NAMI-A
目录号 : GC33045
NAMI-A是一种钌基试剂，其特征在于对肿瘤转移的选择性活性，抑制粘附和迁移。
Cas No.:201653-76-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
NAMI-A is a ruthenium-based drug characterised by the selective activity against tumour metastases, inhibits the adhesion and migration.In vitro: NAMI-A can significantly affect tumor cells with metastatic ability.The half lifetime of NAMI-A elimination from the lungs is longer than for liver, kidney, and primary tumor. NAMI-A bound to collagen is active on tumor cells as shown in vitro by an invasion test, using a modified Boyden chamber and Matrigel, and it inhibits the matrix metallo-proteinases MMP-2 and MMP-9 at micromolar concentrations. [1] The ruthenium drug NAMI-A inhibits the adhesion and migration of colorectal cancer cells. NAMI-A decreases α5β1 integrin expression and FAK auto-phosphorylation on Tyr 397. [2]In vivo: The reference for NAMI-A is 35 mg/kg/day. [1]
[1]. Sava G et al. Dual Action of NAMI-A in inhibition of solid tumor metastasis: selective targeting of metastatic cells and binding to collagen. Clin Cancer Res. 2003 May;9(5):1898-905. [2]. Pelillo C et al. Inhibition of adhesion, migration and of α5β1 integrin in the HCT-116 colorectal cancer cells treated with the ruthenium drug NAMI-A. J Inorg Biochem. 2016 Jul;160:225-35.
| Cas No. | 201653-76-1 | SDF | |
| Canonical SMILES | Cl[Ru](Cl)(Cl)(Cl)(C)[N]1=CNC=C1.O=S(C)C.[-].[H+].C2=CNC=N2 | ||
| 分子式 | C5H10Cl4N2ORuS . C3H4N2 . H | 分子量 | 458.18 |
| 溶解度 | Water : 8.28 mg/mL (18.07 mM) | 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.1825 mL | 10.9127 mL | 21.8255 mL |
| 5 mM | 0.4365 mL | 2.1825 mL | 4.3651 mL |
| 10 mM | 0.2183 mL | 1.0913 mL | 2.1825 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。
NAMI-A and KP1019/1339, Two Iconic Ruthenium Anticancer Drug Candidates Face-to-Face: A Case Story in Medicinal Inorganic Chemistry
Molecules 2019 May 24;24(10):1995.PMID:31137659DOI:10.3390/molecules24101995.
NAMI-A ((ImH)[trans-RuCl4(dmso-S)(Im)], Im = imidazole) and KP1019/1339 (KP1019 = (IndH)[trans-RuCl4(Ind)2], Ind = indazole; KP1339 = Na[trans-RuCl4(Ind)2]) are two structurally related ruthenium(III) coordination compounds that have attracted a lot of attention in the medicinal inorganic chemistry scientific community as promising anticancer drug candidates. This has led to a considerable amount of studies on their respective chemico-biological features and to the eventual admission of both to clinical trials. The encouraging pharmacological performances qualified KP1019 mainly as a cytotoxic agent for the treatment of platinum-resistant colorectal cancers, whereas the non-cytotoxic NAMI-A has gained the reputation of being a very effective antimetastatic drug. A critical and strictly comparative analysis of the studies conducted so far on NAMI-A and KP1019 allows us to define the state of the art of these experimental ruthenium drugs in terms of the respective pharmacological profiles and potential clinical applications, and to gain some insight into the inherent molecular mechanisms. Despite their evident structural relatedness, deeply distinct biological and pharmacological profiles do emerge. Overall, these two iconic ruthenium complexes form an exemplary and unique case in the field of medicinal inorganic chemistry.
The Deceptively Similar Ruthenium(III) Drug Candidates KP1019 and NAMI-A Have Different Actions. What Did We Learn in the Past 30 Years?
Met Ions Life Sci 2018 Feb 5;18:/books/9783110470734/9783110470734-007/9783110470734-011.xml.PMID:29394024DOI:10.1515/9783110470734-011.
The general interest in anticancer metal-based drugs and some encouraging pharmacological results obtained at the beginning of the investigations on innovative Ru-based drugs triggered a lot of attention on NAMI-A and KP1019, the two Ru(III) coordination compounds that are the subject of this review. This great attention led to a considerable amount of scientific results and, more importantly, to their eventual admission into clinical trials. Both complexes share a relatively low systemic toxicity that allows reaching rather high dosages, comparable to those of carboplatin. Soon it became evident that NAMI-A and KP1019, in spite of their structural similarity, manifest very distinct chemical and biological properties. The pharmacological performances qualified KP1019 mainly as a cytotoxic drug for the treatment of platinum-resistant colorectal cancers, whereas NAMI-A gained the reputation of a potential anticancer drug with negligible effects on the primary tumor but a pronounced ability to affect metastases. We believe that a strictly comparative exam of NAMI-A and KP1019, based on the substantial body of studies accomplished since their discovery almost 30 years ago, might be an useful exercise, both for assessing the state of the art in terms of biological and clinical profiles, and of the inherent mechanisms, and for envisaging possible future developments in the light of past achievements.
Evaluation of NAMI-A Cytotoxic Effects toward Leukemia Cell Lines: A Slippery Ground Giving Misleading Messages
Crit Rev Oncog 2021;26(2):73-78.PMID:34347974DOI:10.1615/CritRevOncog.2020036010.
The expansion of metal-based complexes in the last 20 years has been very intense and many metals have been involved. Among the many compounds studied, the ruthenium-based complex NAMI-A embodies the unique paradigm of the ability to selectively inhibiting and preventing the development and the growth of distant metastases originating from solid tumors in all the tumor models on which it has been tested. An activity that can be detected only in vivo since the compound is virtually free of measurable direct cell cytotoxicity in vitro. Recently, a published paper reported on a significant in vitro cytotoxicity against some leukemic cells. The present study was undertaken to reproduce those experiments to further support this novel antileukemic activity that would have put NAMI-A on a new trajectory for development. Our results do not confirm the efficacy of NAMI-A in vitro against the human HL-60 promyelocytic leukemia cell line either using test cultures identical to those reported in the study of reference or in even more stressed conditions, supporting the lack of in vitro direct cell cytotoxicity of NAMI-A. The present study also helps to elucidate that many factors can influence the outcome of in vitro tests of cytotoxicity and suggests caution to speculate on possible therapeutic properties based on the results of simple and reductive in vitro tests of cytotoxicity.
NAMI-A preferentially reacts with the Sp1 protein: understanding the anti-metastasis effect of the drug
Chem Commun (Camb) 2020 Jan 30;56(9):1397-1400.PMID:31912815DOI:10.1039/c9cc08775c.
NAMI-A is highly reactive to Sp1, a tumor metastasis related protein, resulting in the perturbation of the protein structure and disruption of the DNA recognition of Sp1. Interestingly, Sp1 is more susceptible than other zinc finger proteins to NAMI-A, suggesting that Sp1 could be the anti-metastasis target of NAMI-A.
Comparison of KP1019 and NAMI-A in tumour-mimetic environments
Metallomics 2016 Aug 1;8(8):762-73.PMID:27460862DOI:10.1039/c6mt00145a.
NAMI-A and KP1019 are Ru(III)-based anti-metastatic and cytotoxic anti-cancer drugs, respectively, and have been proposed to be activated by reduction to Ru(II). The potential reduction of NAMI-A and KP1019 in the hypoxic environment of a tumour model of neuroblastoma was examined. Normoxic, hypoxic and necrotic tumour tissues were modelled by multicellular spheroids of SH-SY5Y human neuroblastoma cells of various diameters (50-800 μm). The variation in spheroid environment was confirmed with pimonidazole staining. Laser-ablation inductively-coupled plasma mass spectrometry showed KP1019 and NAMI-A penetration into the spheroid hypoxic region. XANES showed that the speciation of NAMI-A biotransformation products did not change significantly as hypoxia levels increased. KP1019 metabolites showed a correlation between the degree of spheroid hypoxia and the Ru K-edge energy consistent with either partial reduction of Ru(III) to Ru(II) in tumour microenvironments, increased S/Cl coordination or a reduced fraction of polynuclear Ru species. EXAFS spectroscopy was undertaken in an attempt to distinguish between these scenarios but was inconclusive.