org/wiki/Iodide,
Iodide – an overview | ScienceDirect Topics – ScienceDirect.com

Lee, Shin Heon published the artcileMacrophage migration inhibitory factor (MIF) inhibitor 4-IPP downregulates stemness phenotype and mesenchymal trans-differentiation after irradiation in glioblastoma multiforme, Product Details of C10H7IN2, the publication is PLoS One (2021), 16(9), e0257375, database is CAplus and MEDLINE.

Radiation therapy is among the most essential treatment methods for glioblastoma multiforme (GBM). Radio-resistance and cancer stem cell properties can cause therapeutic resistance, cancer heterogeneity, and poor prognoses in association with GBM. Furthermore, the GBM subtype transition from proneural to the most malignant mesenchymal subtype after radiation therapy also accounts for high resistance to conventional treatments. Here, we demonstrate that the inhibition of macrophage migration inhibitory factor (MIF) and D-dopachrome tautomerase (DDT) by 4-iodo-6-phenylpyrimidine (4-IPP), a dual inhibitor targeting MIF and DDT, downregulates stemness phenotype, intracellular signaling cascades, mesenchymal trans-differentiation, and induces apoptosis in proneural glioma stem cells (GSCs). In an anal. of The Cancer Genome Atlas, high MIF and DDT expression were associated with poor prognosis. GSC growth was effectively inhibited by 4-IPP in a time- and dose-dependent manner, and 4-IPP combined with radiation therapy led to significantly reduced proliferation compared with radiation therapy alone. The expression of stemness factors, such as Olig2 and SOX2, and the expression of pAKT, indicating PI3K signaling pathway activation, were decreased in association with both 4-IPP monotherapy and combination treatment. The expression of mesenchymal markers, TGM2 and NF-κB, and expression of pERK (indicating MAPK signaling pathway activation) increased in association with radiation therapy alone but not with 4-IPP monotherapy and combination therapy. In addition, the combination of 4-IPP and radiation therapy significantly induced apoptosis compared to the monotherapy of 4-IPP or radiation. In vivo results demonstrated a significant tumor-suppressing effect of 4-IPP when combined with radiation therapy. Collectively, our results showed that the targeted inhibition of MIF and DDT has the potential to strengthen current clin. strategies by enhancing the anticancer effects of radiation therapy.

PLoS One published new progress about 41270-96-6. 41270-96-6 belongs to iodides-buliding-blocks, auxiliary class Pyrimidine,Iodide,Benzene,Immunology/Inflammation,MIF, name is 4-Iodo-6-phenylpyrimidine, and the molecular formula is C10H7IN2, Product Details of C10H7IN2.

Referemce:
https://en.wikipedia.org/wiki/Iodide,
Iodide – an overview | ScienceDirect Topics – ScienceDirect.com