Once-daily dosing to fit your patient’s routine1

Continue IMBRUVICA® treatment until disease progression or unacceptable toxicity.
- Administer IMBRUVICA® at approximately the same time each day with a glass of water
- Swallow tablets or capsule whole. Do not open, break, or chew the capsules. Do not cut, crush, or chew the tablets
- If a dose of IMBRUVICA® is not taken at the scheduled time, it can be taken as soon as possible on the same day with a return to the normal schedule the following day. Do not take extra doses of IMBRUVICA® to make up for the missed dose
*Other BTKi treatments have dose modifications for ARs and drug-drug interactions that can result in one-tablet, once-daily dosing.
†Agents administered in combination with IMBRUVICA® require infusion. When administering IMBRUVICA® in combination with rituximab or obinutuzumab, consider administering IMBRUVICA® prior to rituximab or obinutuzumab when given the same day.
I liked the
idea that
it
was an oral
medication that
I could take
once a day.”

Bob
CLL Patient
Once-daily dosing is necessary to ensure inhibition of BTK enzymatic activity1
Inhibition of BTK by IMBRUVICA® has a disruptive effect on 3 key B-cell processes as shown by in vitro and in vivo studies1:
- Inhibits survival and proliferation1-6
- Inhibits adhesion1,6-11
- Modulates chemotaxis and trafficking1,5,7,9,11-13

Discontinuation and dose reduction rates in the CLL/SLL registration studies1
The data below are pooled from 5 randomized controlled clinical trials (RESONATE™, RESONATE™-2, HELIOS, iLLUMINATE™, and E1912) and 1 single-arm, open-label clinical trial (Study 1102) in patients with CLL/SLL (N=2,016 total and n=1,133 patients exposed to IMBRUVICA®)
- 4% to 10% of patients discontinued due to ARs
- ARs leading to discontinuation included pneumonia, hemorrhage, atrial fibrillation, neutropenia, arthralgia, rash, and thrombocytopenia
- Approximately 9% of patients had a dose reduction due to ARs


- Patients requiring a dose reduction can exchange their unused tablets for the same number of tablets at the reduced dose strength
- Your patient can receive their new dose before returning their unused tablets
- In this safety-based returns program, there will be no additional cost to the patient for any tablets provided at the reduced dose strength
‡Patients must enroll in the program to apply. To be eligible for participation in the IMBRUVICA® By Your Side Dose Exchange Program, patients must have remaining pills from a current prescription for an FDA-approved indication for IMBRUVICA® and must return their remaining pills.
Abbreviations
ARs=adverse reactions, BR=bendamustine + rituximab, BTK=Bruton's tyrosine kinase, BTKi=Bruton’s tyrosine kinase inhibitor, CLL=chronic lymphocytic leukemia, SLL=small lymphocytic lymphoma.
References
- IMBRUVICA® (ibrutinib) Prescribing Information.
- Burger JA, Buggy JJ. Bruton tyrosine kinase (BTK) inhibitor ibrutinib (PCI-32765). Leuk Lymphoma. 2013;54(11):2385-2391.
- Honigberg LA, Smith AM, Sirisawad M, et al. The Bruton tyrosine kinase inhibitor PCI-32765 blocks B-cell activation and is efficacious in models of autoimmune disease and B-cell malignancy. Proc Natl Acad Sci USA. 2010;107(29):13075-13080.
- Cinar M, Hamedani F, Mo Z, et al. Bruton tyrosine kinase is commonly overexpressed in mantle cell lymphoma and its attenuation by ibrutinib induces apoptosis. Leuk Res. 2013;37(10):1271-1277.
- Ponader S, Chen S-S, Buggy JJ, et al. The Bruton tyrosine kinase inhibitor PCI-32765 thwarts chronic lymphocytic leukemia cell survival and tissue homing in vitro and in vivo. Blood. 2012;119(5):1182-1189.
- Herman SEM, Gordon AL, Hertlein E, et al. Bruton tyrosine kinase represents a promising therapeutic target for treatment of chronic lymphocytic leukemia and is effectively targeted by PCI-32765. Blood. 2011;117(23):6287-6296.
- Chang BY, Francesco M, Steggerda S, et al. Ibrutinib inhibits malignant cell adhesion and migration and reduces tumor burden in lymph node and bone marrow in a murine model of mantle cell dissemination and progression. Presented at: 104th Annual Meeting of the American Association for Cancer Research; April 6-10, 2013; Washington, DC. Abstract 923.
- Binsky I, Lantner F, Grabovsky V, et al. TAp63 regulates VLA-4 expression and chronic lymphocytic leukemia cell migration to the bone marrow in a CD74-dependent manner. J Immunol. 2010;184(9):4761-4769.
- Kurtova AV, Tamayo AT, Ford RJ, Burger JA. Mantle cell lymphoma cells express high levels of CXCR4, CXCR5, and VLA-4 (CD49d): importance for interactions with the stromal microenvironment and specific targeting. Blood. 2009;113(19):4604-4613.
- Chang BY, Francesco M, de Rooij MFM, et al. Egress of CD19+CD5+ cells into peripheral blood following treatment with the Bruton tyrosine kinase inhibitor ibrutinib in mantle cell lymphoma patients. Blood. 2013;122(14):2412-2424.
- de Rooij MFM, Kuil A, Geest CR, et al. The clinically active BTK inhibitor PCI-32765 targets B-cell receptor– and chemokine-controlled adhesion and migration in chronic lymphocytic leukemia. Blood. 2012;119(11):2590-2594.
- Burger JA, Ghia P, Rosenwald A, Caligaris-Cappio F. The microenvironment in mature B-cell malignancies: a target for new treatment strategies. Blood. 2009;114(16):3367-3375.
- Davids MS, Burger JA. Cell trafficking in chronic lymphocytic leukemia. Open J Hematol. 2012;3(S1)-3.