scholarly journals 1-Phenyl-8-[[4-(pyrrolo[1,2-a]quinoxalin-4-yl)phenyl]methyl]-1,3,8-triazaspiro[4.5]decan-4-one: Synthesis, Crystal Structure and Anti-Leukemic Activity

Molbank ◽  
10.3390/m1113 ◽  
2020 ◽  
Vol 2020 (1) ◽  
pp. M1113
Author(s):  
Jean Guillon ◽  
Solène Savrimoutou ◽  
Sandra Rubio ◽  
Stéphane Moreau ◽  
Noël Pinaud ◽  
...  

1-Phenyl-8-[[4-(pyrrolo[1,2-a]quinoxalin-4-yl)phenyl]methyl]-1,3,8-triazaspiro[4.5]decan-4-one has been successfully synthesized via a multi-step pathway starting from 2-nitroaniline. Structure characterization of this original pyrrolo[1,2-a]quinoxaline derivative was achieved by FT-IR, 1H-NMR, 13C-NMR, X-Ray and HRMS spectral analysis. This title compound shows interesting cytotoxic potential against several human leukemia cell lines (K562, HL60, and U937 cells).


Molbank ◽  
10.3390/m1023 ◽  
2018 ◽  
Vol 2018 (4) ◽  
pp. M1023 ◽  
Author(s):  
Jean Guillon ◽  
Solène Savrimoutou ◽  
Sandra Rubio ◽  
Vanessa Desplat

The 1-methyl-3-{4-[(4-(2-oxo-2,3-dihydro-1H-benzimidazol-1-yl)piperidin-1-yl)benzyl]}-2-phenylindole compound has been successfully synthesized via a multistep pathway starting from 2-phenylindole. Structure characterization of this new indole derivative was done by FTIR, 1H-NMR, 13C-NMR, and HRMS spectral analysis. The title compound showed high cytotoxic potential against five leukemia cell lines (K562, HL60, U937, U266, and Jurkat cell lines).



Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2073
Author(s):  
Jing-Ting Chiou ◽  
Liang-Jun Wang ◽  
Yuan-Chin Lee ◽  
Long-Sen Chang

This study aimed to investigate the mechanistic pathway of Naja atra (Taiwan cobra) cardiotoxin 1 (CTX1)–induced death of leukemia cell lines U937 and HL-60. CTX1 increased cytoplasmic Ca2+ and reactive oxygen species (ROS) production, leading to the death of U937 cells. It was found that Ca2+-induced NOX4 upregulation promoted ROS-mediated p38 MAPK phosphorylation, which consequently induced c-Jun and ATF-2 phosphorylation. Using siRNA knockdown, activated c-Jun and ATF-2 were demonstrated to regulate the expression of Fas and FasL, respectively. Suppression of Ca2+-mediated NOX4 expression or ROS-mediated p38 MAPK activation increased the survival of U937 cells exposed to CTX1. FADD depletion abolished CTX1-induced cell death, caspase-8 activation, and t-Bid production, supporting the correlation between the Fas death pathway and CTX1-mediated cytotoxicity. Among the tested N. atra CTX isotoxins, only CTX1 induced Fas and FasL expression. Chemical modification studies revealed that intact Met residues were essential for the activity of CTX1 to upregulate Fas and FasL expression. Taken together, the data in this study indicate that CTX1 induces c-Jun-mediated Fas and ATF-2-mediated FasL transcription by the Ca2+/NOX4/ROS/p38 MAPK axis, thereby activating the Fas death pathway in U937 cells. Furthermore, CTX1 activates Fas/FasL death signaling in the leukemia cell line HL-60.



APOPTOSIS ◽  
2004 ◽  
Vol 9 (4) ◽  
pp. 429-435 ◽  
Author(s):  
M. Tsuruga ◽  
H. Nakajima ◽  
S. Ozawa ◽  
M. Togashi ◽  
Y.-C. Chang ◽  
...  


2016 ◽  
Vol 45 (26) ◽  
pp. 10696-10707 ◽  
Author(s):  
Manuel I. Velasco ◽  
Claudio R. Krapacher ◽  
Rita H. de Rossi ◽  
Laura I. Rossi

The characterization of non-crystalline complexes is very difficult when techniques like X-ray diffraction or NMR are not available. We propose a simple procedure to characterize the physicochemical properties of amorphous new coordination compounds between cyclodextrins (CD) and Cu2+ salts, by several techniques as TGA, FT-IR, EPR.



1987 ◽  
Vol 7 (10) ◽  
pp. 3656-3662 ◽  
Author(s):  
T P Mäkelä ◽  
R Alitalo ◽  
Y Paulsson ◽  
B Westermark ◽  
C H Heldin ◽  
...  

We studied the expression of the genes encoding the A and B chains of platelet-derived growth factor (PDGF) in a number of human leukemia cell lines. Steady-state expression of the A-chain RNA was seen only in the promonocytic leukemia cell line U937 and in the T-cell leukemia cell line MOLT-4. It has previously been reported that both PDGF A and PDGF B genes are induced during megakaryoblastic differentiation of the K562 erythroleukemia cells and transiently during monocytic differentiation of the promyelocytic leukemia cell line HL-60 and U937 cells. In this study we show that PDGF A RNA expression was induced in HL-60 and Jurkat T-cell leukemia cells and increased in U937 and MOLT-4 cells after a 1- to 2-h stimulation with an 8 pM concentration of transforming growth factor beta (TGF-beta). PDGF A RNA remained at a constant, elevated level for at least 24 h in U937 cells, but returned to undetectable levels within 12 h in HL-60 cells. No PDGF A expression was induced by TGF-beta in K562 cells or in lung carcinoma cells (A549). Interestingly, essentially no PDGF B-chain (c-sis proto-oncogene) RNA was expressed simultaneously with PDGF A. In the presence of TGF-beta and protein synthesis inhibitors, PDGF A RNA was superinduced at least 20-fold in the U937 and HL-60 cells. PDGF A expression was accompanied by secretion of immunoprecipitable PDGF to the culture medium of HL-60 and U937 cells. The phorbol ester tumor promoter tetradecanoyl phorbol acetate also increased PDGF A expression with similar kinetics, but with a mechanism distinct from that of TGF-beta. These results suggest a role for TGF-beta in the differential regulation of expression of the PDGF genes.



1987 ◽  
Vol 7 (10) ◽  
pp. 3656-3662
Author(s):  
T P Mäkelä ◽  
R Alitalo ◽  
Y Paulsson ◽  
B Westermark ◽  
C H Heldin ◽  
...  

We studied the expression of the genes encoding the A and B chains of platelet-derived growth factor (PDGF) in a number of human leukemia cell lines. Steady-state expression of the A-chain RNA was seen only in the promonocytic leukemia cell line U937 and in the T-cell leukemia cell line MOLT-4. It has previously been reported that both PDGF A and PDGF B genes are induced during megakaryoblastic differentiation of the K562 erythroleukemia cells and transiently during monocytic differentiation of the promyelocytic leukemia cell line HL-60 and U937 cells. In this study we show that PDGF A RNA expression was induced in HL-60 and Jurkat T-cell leukemia cells and increased in U937 and MOLT-4 cells after a 1- to 2-h stimulation with an 8 pM concentration of transforming growth factor beta (TGF-beta). PDGF A RNA remained at a constant, elevated level for at least 24 h in U937 cells, but returned to undetectable levels within 12 h in HL-60 cells. No PDGF A expression was induced by TGF-beta in K562 cells or in lung carcinoma cells (A549). Interestingly, essentially no PDGF B-chain (c-sis proto-oncogene) RNA was expressed simultaneously with PDGF A. In the presence of TGF-beta and protein synthesis inhibitors, PDGF A RNA was superinduced at least 20-fold in the U937 and HL-60 cells. PDGF A expression was accompanied by secretion of immunoprecipitable PDGF to the culture medium of HL-60 and U937 cells. The phorbol ester tumor promoter tetradecanoyl phorbol acetate also increased PDGF A expression with similar kinetics, but with a mechanism distinct from that of TGF-beta. These results suggest a role for TGF-beta in the differential regulation of expression of the PDGF genes.



2011 ◽  
Vol 233-235 ◽  
pp. 1809-1813
Author(s):  
Yu Ping Tong ◽  
Chang Li Xiao ◽  
Zhong Zheng Yang ◽  
Lu De Lu ◽  
Hao Bing Fu

The zirconium phosphate α-Zr(HPO4)2·H2O (α-ZrP) with layered structure has been synthesized by refluxing method. Power X-ray diffraction (XRD), vibrational spectroscopy (FT-IR, FT-Raman), thermal analysis (TG-DSC), transition electron spectroscopy (TEM), scanning electron microscopy (SEM) and energy dispersive X-ray spectrometer (EDS) was respectively used for structure characterization of the compound α-ZrP. The result of intercalation reactions with tetramethylammonium bromide and cetyltrimethylammonium bromide showed interlayer distances increase of ~ 0.46 nm and ~ 1.68 nm, respectively. The BET surface area of α-ZrP is 12.29 m2·g-1. The cyclic voltammetry behaviors of the compound on Au electrode showed a typical reversible process. Moreover, the strong fluorescent property of the α-ZrP was measured. The maximum emission peaks occurred at ca. 390 nm upon excitation at ca. 288 nm.



Virology ◽  
2002 ◽  
Vol 303 (1) ◽  
pp. 164-173 ◽  
Author(s):  
Sebastian Patzke ◽  
Mats Lindeskog ◽  
Else Munthe ◽  
Hans-Christian Aasheim


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