Mantle cell lymphoma - combination treatment with bendamustine and rituximab

Active Ingredient: Acalabrutinib

Indication for Acalabrutinib

Population group: only adults (18 years old or older)
Therapeutic intent: Curative procedure

Acalabrutinib in combination with bendamustine and rituximab (BR) is indicated for the treatment of adult patients with previously untreated mantle cell lymphoma (MCL) who are not eligible for autologous stem cell transplant (ASCT).

For this indication, competent medicine agencies globally authorize below treatments:

100 mg twice daily until disease progression or unacceptable toxicity

For:

Dosage regimens

Oral, 100 milligrams acalabrutinib, 2 times daily.

Detailed description

The recommended dose of acalabrutinib is 100 mg acalabrutinib twice daily (equivalent to a total daily dose of 200 mg).

The dose interval is approximately 12 hours.

Treatment with acalabrutinib should be continued until disease progression or unacceptable toxicity.

Acalabrutinib should be administered on Day 1 on Cycle 1 (each cycle is 28 days) until disease progression or unacceptable toxicity. Bendamustine should be administered at 90 mg/m² on Days 1 and 2 of each cycle for a total of 6 cycles. Rituximab should be administered at 375 mg/m² on Day 1 each cycle for a total of 6 cycles. Patients achieving a response (partial response [PR] or complete response [CR]) after the first 6 cycles, may receive maintenance rituximab at 375 mg/m² on Day 1 of every other cycle for a maximum of 12 additional doses, starting on Cycle 8 up to Cycle 30.

Missed dose

If a patient misses a dose of acalabrutinib by more than 3 hours, the patient should be instructed to take the next dose at its regularly scheduled time. Double dose of acalabrutinib should not be taken to make up for a missed dose.

Active ingredient

Acalabrutinib

Acalabrutinib is a small-molecule inhibitor of BTK (Bruton's tyrosine kinase). Acalabrutinib and its active metabolite, ACP-5862, form a covalent bond with a cysteine residue in the BTK active site, leading to inhibition of BTK enzymatic activity. In nonclinical studies, acalabrutinib inhibited BTK-mediated activation of downstream signaling proteins CD86 and CD69 and inhibited malignant B-cell proliferation and tumor growth in mouse xenograft models.

Read more about Acalabrutinib

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