Supplementary Materials from JAK1/2 and Pan-Deacetylase Inhibitor Combination Therapy Yields Improved Efficacy in Preclinical Mouse Models of JAK2^V617F-Driven Disease

Abstract

<p>- PDF file 1093K, Supplementary Table S1. Activity and tolerability of ruxolitinib (RUX) and panobinostat (PAN), alone and in combination, in a mouse model of Ba/F3 JAK2V617F cells-driven leukemic disease. Supplementary Table S2. Levels of panobinostat (PAN) and ruxolitinib (RUX) in blood and tissues post-final dose in a mouse model of Ba/F3 JAK2V617F cells-driven leukemic disease. Supplementary Table S3. Exposure to panobinostat (PAN) and ruxolitinib (RUX) in blood and tissues in a mouse model of Ba/F3 JAK2V617F cells-driven leukemic disease. Supplementary Table S4. Levels of panobinostat (PAN) and ruxolitinib (RUX) in blood and tissues post-final dose in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Table S5. Exposure to panobinostat (PAN) and ruxolitinib (RUX) in blood and tissues in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S1. Tolerability of ruxolitinib (RUX) and panobinostat (PAN), alone and in combination, in a mouse model of Ba/F3 JAK2V617F cellsdriven leukemic disease. Supplementary Figure S2. Modulation of aberrant JAK2/STAT5 signaling in vitro and in vivo following treatment with ruxolitinib (RUX) and panobinostat (PAN), alone and in combination. Supplementary Figure S3. Efficacy and tolerability of ruxolitinib (RUX) in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S4. Modulation of STAT5 phosphorylation in spleen and bone marrow following treatment with ruxolitinib (RUX) in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S5. Histological analysis following treatment with ruxolitinib (RUX) in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S6. Efficacy and tolerability of panobinostat (PAN) in a mouse model of JAK2V617F-driven MPN-like disease Supplementary Figure S7. Modulation of protein acetylation and acetylated histone H3 in spleen and bone marrow, respectively, following treatment with 21 panobinostat (PAN) in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S8. Histological analysis following treatment with panobinostat (PAN) in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S9. Efficacy and tolerability of ruxolitinib (RUX) and panobinostat (PAN), alone and in combination, in a mouse model of JAK2V617Fdriven MPN-like disease. Supplementary Figure S10. Impact of ruxolitinib (RUX) and panobinostat (PAN), alone and in combination, on relative levels of retrovirally transduced JAK2V617F in a mouse model of JAK2V617F-driven MPN-like disease. Supplementary Figure S11. Histological analysis following treatment with ruxolitinib (RUX) and panobinostat (PAN), alone and in combination, in a mouse model of JAK2V617F-driven MPN-like disease</p>