| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Targets |
NAMI-A targets the metastatic process rather than directly killing cancer cells. It inhibits tumor angiogenesis, cell migration, and metastasis. The compound's mechanism involves the inhibition of matrix metalloproteinases (MMPs) and disruption of the extracellular matrix, which are critical for cancer cell invasion and metastasis. NAMI-A also affects the expression of genes involved in cell adhesion and migration. The compound exhibits relatively minor effects on primary tumor cell proliferation, making it a unique antimetastatic agent. NAMI-A's ruthenium-based structure allows it to interact with proteins and DNA, but its primary mechanism is anti-metastatic rather than cytotoxic.
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| ln Vitro |
In vitro, NAMI-A exhibits little cytotoxicity towards many cancer cell lines. Instead, it inhibits cell adhesion and migration in cancer cells. The compound's anti-metastatic activity is assessed in vitro using wound healing assays, Transwell migration assays, and adhesion assays. Treatment with NAMI-A at concentrations ranging from 10 to 100 μM results in reduced cell migration and adhesion. The compound does not significantly affect cell proliferation at these concentrations. NAMI-A also inhibits angiogenesis in vitro, as measured by endothelial cell tube formation assays. These in vitro findings support the compound's unique mechanism of action as a metastasis inhibitor.
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| ln Vivo |
In vivo, NAMI-A is a potent antimetastatic compound. In animal models of cancer metastasis, administration of NAMI-A results in significant reduction of metastatic lesions in the lungs and other organs, with relatively minor effects on primary tumor growth. The compound has been shown to be effective against solid tumor metastases, even in advanced stages of growth. NAMI-A's anti-metastatic activity is attributed to its inhibition of tumor angiogenesis, cell migration, and invasion. The compound has been studied in preclinical models and has shown promise as a novel antimetastatic agent.
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| Enzyme Assay |
In vitro enzyme assays for NAMI-A typically involve measuring the inhibition of matrix metalloproteinases (MMPs) or other enzymes involved in metastasis. A typical protocol: recombinant MMP-2 or MMP-9 is incubated with varying concentrations of NAMI-A (1-1000 μM) in assay buffer (50 mM Tris-HCl, pH 7.5, 150 mM NaCl, 10 mM CaCl₂, 0.05% Brij-35) for 30 minutes at 37°C. Fluorogenic substrate (e.g., DQ-gelatin) is added, and fluorescence is monitored continuously for 60-120 minutes. IC₅₀ values are calculated from inhibition curves. For angiogenesis assays, endothelial cells are seeded on Matrigel and treated with NAMI-A, and tube formation is quantified after 6-18 hours. Each concentration is tested in triplicate, and experiments are repeated at least three times.
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| Cell Assay |
In vitro cell-based assays for NAMI-A are performed using cancer cell lines such as B16F10 melanoma, MDA-MB-231 breast cancer, or HT1080 fibrosarcoma. A typical protocol: cells are seeded in 96-well plates or Transwell inserts. For migration assays, cells are treated with NAMI-A at concentrations ranging from 10 to 100 μM for 24-48 hours, and migration is assessed using wound healing or Transwell assays. For adhesion assays, cells are plated on Matrigel- or fibronectin-coated plates and treated with NAMI-A, and adherent cells are counted after 30-60 minutes. Cell viability is assessed using MTT or CellTiter-Glo assays to confirm that observed effects are not due to cytotoxicity. Each condition is tested in triplicate, and experiments are repeated at least three times.
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| Animal Protocol |
In vivo animal studies for NAMI-A are conducted in mouse models of cancer metastasis. A typical protocol: C57BL/6 mice are injected intravenously with B16F10 melanoma cells via the tail vein to establish lung metastasis. NAMI-A is administered via intraperitoneal injection at doses of 10-50 mg/kg, daily or every other day, for 2-4 weeks. At study termination, lungs are harvested and metastatic colonies are counted. For orthotopic models, cancer cells are injected into the mammary fat pad (for breast cancer) or subcutaneously, and primary tumor growth and metastasis are monitored. Efficacy is assessed by comparing metastatic burden between treatment and vehicle control groups.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of NAMI-A have been characterized in preclinical studies. As a ruthenium-based compound, its pharmacokinetics are distinct from organic small molecules. The compound is administered intravenously or intraperitoneally. Its plasma half-life, volume of distribution, protein binding, and clearance have been evaluated in animal models. The compound's ruthenium content allows for detection by atomic absorption spectroscopy or inductively coupled plasma mass spectrometry (ICP-MS). The compound's stability in solution has rarely been reported. It should be stored as recommended by the manufacturer.
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| Toxicity/Toxicokinetics |
Toxicological data for NAMI-A have been evaluated in preclinical studies. The compound is generally well-tolerated at therapeutic doses. Common adverse effects may include gastrointestinal disturbances and hematological effects. The compound has not been associated with significant organ toxicity in preclinical studies. Standard laboratory safety precautions should be followed when handling NAMI-A: use of personal protective equipment (gloves, safety goggles, lab coat) and handling in a well-ventilated fume hood. The compound should be stored as recommended by the manufacturer. Researchers should consult the safety data sheet (SDS) before handling.
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| References |
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| Additional Infomation |
Additional information for NAMI-A: The compound has a CAS number of 201653-76-1. Synonyms include NAMIA, ImH-trans-RuCl4(DMSO)-Im, and imidazolium trans-imidazoledimethyl sulfoxidetetrachlororuthenate. It is a ruthenium-based anticancer agent and metastasis inhibitor. It inhibits tumor angiogenesis, cell migration, and metastasis. It exhibits little cytotoxicity towards many cancer cell lines in vitro. It is a potent antimetastatic compound in vivo. It is for research use only and is not approved for clinical applications. No FDA approvals exist.
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| Molecular Formula |
C8H15CL4N4ORUS
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| Molecular Weight |
458.177895784378
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| Exact Mass |
458.873
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| CAS # |
201653-76-1
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| PubChem CID |
133082692
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| Appearance |
Pink to red solid powder
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
0
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| Heavy Atom Count |
19
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| Complexity |
81.2
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| Defined Atom Stereocenter Count |
0
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| SMILES |
[Ru+3].[Cl-].[Cl-].[Cl-].[Cl-].S(C)(C)=O.[NH+]1C=CNC=1.N1C=NC=C1
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| InChi Key |
RJZBTXZRLXLLKO-UHFFFAOYSA-K
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| InChi Code |
InChI=1S/2C3H4N2.C2H6OS.4ClH.Ru/c2*1-2-5-3-4-1;1-4(2)3;;;;;/h2*1-3H,(H,4,5);1-2H3;4*1H;/q;;;;;;;+3/p-3
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| Chemical Name |
1H-imidazole;1H-imidazol-3-ium;methylsulfinylmethane;ruthenium(3+);tetrachloride
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| Synonyms |
ImH-trans-RuCl4(DMSO)-Im; NAMIA
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~8.28 mg/mL (~18.07 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 6.67 mg/mL (14.56 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).
 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 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 |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.