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How SCEMBLIX works.

SCEMBLIX targets the abnormal protein that causes Ph+ CML-CP 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-CP.

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.

Abnormal protein causing Ph+ CML: Signaling for uncontrolled white blood cell growth in Ph+ CML. Building site of other currently approved TKIs. Switch site: Controls the abnormal protein activity. SCEMBLIX in action: Blocked signaling with SCEMBLIX. SCEMBLIX shuts off activity of the abnormal protein.

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, adosine triphosphate.