Patients HCP
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How SCEMBLIX works. Kat, real SCEMBLIX patient. Kat was compensated for her time.

SCEMBLIX targets the abnormal protein that causes Ph+ CML in chronic phase differently

SCEMBLIX is thought to work by binding to a different site (myristoyl pocket) to help block the activity of the abnormal protein that causes Ph+ CML in chronic phase.

Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) is caused by a continuously active abnormal protein (BCR-ABL) that leads to uncontrolled growth of abnormal white blood cells (also known as leukemic cells).

All other currently approved tyrosine kinase inhibitors (TKIs) bind to this abnormal protein at a site known as the ATP binding site to help block the protein's activity.

SCEMBLIX targets a different site of this abnormal protein to help block the protein's activity.

BCR-ABL abnormal protein. BCR- ABL leads to uncontrolled growth of abnormal white blood cells in Ph+ CML-CP. ATP binding site of other currently approved TKIs. SCEMBLIX binding site (myristoyl pocket). SCEMBLIX in action. SCEMBLIX helps block the activity of BCR-ABL by binding to a different site. SCEMBLIX binding site
SCEMBLIX is the only treatment that is thought to bind to a different site to help block the activity of the abnormal protein that causes Ph+ CML-CP.

ATP, adenosine triphosphate; Ph+ CML-CP, Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase; TKIs, tyrosine kinase inhibitors.

*SCEMBLIX was studied vs GLEEVEC® (imatinib), TASIGNA® (nilotinib), Sprycel ® (dasatinib), and Bosulif ® (bosutinib). Sprycel is a registered trademark of Bristol-Myers Squibb Company. Bosulif is a registered trademark of Pfizer Inc.