Therapeutic Response

CD22 + status confers therapeutic sensitivity to Inotuzumab ozogamicin in patients with Acute Lymphoid Leukemia.

Statements

Source and description
Besponsa (inotuzumab ozogamicin) [package insert]. FDA. The U.S. Food and Drug Administration granted approval to inotuzumab ozogamicin for the treatment of adult and pediatric patients 1 year and older with relapsed or refractory CD22-positive B-cell precursor acute lymphoblastic leukemia (ALL).
Besponsa (inotuzumab ozogamicin) [product information]. EMA. The European Medicines Agency (EMA) has authorized Besponsa (inotuzumab ozogamicin) as a monotherapy for the treatment of adult patients with relapsed or refractory CD22-positive B cell precursor acute lymphoblastic leukemia (ALL). Adult patients with Philidelphia chromosome positive (Ph+) relapsed or refractory B cell precursor ALL should have failed treatment with at least one tyrosine kinase inhibitor (TKI).
Inotuzumab Ozogamicin Monotherapy. NCCP National SACT Regimen. HSE. The Republic of Ireland's Health Service Executive (HSE) has approved inotuzumab ozogamicin for reimbursement as a monotherapy treatment option for the treatment of adult patients with relapsed or refractory CD22-positive B cell precursor acute lymphoblastic leukemia (ALL). The indication further states that adult patients with Philadelphia chromosome positive (Ph+) relapsed or refractory B cell precursor ALL should have failed treatment with at least 1 tyrosine kinase inhibitor (TKI).
Besponsa (inotuzumab ozogamicin) [product information]. EMA. The European Medicines Agency (EMA) has authorized inotuzumab ozogamicin as a monotherapy for the treatment of pediatric patients aged 1 year and older with CD22-positive B cell precursor acute lymphoblastic leukemia (ALL): in first relapse after allo-haematopoietic stem cell transplant (HSCT); after any first relapse in patients with Very High Risk (VHR) disease; after a second or greater relapse; and in those with refactory disease. Patients with Philadelphia chromosome positive (Ph+) disease should have exhausted relevant BCR-ABL targeting treatment options.