Furamidine (hydrochloride)
(Synonyms: 呋喃脒二盐酸盐,DB75 dihydrochloride; NSC 305831 dihydrochloride) 目录号 : GC43715A selective PRMT1 inhibitor and antiprotozoal agent
Cas No.:55368-40-6
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Furamidine is a cell-permeable inhibitor of protein arginine methyltransferase 1 (PRMT1) that is selective for PRMT1 over PRMT5, PRMT6, and PRMT4/coactivator-associated arginine methyltransferase 1 (CARM1) (IC50s = 9.4, 166, 283, and >400 μM, respectively). In vitro, furamidine (20 μM) inhibits Aly protein methylation in HEK293T cells and growth of several leukemia cell lines. It inhibits tyrosyl-DNA phosphodiesterase (Tdp1) activity on both single- and double-stranded DNA substrates with concentrations in the low micromolar range, but it is more potent against a duplex DNA substrate. Furamidine inhibits growth of T. brucei, the parasite that causes sleeping sickness, with IC50 values of 1.5 to 37 nM across various strains. It inhibits the T. brucei P2 aminopurine transporter (Ki = 1.2 μM). It also binds to AT-rich DNA sequences in trypanosome kinetoplast DNA.
| Cas No. | 55368-40-6 | SDF | |
| 别名 | 呋喃脒二盐酸盐,DB75 dihydrochloride; NSC 305831 dihydrochloride | ||
| Canonical SMILES | NC(C1=CC=C(C2=CC=C(C3=CC=C(C(N)=N)C=C3)O2)C=C1)=N.Cl.Cl | ||
| 分子式 | C18H16N4O•2HCl | 分子量 | 377.3 |
| 溶解度 | DMF: 0.5 mg/ml,DMSO: 5 mg/ml,Ethanol: 1 mg/ml,PBS (pH 7.2): Partially soluble | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.6504 mL | 13.2521 mL | 26.5041 mL |
| 5 mM | 0.5301 mL | 2.6504 mL | 5.3008 mL |
| 10 mM | 0.265 mL | 1.3252 mL | 2.6504 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Comparison of EMT mediated tyrosine kinase inhibitor resistance in NSCLC
Biochem Biophys Res Commun 2018 Feb 5;496(2):770-777.PMID:29337056DOI:PMC5801208
In the United States, lung cancer is the second most common cancer in men and women. In 2017, 222,500 new cases and 155,870 deaths from lung cancer are estimated to have occurred. A tyrosine kinase receptor, epidermal growth factor receptor (EGFR), is over expressed or mutated in non-small cell lung cancer (NSCLC) resulting in increased cell proliferation and survival. Tyrosine kinase inhibitors (TKIs) are currently being used as therapy for NSCLC patients, however, they have limited efficacy in NSCLC patients due to acquisition of resistance. This study investigates the role of epithelial-mesenchymal transition (EMT) in the development of resistance against TKIs in NSCLC. Currently, the role of p120-catenin, Kaiso factor and PRMT-1 in reversal of EMT in T790M mutated and TKI-resistant NSCLC cells is a new line of study. In this investigation we found upregulation of cytoplasmic p120-catenin, which was co-localized with Kaiso factor. In the nucleus, binding of p120-catenin to Kaiso factor initiates transcription by activating EMT-transcription factors such as Snail, Slug, Twist, and ZEB1. PRMT-1 was also found to be upregulated, which induces methylation of Twist and repression of E-cadherin activity, thus promoting EMT. We confirmed that TKI-resistant cells have mesenchymal cell type characteristics based on their cell morphology and gene or protein expression of EMT related proteins. EMT proteins, Vimentin and N-cadherin, displayed increased expression, whereas E-cadherin expression was downregulated. Finally, we found that the knockdown of p120-catenin and PRMT-1 by siRNA or use of a PRMT-1 inhibitor Furamidine increased Erlotinib sensitivity and could reverse EMT to overcome TKI resistance.