| Name | N6-(2-Hydroxyethyl)adenosine |
| Description | N6-(2-Hydroxyethyl)adenosine, a Ca2+ antagonist and anti-inflammatory agent, is associated with the regulation of cerebral and coronary circulation and is believed to exhibit sedative activity. |
| In vitro | N6-(2-Hydroxyethyl)adenosine can suppress TGF-β1 or LPS-induced TGF-β1/Smad and NF-κB signaling pathways in vitro. The levels of ECM production, indicated by expression of collagen I, α-SMA and Fibronectin, are significantly reduced by treatment with N6-(2-Hydroxyethyl)adenosine dose-dependently (5, 10, and 20 μg/ml). Similarly, TGF-β and LPS stimulate increased levels of TNF-α, IL-1β and IL-10. N6-(2-Hydroxyethyl)adenosine treatment reduces the elevated levels of TNF-α and IL-1β and increases IL-10 secretion dose-dependently [1]. |
| In vivo | Injury of Kidney Tissue in UUO Mice Ameliorated by Intraperitoneal Administration of N6-(2-Hydroxyethyl) adenosine (2.5, 5, and 7.5 mg/kg; intraperitoneal injection). N6-(2-Hydroxyethyl) adenosine treatment prevents the accumulation of fibrosis-related proteins (TGF-β1, α-SMA, collagen I, and Fibronectin) and inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-10) associated with renal interstitial fibrosis. N6-(2-Hydroxyethyl) adenosine could block the accumulation of M1 macrophages, and induced the accumulation of M2 macrophages in ligated kidneys [1]. |
| Storage | Shipping with blue ice. |
| Solubility Information | DMSO : 4.8 mg/mL (15.42 mM)
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| Inhibitors Related | Nisoldipine | Nimodipine | 2,5-Di-tert-butylhydroquinone | Diltiazem hydrochloride | Levetiracetam | L-Ascorbic acid | Lanthanum(III) chloride heptahydrate | Ethyl cinnamate | 1-Octanol | Otilonium bromide |
| Related Compound Libraries | Pain-Related Compound Library | Bioactive Compound Library | Neuronal Signaling Compound Library | Membrane Protein-targeted Compound Library | Neuroprotective Compound Library | Anti-Aging Compound Library | Bioactive Compounds Library Max | Ion Channel Targeted Library |
United States
