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产品名称 | AhR ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
StemRegenin 1 |
++
Aryl hydrocarbon receptor (AhR), IC50: 127 nM |
99%+ | |||||||||||||||||
CH-223191 |
+++
AhR, IC50: 30 nM |
99%+ | |||||||||||||||||
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 |
描述 | GNF351 is an AHR antagonist with an IC50 value of 62 nM. GNF351 has minimal toxicity to mouse or human keratinocytes[1].Treatment of cells with GNF351 at a concentration of 500 nM for 48 hours significantly reduced the percentage of Ki67-positive cells and the number of cells in a proliferative monolayer culture assay of human keratinocytes[1]. |
Concentration | Treated Time | Description | References | |
Primary HFLS-RA cells | 100 nM | 1 h | Inhibits IL1B-induced inflammatory signaling | Ann Rheum Dis. 2013 Oct;72(10):1708-16 |
HN13 cells | 100 nM | 48 hours | Reduction in MMP9 secretion | Mol Cancer Res. 2012 Oct;10(10):1369-79 |
Primary esophageal epithelial cells | 2 μM | 30 minutes | GNF-351 pretreatment was used to evaluate the role of the AHR signaling pathway in PPI-induced transcriptional responses. Results showed that GNF-351 inhibited PPI-induced expression of CYP1A1 and HMOX1 genes, indicating that the AHR signaling pathway plays a partial role in PPI-mediated transcriptional responses. | J Allergy Clin Immunol. 2021 May;147(5):1924-1935 |
EPC2 cells | 2 μM | 30 minutes | GNF-351, a high-affinity antagonist of the AHR signaling pathway, was used to block the transcriptional responses mediated by PPIs through the AHR signaling pathway. Results showed that GNF-351 pretreatment significantly inhibited the PPI-induced expression of CYP1A1 and CYP1B1 genes but had no effect on the induction of MT1H gene. | J Allergy Clin Immunol. 2021 May;147(5):1924-1935 |
human bone-derived mesenchymal stem cells (hBMSCs) | 100 nM | 17 days | To evaluate the impact of TCDD on osteogenic differentiation of hBMSCs. Results showed that 10 nM TCDD consistently attenuated alkaline phosphatase (ALP) activity and matrix mineralization, downregulated osteogenic markers (ALP, OPN, and IBSP), and upregulated FGF9 and FGF18 expression. Coexposure with the AhR antagonist GNF351 blocked TCDD-mediated attenuation of matrix mineralization and partially or fully rescued expression of genes associated with osteogenic regulation. | Toxicol Sci. 2019 Jan 1;167(1):145-156 |
Primary FLS | 500 nM | 1 hours | AHR activation in TCDD-treated COS-1 cells leads to enhanced transcriptional activity of VEGF-A, EREG, and AREG promoters | J Pharmacol Exp Ther. 2014 Feb;348(2):236-45 |
HN2095 cells | 100 nM | 12 hours | Reduction in IL6 transcription and CYP1A1 activity | Mol Cancer Res. 2012 Oct;10(10):1369-79 |
HN30 cells | 100 nM | 24 hours | Reduction in IL6 transcription and CYP1A1 activity | Mol Cancer Res. 2012 Oct;10(10):1369-79 |
K4IM cells | 500 nM | 1 h | Inhibits IL1B-induced inflammatory signaling | Ann Rheum Dis. 2013 Oct;72(10):1708-16 |
Primary HFLS-N cells | 100 nM | 1 h | Inhibits IL1B-induced inflammatory signaling | Ann Rheum Dis. 2013 Oct;72(10):1708-16 |
Mouse intestinal microsomes | 100 μM | 30 minutes | Identification of GNF-351 metabolites, including two oxidized GNF-351 and one tri-demethylated GNF-351 | Br J Pharmacol. 2014 Apr;171(7):1735-46 |
Human intestinal microsomes | 100 μM | 30 minutes | Identification of GNF-351 metabolites, including two oxidized GNF-351 and one tri-demethylated GNF-351 | Br J Pharmacol. 2014 Apr;171(7):1735-46 |
Mouse liver microsomes | 100 μM | 30 minutes | Identification of GNF-351 metabolites, including two oxidized GNF-351 and one tri-demethylated GNF-351 | Br J Pharmacol. 2014 Apr;171(7):1735-46 |
Human liver microsomes | 100 μM | 30 minutes | Identification of GNF-351 metabolites, including two oxidized GNF-351 and one tri-demethylated GNF-351 | Br J Pharmacol. 2014 Apr;171(7):1735-46 |
normal human epidermal keratinocytes | 100 nM | 24 hours | GNF351 inhibited the TCDD-mediated RNA and transcriptional increases | J Invest Dermatol. 2023 Oct;143(10):1964-1972. e4 |
Primary FLS cells from RA patients | 500 nM | 4 hours | GNF351 significantly inhibits IL1B-mediated enhanced expression of EREG, AREG, VEGF-A, and FGF-2 mRNA | J Pharmacol Exp Ther. 2014 Feb;348(2):236-45 |
Primary FLS cells from healthy individuals | 500 nM | 4 hours | GNF351 significantly inhibits IL1B-mediated enhanced expression of EREG, AREG, VEGF-A, and FGF-2 mRNA | J Pharmacol Exp Ther. 2014 Feb;348(2):236-45 |
Huh7 cells | 1 μM | 1-hour pretreatment followed by 6 hours | Evaluate the inhibitory effect of GNF351 on acute-phase gene expression, results showed GNF351 failed to inhibit SAA1 expression | J Pharmacol Exp Ther. 2011 Jul;338(1):318-27 |
H1L1.1.1c2 cells | 100 nM | 4 hours | Evaluate the antagonistic effect of GNF351 on mouse AHR, results showed GNF351 could antagonize TCDD-induced AHR activity | J Pharmacol Exp Ther. 2011 Jul;338(1):318-27 |
HepG2 40/6 cells | 100 nM to 10 μM | 4 hours | Evaluate the agonist activity of GNF351 on AHR, results showed no significant agonist activity was observed in the tested concentration range | J Pharmacol Exp Ther. 2011 Jul;338(1):318-27 |
Administration | Dosage | Frequency | Description | References | ||
Mouse | C57BL/6J mice | Oral | 5 mg/kg | Single dose, observed for 24 hours | Evaluation of GNF-351 absorption and metabolism, results showed GNF-351 was not detected in serum and mostly found in feces | Br J Pharmacol. 2014 Apr;171(7):1735-46 |
计算器 | ||||
存储液制备 | ![]() |
1mg | 5mg | 10mg |
1 mM 5 mM 10 mM |
2.43mL 0.49mL 0.24mL |
12.15mL 2.43mL 1.22mL |
24.30mL 4.86mL 2.43mL |
CAS号 | 1227634-69-6 |
分子式 | C24H25N7 |
分子量 | 411.5 |
SMILES Code | CC1=CN=CC(C2=NC(NCCC3=CNC4=C3C=CC=C4)=C5N=CN(C(C)C)C5=N2)=C1 |
MDL No. | MFCD23726597 |
别名 | |
运输 | 蓝冰 |
InChI Key | ABXIUYMKZDZUDC-UHFFFAOYSA-N |
Pubchem ID | 46216378 |
存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Keep in dark place, inert atmosphere, 2-8°C |
溶解方案 |
DMSO: 120 mg/mL(291.61 mM),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 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
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