Javascript must be enabled to continue!
Abstract 971: Chaperone-mediated protein degradation (CHAMP): A novel technology for tumor-targeted protein degradation
View through CrossRef
Abstract
The HSP90 chaperone mediates folding of many important client proteins and mutated oncoproteins, but can also direct its substrates towards degradation by the ubiquitin-proteasome system. Further, in tumor tissues, HSP90 complexes are in a highly activated state relative to normal tissues, which results in HSP90-binding small molecule compounds displaying unique tumor-selective pharmacokinetics. In order to take advantage of these attributes of HSP90 to degrade the transcription factor BRD4 in a tumor-selective fashion, hetero-bifunctional small molecule compounds were synthesized, termed chaperone-mediated protein degraders (CHAMPs), that chemically induced proximity between BRD4 and HSP90. In vitro, treatment of MV-4-11 leukemia cells with a BRD4-CHAMP compound resulted in formation of a BRD4:CHAMP:HSP90 ternary complex and subsequent proteasome-dependent BRD4 degradation and inhibition of cell proliferation. CHAMPs were identified that induced selective degradation of BRD4 and displayed only minimal effects on other HSP90-regulated client proteins. While BRD4 is a known HSP90 client protein, non-HSP90 clients such as mutated KRAS could also be degraded using this approach. In vivo, in the MV-4-11 mouse xenograft model, a selective BRD4-CHAMP compound displayed prolonged pharmacokinetics in tumors relative to plasma and normal tissues, with its tumor concentration remaining above the in vitro cytotoxicity EC50 value for at least 7 days following a single dose. This resulted in greater than 90% and prolonged degradation of BRD4 in tumors, as well as decreased expression of the BRD4-regulated MYC gene. Treatment with BRD4-CHAMP at its MTD resulted in dramatic tumor regressions after a single dose and the majority of tumors were undetectable following 3 weekly doses. In contrast, daily dosing of a clinical stage pan-BET inhibitor at its MTD resulted in stable to progressive disease, indicating that BRD4-CHAMP has a greatly improved therapeutic index in this model. CHAMP technology has a number of advantages relative to other targeted protein degradation approaches, such as PROTAC, including an improved safety margin due to selective accumulation in tumor tissues.
Citation Format: Kevin P. Foley, Long Ye, Mingkai Wang, Chenghao Ying, Wei Yin, Lingjie Zhang, Weiwen Ying. Chaperone-mediated protein degradation (CHAMP): A novel technology for tumor-targeted protein degradation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 971.
American Association for Cancer Research (AACR)
Title: Abstract 971: Chaperone-mediated protein degradation (CHAMP): A novel technology for tumor-targeted protein degradation
Description:
Abstract
The HSP90 chaperone mediates folding of many important client proteins and mutated oncoproteins, but can also direct its substrates towards degradation by the ubiquitin-proteasome system.
Further, in tumor tissues, HSP90 complexes are in a highly activated state relative to normal tissues, which results in HSP90-binding small molecule compounds displaying unique tumor-selective pharmacokinetics.
In order to take advantage of these attributes of HSP90 to degrade the transcription factor BRD4 in a tumor-selective fashion, hetero-bifunctional small molecule compounds were synthesized, termed chaperone-mediated protein degraders (CHAMPs), that chemically induced proximity between BRD4 and HSP90.
In vitro, treatment of MV-4-11 leukemia cells with a BRD4-CHAMP compound resulted in formation of a BRD4:CHAMP:HSP90 ternary complex and subsequent proteasome-dependent BRD4 degradation and inhibition of cell proliferation.
CHAMPs were identified that induced selective degradation of BRD4 and displayed only minimal effects on other HSP90-regulated client proteins.
While BRD4 is a known HSP90 client protein, non-HSP90 clients such as mutated KRAS could also be degraded using this approach.
In vivo, in the MV-4-11 mouse xenograft model, a selective BRD4-CHAMP compound displayed prolonged pharmacokinetics in tumors relative to plasma and normal tissues, with its tumor concentration remaining above the in vitro cytotoxicity EC50 value for at least 7 days following a single dose.
This resulted in greater than 90% and prolonged degradation of BRD4 in tumors, as well as decreased expression of the BRD4-regulated MYC gene.
Treatment with BRD4-CHAMP at its MTD resulted in dramatic tumor regressions after a single dose and the majority of tumors were undetectable following 3 weekly doses.
In contrast, daily dosing of a clinical stage pan-BET inhibitor at its MTD resulted in stable to progressive disease, indicating that BRD4-CHAMP has a greatly improved therapeutic index in this model.
CHAMP technology has a number of advantages relative to other targeted protein degradation approaches, such as PROTAC, including an improved safety margin due to selective accumulation in tumor tissues.
Citation Format: Kevin P.
Foley, Long Ye, Mingkai Wang, Chenghao Ying, Wei Yin, Lingjie Zhang, Weiwen Ying.
Chaperone-mediated protein degradation (CHAMP): A novel technology for tumor-targeted protein degradation [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21.
Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 971.
Related Results
Complex Collision Tumors: A Systematic Review
Complex Collision Tumors: A Systematic Review
Abstract
Introduction: A collision tumor consists of two distinct neoplastic components located within the same organ, separated by stromal tissue, without histological intermixing...
Abstract 1649: Chemically induced chaperone-mediated protein degradation (CHAMP) of KRAS(G12C)
Abstract 1649: Chemically induced chaperone-mediated protein degradation (CHAMP) of KRAS(G12C)
Abstract
Covalent KRAS(G12C) inhibitors have recently shown promising efficacy in the clinic. However, the rapid development of drug resistance compromises their lon...
Giant Sacrococcygeal Teratoma in Infant: Systematic Review
Giant Sacrococcygeal Teratoma in Infant: Systematic Review
Abstract
Introduction
Sacrococcygeal teratoma (SCT) is a rare embryonal tumor that occurs in the sacrococcygeal region, with an incidence of about 1 in 35,000 to 40,000 live births...
Hsp90 and associates shaping parasite biology
Hsp90 and associates shaping parasite biology
ABSTRACT
Hsp90 is considered to be the master regulator of chaperone activity within the cellular context. In addition t...
Spatial filtering for flood illumination ophthalmoscope
Spatial filtering for flood illumination ophthalmoscope
Filtrage spatial pour ophtalmoscope plein champ
La transparence de l’œil permet d’observer la rétine de manière non-invasive par des moyens optiques, dans le but d’...
Supplementary Data from Targeted BiTE Expression by an Oncolytic Vector Augments Therapeutic Efficacy Against Solid Tumors
Supplementary Data from Targeted BiTE Expression by an Oncolytic Vector Augments Therapeutic Efficacy Against Solid Tumors
<p>Supplementary Methods, Supplementary Figures S1-S15 Fig. S1. Purification and binding specificity of MV-encoded BiTEs. (A) Purification of MV-expressed BiTEs. Vero cells w...
Alterations of the Hsp70/Hsp90 chaperone and the HOP/CHIP co-chaperone system in cancer
Alterations of the Hsp70/Hsp90 chaperone and the HOP/CHIP co-chaperone system in cancer
AbstractActivation of the Hsp90 chaperone system is a characteristic of cancer cells. The regulation of chaperone activities involves their interaction with cochaperones; therefore...
Mycobacterium tuberculosisRv0991c is a redox-regulated molecular chaperone
Mycobacterium tuberculosisRv0991c is a redox-regulated molecular chaperone
ABSTRACTThe bacterial pathogenMycobacterium (M.) tuberculosisis the leading cause of death by an infectious disease among humans. Here, we describe a previously uncharacterizedM. t...

