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Recilisib is a radioprotectant, which can activate AKT, PI3K activities in cells.

Recilisib Sodium (up to 50 &#181M) shows a normal distribution of cells throughout the cell cycle, with a slight reduction in the number of cells in S-phase at 50 &#181M. Continuous exposure of Recilisib Sodium (100 &#181M) does not result in cell death. Recilisib Sodium does not inhibit the ability of human bone marrow to form colonies in methylcellulose at either timepoint. Recilisib Sodium treatment does not inhibit the colony forming potential of human bone marrow cells. Recilisib Sodium provides dose dependent protection of human bone marrow cells at all three doses of IR. Recilisib Sodium activates the phosphorylation of AKT and GSK3α/β in HFL cells. Recilisib Sodium increases PI3K activity in HFL-1 cells and murine bone marrow cells in response to radiation exposure. Recilisib Sodium treatment in combination with radiation alters the MAPK signaling pathway[1].

Recilisib Sodium (500 mg/kg) significantly increases the rate of recovery and differentiation of primitive bone marrow myeloid progenitor cells in mice. Recilisib Sodium in combination with radiation reduces CFU numbers in mice, but the Recilisib Sodium-treated mice consistently retain a capability to form differentiated colonies. Recilisib Sodium treated mice have a progenitor cell population that is never completely depleted by radiation exposure[1].

[1]. Kang AD, et al. ON01210.Na (Ex-RAD) mitigates radiation damage through activation of the AKT pathway. PLoS One. 2013;8(3):e58355.

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