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Abstract 2311: Determinants of CDK4 target engagement by palbociclib, ribociclib and abemaciclib
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Abstract
Palbociclib, ribociclib and abemaciclib compose a class of ATP-competitive CDK4 and CDK6 inhibitors that have demonstrated preclinical and clinical efficacy against various tumor types. While these inhibitors have favorably altered the landscape of cancer therapeutics, identification of patients likely to respond to CDK4/6 inhibition remains a challenge. Previously, we used our chemoproteomics platform (KiNativ), which measures competition of an ATP- or ADP-acyl-phosphate probe, to profile lysates generated from cells that were treated with palbociclib. We showed that palbociclib-CDK4 target engagement is cell line specific and that engagement correlates with sensitivity of the cell line to palbociclib-mediated growth inhibition. However, the circumstances that determine whether target engagement is achieved were not understood. In an effort to understand the molecular mechanisms that influence CDK4 target engagement, we used the same proteomics platform to interrogate the contribution of various known CDK regulators. We identified a family of proteins that prevents palbociclib target engagement upon overexpression and whose lack of expression correlates with palbociclib sensitivity. This interaction is specific for CDK4/6 as modulation of the drug's interaction with off-target kinases was not affected by overexpression of these proteins. Furthermore, we found that these proteins similarly prevent CDK4 target engagement by ribociclib and abemaciclib. Incorporation of the proteins identified here into a biomarker strategy should help to enrich for patients likely to respond to CDK4/6 inhibition therapy and expand the utility of these inhibitors.
Citation Format: Jennifer L. Green, Tyzoon Nomanbhoy. Determinants of CDK4 target engagement by palbociclib, ribociclib and abemaciclib [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2311.
American Association for Cancer Research (AACR)
Title: Abstract 2311: Determinants of CDK4 target engagement by palbociclib, ribociclib and abemaciclib
Description:
Abstract
Palbociclib, ribociclib and abemaciclib compose a class of ATP-competitive CDK4 and CDK6 inhibitors that have demonstrated preclinical and clinical efficacy against various tumor types.
While these inhibitors have favorably altered the landscape of cancer therapeutics, identification of patients likely to respond to CDK4/6 inhibition remains a challenge.
Previously, we used our chemoproteomics platform (KiNativ), which measures competition of an ATP- or ADP-acyl-phosphate probe, to profile lysates generated from cells that were treated with palbociclib.
We showed that palbociclib-CDK4 target engagement is cell line specific and that engagement correlates with sensitivity of the cell line to palbociclib-mediated growth inhibition.
However, the circumstances that determine whether target engagement is achieved were not understood.
In an effort to understand the molecular mechanisms that influence CDK4 target engagement, we used the same proteomics platform to interrogate the contribution of various known CDK regulators.
We identified a family of proteins that prevents palbociclib target engagement upon overexpression and whose lack of expression correlates with palbociclib sensitivity.
This interaction is specific for CDK4/6 as modulation of the drug's interaction with off-target kinases was not affected by overexpression of these proteins.
Furthermore, we found that these proteins similarly prevent CDK4 target engagement by ribociclib and abemaciclib.
Incorporation of the proteins identified here into a biomarker strategy should help to enrich for patients likely to respond to CDK4/6 inhibition therapy and expand the utility of these inhibitors.
Citation Format: Jennifer L.
Green, Tyzoon Nomanbhoy.
Determinants of CDK4 target engagement by palbociclib, ribociclib and abemaciclib [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL.
Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2311.
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