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Acute lymphoblastic leukemia (ALL)

Protein kinase B (PKB; PKBA; AKT; AKT1)

Studies in cell culture and mice suggest AKT inhibitors could be useful for treating glucocorticoid-resistant ALL. Glucocorticoids are a standard component of first-line therapy for ALL. In cultured T ALL (T-ALL) cells, forced activation of AKT inhibited the ability of glucocorticoids to promote apoptosis, whereas normal AKT activity did not. In a xenograft mouse model of T-ALL, the AKT inhibitor MK-2206 restored tumor sensitivity to glucocorticoids and increased survival compared with vehicle. Next steps could include clinical testing of AKT inhibitors as an adjunct to T-ALL therapy.
Merck & Co. Inc.'s MK-2206 is in Phase I and
Phase II testing in a range of solid tumors.

SciBX 7(3); doi:10.1038/scibx.2014.80
Published online Jan. 23, 2014

Patent and licensing status undisclosed

Piovan, E. et al. Cancer Cell;
published online Nov. 27, 2013;
Contact: Adolfo A. Ferrando,
Columbia University, New York, N.Y.
Contact: Andrea Califano,
same affiliation as above