For research use only. Not for use in humans.
Molecular Weight(MW): 393.23
Reversine is a potent human A3 adenosine receptor antagonist with Ki of 0.66 μM, and a pan-aurora A/B/C kinase inhibitor with IC50 of 12 nM/13 nM/20 nM, respectively. Also used for stem cell dedifferentiation.
Selleck's Reversine has been cited by 5 publications
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Immunofluorescence of acetylated a-tubulin (red) in control (a), reversin-treated (b), and BI 2536/Reversin mixture-treated embryos (c).The embryos treated with Reversine completed first mitosis, but the nuclei of their blastomeres were fragmented (b, arrows). Embryos inhibited withthe BI 2536/Reversine mixture arrested before the onset of anaphase. Microtubules of the spindle are disorganized (c, double-arrow) and thechromosomes are misaligned (c, arrows) in these inhibited embryos. DNA is counter-stained with DAPI (blue). Scale bar, 10 μm.
Mol Reprod Dev, 2013, 80(7):522-34.. Reversine purchased from Selleck.
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|Description||Reversine is a potent human A3 adenosine receptor antagonist with Ki of 0.66 μM, and a pan-aurora A/B/C kinase inhibitor with IC50 of 12 nM/13 nM/20 nM, respectively. Also used for stem cell dedifferentiation.|
Reversine induces myogenic lineage-committed cells to become multipotent mesenchymal progenitor cells, which proliferates and redifferentiates into bone and fat cells.  Reversine, as an A3 adenosine receptor antagonist, competitively inhibits forskolin-stimulated cAMP production in stably transfected Chinese hamster ovary (CHO) cells.  Reversine inhibits the phosphorylation of a well-known Aurora target, histone H3 in HCT116 cells. Moreover, Reversine potently blocks proliferation of multiple tumor cell types, and induces cell death. In primary human tumor samples, Reversine also inhibits colony formation of leukemic cells.  When treated in combination, reversine and aspirin synergistically inhibit growth of cervical cancer cells and induce cell apoptosis. 
|In vivo||In mice inoculated with U14 tumors, Reversine (10 mg/kg i.p.) and aspirin cause more reduced tumor weight and tumor volume when compared with the control agents. |
|Kinase Assay: ||
Radioligand Binding Assays:Each tube in the A3 AR competitive binding assay contains 100 μL of membrane suspension (20 μg of protein), 50 μL of [125I]4-amino-3-iodobenzyl)adenosine-5′-N-methyluronamide (0.5 nM), and 50 μL of increasing concentrations of the test ligands in Tris-HCl buffer (50 mM, pH 7.4) containing 10 mM MgCl2 and 1 mM EDTA. Nonspecific binding is determined using 10 mM 5′-N-ethylcarboxamidoadenosine in the buffer. The mixtures are incubated at 25°C for 60 min. Binding reactions are terminated by filtration through Whatman GF/B filters under reduced pressure using a MT-24 cell harvester. Filters are washed three times with 9 mL of ice-cold buffer. Radioactivity is determined using a Beckman γ-counter, and the percent inhibition is calculated.
|Animal Research: ||
|In vitro||DMSO||5 mg/mL warmed (12.71 mM)|
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