ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor.

By Chris Tse, A. Shoemaker, Jessica Adickes, Mark G. Anderson, Jun Chen, Sha S. Jin, Eric F. Johnson, K. Marsh, M. Mitten, Paul M Nimmer and 8 more. Cancer Research, 2008

1,864 citations recorded by the source corpus.

Subfields: Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/18f8c0de3052c535dc82a6d672d4b1c7993bb944

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In Molecular Biology

1. J. Brunelle
2. S. Tait
3. T. Tchkonia
4. Yi Zhu
5. Michael N. Hall
6. P. Colman
7. J. Hardwick
8. David W. Andrews

Citations in the corpus

• Mitochondrial apoptosis: killing cancer using the enemy within (2015, background): “Unfortunately, the clinical application of ABT-263 is limited because it induces thrombocytopenia (Tse et al, 2008; Josefsson et al, 2011).”
• BCL-2 family antagonists for cancer therapy (2008, background): “First, the compound kills BAK/BAX double-knockout MEFs as potently (EC 50 ∼5 μM) as it kills wild-type cell”
• Rapamycin passes the torch: a new generation of mTOR inhibitors (2011, background): “, and ABT263 (Navitoclax, Genentech and Abbott), which inhibits the anti-apoptotic effect of BCL-2 and BCL-xL in cancer cell lines by preventing their ability to bind and sequester pro-apoptotic factors such as BI”
• Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “So far, nearly a dozen BH3 mimetics are under investigation as Bcl-2 inhibitors in different phases of human clinical trials such as AT-101 (R-(-)-gossypol) [83,84], ABT199 (venetoclax) [85], ABT-737 [86], ABT-263 (navitoclax, orally available derivative of ABT-737) [87,88], GX15-070 (obatoclax) [89”
• Multiple Functions of BCL-2 Family Proteins (2013, background): “ABT-737 derivatives are in clinical trials as anticancer agents with promising early results, and additional therapeutics specific to antiapoptotic MCL-1, which is not targeted by ABT-737, are being pursued (Tse et al. 2008; Yecies et al. 2010; Gandhi et al. 2011).”
• BCL-2 family proteins: changing partners in the dance towards death (2017, background): “Small molecule BH3 mimetics, like ABT-263 (Navitoclax) and ABT-199 (Venetoclax), mimic the binding of BH3 peptides to the hydrophobic BH3 domain-binding groove of anti-apoptotic proteins and thus displace BH3-only proteins and active BAX/BAK from anti-apoptotic proteins.(107,108) By binding to the B”
• Identification of a novel senolytic agent, navitoclax, targeting the Bcl‐2 family of anti‐apoptotic factors (2016, background): “Additionally, N can cause bleeding by affecting platelets and can cause neutropenia, while newer congeners may have less of these effects (Tse et al., 2008; Souers et al., 2013), further emphasizing a need for medicinal chemical optimization.”
• Fisetin is a senotherapeutic that extends health and lifespan (2018, background): “Navitoclax, and could be repurposed as senolytics, but cause considerable toxicity including neutropenia and platelet deficiency [40,41].”
• Recent advances in the development of protein–protein interactions modulators: mechanisms and clinical trials (2020, background): “3d) is the second generation of Bcl-2 anti-apoptotic protein inhibitor based on the structure of ABT-737.(85,86) It can bind with Bcl-2 (Ki < 1 nM), Bcl-XL (Ki < 0.”