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ABT-199 (venetoclax) and BCL-2 inhibitors in clinical development.

ABSTRACT: With the advent of new agents targeting CD20, Bruton's tyrosine kinase, and phosphoinositol-3 kinase for chronic lymphoid leukemia (CLL), more treatment options exist than ever before. B-cell lymphoma-2 (BCL-2) plays a major role in cellular apoptosis and is a druggable target. Small molecule inhibitors of BCL-2 are in active clinical studies. ABT-199 (venetoclax, RG7601, GDC-0199) has been granted breakthrough designation by FDA for relapsed or refractory CLL with 17p deletion. In this review, we summarized the latest clinical development of ABT-199/venetoclax and other novel agents targeting the BCL-2 proteins.

SUBMITTER: Cang S

PROVIDER: S-EPMC4654800 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

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ABT-199 (venetoclax) and BCL-2 inhibitors in clinical development.

Cang Shundong S Iragavarapu Chaitanya C Savooji John J Song Yongping Y Liu Delong D

Journal of hematology & oncology 20151120

With the advent of new agents targeting CD20, Bruton's tyrosine kinase, and phosphoinositol-3 kinase for chronic lymphoid leukemia (CLL), more treatment options exist than ever before. B-cell lymphoma-2 (BCL-2) plays a major role in cellular apoptosis and is a druggable target. Small molecule inhibitors of BCL-2 are in active clinical studies. ABT-199 (venetoclax, RG7601, GDC-0199) has been granted breakthrough designation by FDA for relapsed or refractory CLL with 17p deletion. In this review, ...[more]

PMID: 26589495

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A novel CDK9 inhibitor increases the efficacy of venetoclax (ABT-199) in multiple models of hematologic malignancies.

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Pharmacological and Protein Profiling Suggests Venetoclax (ABT-199) as Optimal Partner with Ibrutinib in Chronic Lymphocytic Leukemia.

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Bcl-2 phosphorylation confers resistance on chronic lymphocytic leukaemia cells to the BH3 mimetics ABT-737, ABT-263 and ABT-199 by impeding direct binding.

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2013-06-09 | E-GEOD-47369 | biostudies-arrayexpress

Selective BCL-2 inhibition by ABT-199 causes on-target cell death in acute myeloid leukemia.

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