Recilisib

• CAT Number: M020528
• CAS Number: 334969-03-8
• Molecular Formula: C16H13ClO4S
• Molecular Weight: 336.79
• Purity: ≥95%
• Synonyms: 4-[(E)-2-[(4-chlorophenyl)methylsulfonyl]ethenyl]benzoic acid
• InChI: InChI=1S/C16H13ClO4S/c17-15-7-3-13(4-8-15)11-22(20,21)10-9-12-1-5-14(6-2-12)16(18)19/h1-10H,11H2,(H,18,19)/b10-9+
• InChIKey: KBEKQQJUNVQLDZ-MDZDMXLPSA-N
• SMILES: C1=CC(=CC=C1CS(=O)(=O)C=CC2=CC=C(C=C2)C(=O)O)Cl

Recilisib (ON 01210) is a radioprotectant, which can activate AKT, PI3K activities in cells[1].
Recilisib (up to 50 μM) shows a normal distribution of cells throughout the cell cycle, with a slight reduction in the number of cells in S-phase at 50 μM. Continuous exposure of Recilisib (100 μM) does not result in cell death. Recilisib treatment does not inhibit the colony forming potential of human bone marrow cells. Recilisib provides dose dependent protection of human bone marrow cells at all three doses of IR. Recilisib activates the phosphorylation of AKT and GSK3α/β in HFL cells. Recilisib increases PI3K activity in HFL-1 cells and murine bone marrow cells in response to radiation exposure. Recilisib treatment in combination with radiation alters the MAPK signaling pathway[1].
Recilisib (500 mg/kg) significantly increases the rate of recovery and differentiation of primitive bone marrow myeloid progenitor cells in mice. Recilisib in combination with radiation reduces CFU numbers in mice, but the Recilisib-treated mice consistently retain a capability to form differentiated colonies. Recilisib treated mice have a progenitor cell population that is never completely depleted by radiation exposure[1].

Reference

[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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