BEC HCl is a slow-binding and competitive Arginase II inhibitor with Ki of 0.31 μM (ph 7.5).
In Vitro
BEC HCl causes significant enhancement of NO-dependent smooth muscle relaxation in this tissue. [2] BEC HCl enhances perivascular and peribronchiolar lung inflammation, mucus metaplasia, NF-κB DNA binding, and mRNA expression of the NF-κB-driven chemokine genes CCL20 and KC, and lead to further increases in airways hyperresponsiveness. [3] In vivo: BEC HCl increased contractility in isolated myocytes from WT and NOS3 but not NOS1 knockout mice. [4]
In Vivo
No in vivo data are provided in the current product source. Contact us for further information.
Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.
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