产品说明书

GANT 58

Print
Chemical Structure| 64048-12-0 同义名 : NSC 75503
CAS号 : 64048-12-0
货号 : A430364
分子式 : C24H16N4S
纯度 : 99%+
分子量 : 392.476
MDL号 : MFCD01103196
存储条件:

粉末 Keep in dark place,Sealed in dry,2-8°C

液体 -20°C:3-6个月-80°C:12个月

溶解度 :

DMSO: 8 mg/mL(20.38 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

无水乙醇: 20 mg/mL(50.96 mM),配合低频超声助溶,注意:无水乙醇开封后,易挥发,也会吸收空气中的水分,导致溶解能力下降,请避免使用开封较久的乙醇

动物实验配方:
生物活性
描述 Glioma-associated oncogene homolog 1 (GLI1) is an amplified gene in human glioblastoma cells. It is a krupple like transcription factor, belonging to the zinc finger family. The basic function of GLI1 is normal neural development at various stages of human[3].GANT58 (NSC75503) has been shown to inhibit transcriptional activation by GLI1 (as well as by the other GLI species). GANT58 has been shown to inhibit GLI transactivation[4].GANT 58 (NSC 75503) is a potent GLI antagonist that inhibits GLI1-induced transcription with IC50 of 5 μM. Nude mice are treated with every second-day s.c. injections at a concentration of 50 mg/kg of cyclopamine, GANT61, GANT58, or solvent only (n=4-5 for each group). Although mice treated with these compounds showed no such signs of toxicity, this protocol is also introduced for the GANTs to be able to compare all compounds. All injections are done 2-3 cm away from the tumors. Suppression of tumor cell growth is observed for all compounds, during an 18-day treatment period. Treatment with cyclopamine or GANT58 results in the inhibition of additional xenograft growth and limited the increase in tumor size[5].GANT-58 at 5μM significantly abolished oxytocin-induced mRNA and protein expression of HIF-1α, while the nuclear abundance of Gli1 was significantly reduced by atosiban at 10μM, but was increased by oxytocin at 0.1μM in human umbilical vein endothelial cells(HUVECs). GANT-58 at 5μM also significantly abolished oxytocin-enhanced angiogenic properties of HUVECs[6].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.55mL

0.51mL

0.25mL

12.74mL

2.55mL

1.27mL

25.48mL

5.10mL

2.55mL

参考文献

[1]Joo J, Christensen L, et al. GLI1 is a central mediator of EWS/FLI1 signaling in Ewing tumors. PLoS One. 2009 Oct 27;4(10):e7608.

[2]Lauth M, Bergstrom A, et al. Inhibition of GLI-mediated transcription and tumor cell growth by small-molecule antagonists. Proc Natl Acad Sci U S A. 2007 May 15;104(20):8455-60. Epub 2007 May 9.

[3]Prasuja Rokkam,et al. Prognostic Role of Hedgehog-GLI1 Signaling Pathway in Aggressive and Metastatic Breast Cancers. Curr Drug Metab. 2020;21(1):33-43.

[4] Joo J, et al. GLI1 is a central mediator of EWS/FLI1 signaling in Ewing tumors. PLoS One. 2009 Oct 27;4(10):e7608.

[5] Lauth M, et al. Inhibition of GLI-mediated transcription and tumor cell growth by small-molecule antagonists. Proc Natl Acad Sci U S A. 2007 May 15;104(20):8455-60.

[6]Ji Zhu,et al. Regulation of angiogenic behaviors by oxytocin receptor through Gli1-indcued transcription of HIF-1α in human umbilical vein endothelial cells. Biomed Pharmacother. 2017 Jun;90:928-934.