NSC5844 (RE-640) is a 4-aminoquinoline derivative, with antitumor and antimalarial activity.
IC50 & Target
Parasite[2]
体外研究 (In Vitro)
NSC5844 (Compound 10) is a 4-aminoquinoline derivative, and has antitumor activity with GI50s of 7.35 ± 0.10 μM and 14.80 ± 0.35 μM against MDA-MB-468 and MCF-7 cells, respectively[1]. NSC5844 (Compound 1) is cytotoxic to P. falciparum, inhibits the growth of chloroquine-sensitive (D-6) and -resistant (W-2) clones of P. falciparum, with IC50s of 17 and 27 nM, respectively[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
383.27
Formula
C20H16Cl2N4
CAS 号
140926-75-6
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Powder
-20°C
3 years
4°C
2 years
In solvent
-80°C
6 months
-20°C
1 month
参考文献
[1]. Zhang H, et al. Synthesis and in vitro cytotoxicity evaluation of 4-aminoquinoline derivatives. Biomed Pharmacother. 2008 Feb;62(2):65-9. Epub 2007 May 24.
[2]. Vennerstrom JL, et al. Bisquinolines. 1. N,N-bis(7-chloroquinolin-4-yl)alkanediamines with potential against chloroquine-resistant malaria. J Med Chem. 1992 May 29;35(11):2129-34.
Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
IC50 & Target[1][2]
Aβ1-40
Aβ1-42
NF-κB
JNK
Human Endogenous Metabolite
体外研究 (In Vitro)
Ginsenoside Re is a well-known traditional Chinese medicine, which decreases the β-site amyloid precursor protein cleaving enzyme 1 (BACE1) mRNA and protein levels and inhibits BACE1 activity in the N2a/APP695 cells. Ginsenoside Re also significantly increases the PPARγ protein and mRNA levels.To prevent Ginsenoside Re from having a cytotoxic effect on the N2a/APP695 cells, the cell viability is first determined by the MTT assay. The N2a/WT and N2a/APP695 cells are treated with increasing concentrations of Ginsenoside Re (0-200 µM) for 24 h. Ginsenoside Re concentrations under 100 µM do not affect the viability of the N2a/WT and N2a/APP695 cells, whereas the 150 µM Ginsenoside Re concentration markedly decreases the survival rate of the N2a/WT and N2a/APP695 cells. Incubation with Ginsenoside Re at a 200 µM concentration for 24 h reduces the viability of the N2a/WT and N2a/APP695 cells by 15.58% and 26.82%, respectively. These data indicate that Ginsenoside Re treatment within the range of 0-100 µM for 24 h is safe for the N2a/WT and N2a/APP695 cells (P>0.05)[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Ginsenoside Re reduces insulin resistance in 3T3-L1 adipocytes and high-fat diet (HFD) rats through inhibition of JNK and NF-κB activation[2]. Intraperitoneal injection of lipopolysaccharide (LPS) at a dose of 20 mg/kg is lethal to mice, and 70% to 80% of the mice die within 60 h. However, pretreatment of the mice with Rg1 or Ginsenoside Re increases their survival rates in a dose-dependent manner. With the doses of Rg1 or Ginsenoside Re increase from 2.5 to 5 mg/kg, the survival rate is elevated from 60% to 90% (Rg1) or from 30% to 40% (Ginsenoside Re). All the mice administered Rg1 at a minimal dose of 10 mg/kg are protected from death compared to 80% survival of mice treated with an equal dose of Ginsenoside Re. To protect all the mice, 20 mg/kg Ginsenoside Re is needed. To investigate the anti-inflammatory potential of Rg1 and Ginsenoside Re, 1 mg/kg Rg1 or Ginsenoside Re is injected into rats and then challenged the animals with LPS. The injection procedure itself causes a transient stress-induced increase in body temperature of ~1.2°C in each group. Thereafter, LPS-challenged rats without pretreatment develope a robust biphasic fever, with the first peak reaching ~1.5°C at 2 h and the second peak reaching 1.8°C at 4 h. In contrast, the temperature changes for the Rg1-, Ginsenoside Re-, and TAK-242-treated groups are only 0.9, 1.2, and 0.8°C at 2 h and 1.3, 1.4, and 1.0°C at 4 h, respectively. Pretreatment with Rg1, Ginsenoside Re, or TAK-242 significantly attenuates LPS-induced alterations in body temperature[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
947.15
Formula
C48H82O18
CAS 号
52286-59-6
中文名称
人参皂苷 Re
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Cao G, et al. Ginsenoside Re reduces Aβ production by activating PPARγ to inhibit BACE1 in N2a/APP695 cells. Eur J Pharmacol. 2016 Dec 15;793:101-108.
[2]. Su F, et al. Protective effect of ginsenosides Rg1 and Re on lipopolysaccharide-induced sepsis by competitive binding to Toll-like receptor 4. Antimicrob Agents Chemother. 2015 Sep;59(9):5654-63.
[3]. Zhang Z, et al. Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB. Mol Endocrinol. 2008 Jan;22(1):186-95.
Cell Assay [1]
To explore the cytotoxic effect of Ginsenoside Re on N2a/APP695 cells, cell proliferation is assessed using the MTT assay. The cells are treated with increasing doses of Ginsenoside Re (0, 25, 50, 100, 150, and 200 µM) for 24 h. The MTT assay is performed after the treatments. The cells are incubated for 4 h at 37 °C with 0.5 mg/mL of MTT dissolved in fresh complete medium. The dark blue formazan crystals are dissolved in DMSO, and the absorbance is measured on a microplate reader using a reference wavelength of 630 nm and a test wavelength of 490 nm. The data are expressed as the mean percentages of viable cells versus the control[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [3]
Mice[3] To examine the prophylactic effect of Rg1 and Ginsenoside Re on LPS-induced lethality, 6- to 8-week-old BALB/c mice are randomly assigned to 7 groups with 10 mice in each group. The mice are either left untreated or subcutaneously injected with 2.5, 5, 10, or 20 mg/kg Rg1, 20 mg/kg Ginsenoside Re, or 5 mg/kg TAK-242 3 times at 30-min intervals and then challenged with LPS (20 mg/kg) 15 min later. To test the therapeutic effect of Rg1 and Ginsenoside Re on LPS-induced lethality, BALB/c mice are assigned to 5 groups with 10 mice in each group. The mice are injected intraperitoneally (i.p.) with 20 mg/kg LPS. Fifteen minutes later, mice are subcutaneously injected with 10 mg/kg Rg1, 20 mg/kg Ginsenoside Re, or 5 mg/kg TAK-242 3 times at 30-min intervals or left untreated. Survival rates are recorded for 60 h. Rats[3] Sprague Dawley rats are intravenously administered saline solution, 1 mg of Rg1/kg body weight (1 mg/kg Rg1), 1 mg/kg Ginsenoside Re, or 1 mg/kg TAK-242. Fifteen minutes later, rats are challenged with 2.5 μg/kg LPS. Body temperature is measured before and after drug administration. Anticoagulated blood samples with EDTA are collected for white blood cell (WBC) counts at indicated time points using a ProCyte Dx automatic blood cell analyzer. Additional blood samples are collected at 4 h post-drug injection and used for preparation of serum to analyze proinflammatory mediators. The proinflammatory cytokine responses are detected by Western blot assay.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Cao G, et al. Ginsenoside Re reduces Aβ production by activating PPARγ to inhibit BACE1 in N2a/APP695 cells. Eur J Pharmacol. 2016 Dec 15;793:101-108.
[2]. Su F, et al. Protective effect of ginsenosides Rg1 and Re on lipopolysaccharide-induced sepsis by competitive binding to Toll-like receptor 4. Antimicrob Agents Chemother. 2015 Sep;59(9):5654-63.
[3]. Zhang Z, et al. Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB. Mol Endocrinol. 2008 Jan;22(1):186-95.
JH-RE-06, a potent REV1-REV7 interface inhibitor (IC50=0.78 μM; Kd=0.42 μM), targets REV1 that interacts with the REV7 subunit of POLζ. JH-RE-06 disrupts mutagenic translesion synthesis (TLS) by preventing recruitment of mutagenic POLζ. JH-RE-06 improves chemotherapy[1][2].
JH-RE-06 unexpectedly induces dimerization of the REV1 CTD at its REV7-binding surface and blocks the REV1-REV7 interaction[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
JH-RE-06 inhibits mutagenic TLS and enhances cisplatin-induced toxicity in cultured human and mouse cell lines[1]. Co-administration of JH-RE-06 with cisplatin suppresses the growth of xenograft human melanomas in mice[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
468.72
Formula
C20H16Cl3N3O4
CAS 号
1361227-90-8
运输条件
Room temperature in continental US; may vary elsewhere.