Ewing’s sarcoma is characterized by the formation of an oncogenic fusion protein, EWS-FLI1, which binds to RNA helicase central to disease. YK-4-279 binds to EWS-FLI1 (K_d = 9.48 μM), blocking the interaction of EWS-FLI1 and RNA helicase and driving apoptosis in Ewing’s sarcoma family tumors.¹ Through these effects, YK-4-279 reduces the growth of Ewing’s sarcoma orthotopic xenografts. Importantly, it is effective in Ewing’s sarcoma cells, both in vitro and in vivo, that are chemotherapy-resistant.² YK-4-279 also binds the ETS transcription factors ERG and ETV1 (K_d = 11.7 and 17.4, respectively), which form fusion proteins that contribute to some types of prostate cancer.³ (+)-YK-4-279 is a highly purified enantiomer of YK-4-279. Its properties have not been characterized.

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1.Erkizan, H.V.,Kong, Y.,Merchant, M., et al. A small molecule blocking oncogenic protein EWS-FLI1 interaction with RNA helicase A inhibits growth of Ewing’s sarcoma. Nature Medicine 15(7), 750-756 (2009).

2.Awad, O.,Yustein, J.T.,Shah, P., et al. High ALDH activity identifies chemotherapy-resistant Ewing’s sarcoma stem cells that retain sensitivity to EWS-FLI1 inhibition. PLoS One 5(11), 1-17 (2010).

3.Rahim, S.,Beauchamp, E.M.,Kong, Y., et al. YK-4-279 inhibits ERG and ETV1 mediated prostate cancer cell invasion. PLoS One 6(4), 1-8 (2011).