A closer look at how TAZVERIK® works
A closer look at how TAZVERIK® works
A closer look at how TAZVERIK® works
Watch the unique mechanism of action to see how TAZVERIK can help reduce aberrant B-cell proliferation, associated with the development of FL.1,2
This information is derived from animal studies and does not demonstrate clinical efficacy and safety.
EZH2 plays a critical role in normal B-cell development1,3-5
EZH2 is an epigenetic regulator of B-cell identity in the germinal center1,3
- EZH2 activity represses the expression of genes involved in differentiation, negative cell cycle regulation, and apoptosis. Thus allowing B cells to proliferate and survive.1,4,6
- In healthy cells, EZH2 activity is subsequently downregulated to allow for B-cell differentiation and apoptosis.6,7
EZH2=enhancer of zeste homolog 2.
EZH2 plays a critical role in follicular lymphoma1,3-5
B cells locked in a proliferative germinal center state can lead to the accumulation of malignant B cells and the development of FL8
- FL is caused by heterogenous combinations of oncogenic hits, leading to high EZH2 activity, which may enable persistent epigenetic silencing of the genes involved in differentiation, negative cell cycle regulation, and apoptosis.1,4-6
EZH2=enhancer of zeste homolog 2.
TAZVERIK can help reduce aberrant B-cell proliferation associated with the development of FL1-5,8-10
- Inhibition of EZH2 activity by TAZVERIK may enable epigenetic expression of genes that allow for germinal center exit.1,2,11
- Regardless of oncogenic mutation, follicular lymphoma (FL) tumors have a critical dependence on EZH2 for growth and survival.2,12
This information is derived from animal studies and does not demonstrate clinical efficacy and safety.
EZH2=enhancer of zeste homolog 2.
References: 1. Béguelin W, Popovic R, Teater M, et al. EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. Cancer Cell. 2013;23:677-692. 2. TAZVERIK (tazemetostat) Prescribing Information. Cambridge, MA: Epizyme, Inc., July 2020. 3. Velichutina I, Shaknovich R, Geng H, et al. EZH2-mediated epigenetic silencing in germinal center B cells contributes to proliferation and lymphomagenesis. Blood. 2010;116(24):5247-5255. 4. Huet S, Sujobert P, Salles G. From genetics to the clinic: A translational perspective on follicular lymphoma. Nat Rev Cancer. 2018;18:224-239. 5. Lackraj T, Goswami R, Kridel R. Pathogenesis of follicular lymphoma. Best Pract Res Cl Ha. 2018;31:2-14. 6. Lue JK, Amengual JE. Emerging EZH2 inhibitors and their application in lymphoma. Curr Hematol Malig Rep. 2018;13:369-382. 7. Wang GG, Konze KD, Tao J. Polycomb genes, miRNA, and their deregulation in B-cell malignancies. Blood. 2015;125(8):1217-1225. 8. Mamessier E, Broussais-Guillaumot F, Chetaille B, et al. Nature and importance of follicular lymphoma precursors. Haematologica. 2014;9(5):802-810. 9. Naradikian MS, Scholz JL, Oropallo MA, Cancro MP. Understanding B cell biology. In: Bosch X, Ramos-Casals M, Khamashta MA (eds.). Drugs Targeting B-Cells in Autoimmune Diseases. Springer;2014. 10. Klein U and Dalla-Favera R. Germinal centres: role in B‐cell physiology and malignancy. Nat Rev Immunol. 2008;8(1):22-33. 11. Noushin Mossadegh-Keller, Gabriel Brisou, Alicia Beyou, et al. Human B Lymphomas Reveal Their Secrets Through Genetic Mouse Models. Front Immunol. 2021 Jul 16;12:683597. 12. von Keudell G and Salles G. The role of tazemetostat in relapsed/refractory follicular lymphoma. Ther Adv Hematol. 2021;12:1-8.