Select secondary endpoints: CR, CR+CRh1,3 | ||
---|---|---|
Endpoint | VEN+AZA (N=286) | AZA (N=145) |
CR, n (%), (95% CI) | 105 (37), (31, 43) | 26 (18), (12, 25) |
P value | <0.001 | |
Median DOCR (months), (95% CI) | 18 (15.3, –) | 13.4 (8.7, 17.6) |
CR+CRh, n (%), (95% CI) | 185 (65), (59, 70) | 33 (23), (16, 30) |
P value | <0.001 | |
Median DOCR+CRh (months), (95% CI) | 17.8 (15.3, –) | 13.9 (10.4, 15.7) |
Secondary endpoint: CR+CRh by initiation of Cycle 23
In an exploratory post hoc analysis of CR+CRh in the VEN+AZA ITT population4:
Managing Grade 4 neutropenia with or without fever or infection, or Grade 4 thrombocytopenia
Occurrence before remission†‡
STAY ON VENCLEXTA REGIMEN: In most instances, do not interrupt the VENCLEXTA regimen due to cytopenias.
Occurrence after remission†‡ is achieved and lasting at least 7 days
STAY ON VENCLEXTA REGIMEN: In most instances, do not interrupt the VENCLEXTA regimen due to cytopenias.
DELAY subsequent cycle of VENCLEXTA regimen and monitor blood counts
For 1st occurrence
RESUME VENCLEXTA therapy at 400 mg§ in combination with azacitidine or decitabine or at 600 mg in combination with low-dose cytarabine upon resolution to Grade 1 or 2 and resume 28-day treatment cycle
For subsequent occurrences
RESUME VENCLEXTA therapy at 400 mg§ in combination with azacitidine or decitabine or at 600 mg§ in combination with low-dose cytarabine upon resolution to Grade 1 or 2 and reduce treatment cycle by 7 days for each subsequent cycle
(eg, for 2nd occurrence, VENCLEXTA would be dosed for 21 days of a 28-day cycle)
Non-hematologic adverse reactions
Grade 3 or 4 non-hematologic toxicities
Any occurrence
Interrupt VENCLEXTA if not resolved with supportive care. Upon resolution to Grade 1 or baseline level, resume VENCLEXTA at the same dose.
In VIALE-A:
*Defined as less than 5% leukemia blasts with cytopenia.1
†Recommend bone marrow evaluation.1
‡Remission is defined as achieving a CR or CRh.1
§Dose may vary based on drug-drug interactions or severe hepatic impairment.1
IIOf patients who achieved a morphologic leukemia-free state of response or better.7
Complete remission (CR) was defined as ANC >1,000/microliter, platelets >100,000/microliter, red blood cell transfusion independence, and bone marrow with <5% blasts. Absence of circulating blasts and blasts with Auer rods; absence of extramedullary disease.1
Complete remission with partial hematologic recovery (CRh) was defined as <5% of blasts in the bone marrow, no evidence of disease, and partial recovery of peripheral blood counts (platelets >50,000/microliter and ANC >500/microliter).1
DOCR (duration of CR) is defined as the number of days from the date of first response of CR to the date of earliest evidence of confirmed morphologic relapse, confirmed progressive disease, or death due to disease progression.1
DOCR+CRh (duration of CR+CRh) is defined as the number of days from the date of first response of CR+CRh (the first of either CR or CRh) to the date of earliest evidence of confirmed morphologic relapse, confirmed progressive disease, or death due to disease progression.1
AML=acute myeloid leukemia; ANC=absolute neutrophil count; AZA=azacitidine; ITT=intent to treat; PBO=placebo; VEN=VENCLEXTA.
VENCLEXTA® and its design are registered trademarks of AbbVie Inc.
VENCLEXTA Prescribing Information.
VENCLEXTA Prescribing Information.
Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Acute Myeloid Leukemia V.3.2023. © National Comprehensive Cancer Network, Inc. 2023. All rights reserved. Accessed January 13, 2023. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.
Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Acute Myeloid Leukemia V.3.2023. © National Comprehensive Cancer Network, Inc. 2023. All rights reserved. Accessed January 13, 2023. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.
DiNardo CD, Jonas BA, Pullarkat V, et al. Azacitidine and venetoclax in previously untreated acute myeloid leukemia. N Engl J Med. 2020;383(7):617-629.
DiNardo CD, Jonas BA, Pullarkat V, et al. Azacitidine and venetoclax in previously untreated acute myeloid leukemia. N Engl J Med. 2020;383(7):617-629.
Data on file, AbbVie Inc. ABVRRTI71211.
Data on file, AbbVie Inc. ABVRRTI71211.
Data on file, AbbVie Inc. ABVRRTI71272.
Data on file, AbbVie Inc. ABVRRTI71272.
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Data on file, AbbVie Inc. ABVRRTI67697.
Data on file, AbbVie Inc. ABVRRTI71500.
Data on file, AbbVie Inc. ABVRRTI71500.
CRESEMBA Prescribing Information.
CRESEMBA Prescribing Information.
Drug development and drug interactions: table of substrates, inhibitors and inducers. US Food and Drug Administration website. https://www.fda.gov/drugs/developmentapprovalprocess/developmentresources/druginteractionslabeling/ucm093664.htm. Updated March 6, 2020. Accessed October 15, 2020.
Drug development and drug interactions: table of substrates, inhibitors and inducers. US Food and Drug Administration website. https://www.fda.gov/drugs/developmentapprovalprocess/developmentresources/druginteractionslabeling/ucm093664.htm. Updated March 6, 2020. Accessed October 15, 2020.
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Perl AE. The role of targeted therapy in the management of patients with AML. Blood Adv. 2017;1(24):2281-2294.
Karakas T, Maurer U, Weidmann E, Miething CC, Hoelzer D, Bergmann L. High expression of bcl-2 mRNA as a determinant of poor prognosis in acute myeloid leukemia. Ann Oncol. 1998;9(2):159-165.
Karakas T, Maurer U, Weidmann E, Miething CC, Hoelzer D, Bergmann L. High expression of bcl-2 mRNA as a determinant of poor prognosis in acute myeloid leukemia. Ann Oncol. 1998;9(2):159-165.
Mehta SV, Shukla SN, Vora HH. Overexpression of Bcl2 protein predicts chemoresistance in acute myeloid leukemia: its correlation with FLT3. Neoplasma. 2013;60(6):666-675.
Mehta SV, Shukla SN, Vora HH. Overexpression of Bcl2 protein predicts chemoresistance in acute myeloid leukemia: its correlation with FLT3. Neoplasma. 2013;60(6):666-675.
Tzifi F, Economopoulou C, Gourgiotis D, Ardavanis A, Papageorgiou S, Scorilas A. The role of BCL2 family of apoptosis regulator proteins in acute and chronic leukemias. Adv Hematol. 2012;2012:524308.
Tzifi F, Economopoulou C, Gourgiotis D, Ardavanis A, Papageorgiou S, Scorilas A. The role of BCL2 family of apoptosis regulator proteins in acute and chronic leukemias. Adv Hematol. 2012;2012:524308.
Banker DE, Groudine M, Norwood T, Appelbaum FR. Measurement of spontaneous and therapeutic agent-induced apoptosis with BCL-2 protein expression in acute myeloid leukemia. Blood. 1997;89(1):243-255.
Banker DE, Groudine M, Norwood T, Appelbaum FR. Measurement of spontaneous and therapeutic agent-induced apoptosis with BCL-2 protein expression in acute myeloid leukemia. Blood. 1997;89(1):243-255.
Data on file, Genentech, Inc. 07/2022.
Data on file, Genentech, Inc. 07/2022.
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