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Clinical activity of alvocidib flavopiridol in acute myeloid leukemia. The alkylating prodrug J1 can be activated by aminopeptidase N, leading to a possible target directed release of melphalan. Leukemic cells ware obtained from 82 bone marrow or peripheral samples in 73 patients median age 54 yrs with AML. Since APN mediates cleavage of melflufen to its parental drug melphalan in the tumor cell cytoplasm, or in environment with high concentration of APN, a clinical usability of melflufen in AML is suggested [ 4 ]. The sampling was approved by the Ethics committee of Uppsala University.

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The cells were stimulated towards the granulocyte-macrophage lineage in a 7-day assay FMCA-GM7where cells were exposed to drugs day 0—7 of differentiation and cell survival was analyzed with the FMCA on day 7 [ 39 ].

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Johannes Zuber

A plausible explanation is that melflufen may increase the proportion of cells in S-phase during the first 24 hours after exposure, as recently shown in lymphoma cell lines [ 31 ], which would increase cytarabine potency. In conclusion, melflufen demonstrates high and significant preclinical activity in AML and further clinical evaluation seem warranted in this disease. Activity of hydrolytic enzymes in tumour cells is a determinant for anti-tumour efficacy of the melphalan containing prodrug J1. In AML, APN is and is expressed on stem cells and leukemic blasts [ 610 ], on the cell surface [ 1112 ] and in the cytoplasm [ 12 ], and recently occurrence of APN was also demonstrated in microvesicles from patients with myeloid tumors [ 13 ]. Notably, clinically beneficial partial responses was observed also in patients refractory to high dose melphalan [ 22 ]. Improved patient survival for acute myeloid leukemia:

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