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ePoster Display

560TiP - A phase I/IIa study to evaluate the safety and efficacy of CCS1477, a first in clinic inhibitor of p300/CBP, as monotherapy in patients with selected molecular alterations

Date

16 Sep 2021

Session

ePoster Display

Topics

Cytotoxic Therapy;  Clinical Research;  Targeted Therapy;  Cancer Biology

Tumour Site

Presenters

Simon Crabb

Citation

Annals of Oncology (2021) 32 (suppl_5): S583-S620. 10.1016/annonc/annonc699

Authors

S. Crabb1, R. Plummer2, A. Greystoke2, L. Carter3, S. Pacey4, H. Walter5, V.M. Coyle6, T. Knurowski7, K. Clegg7, F. Ashby7, N. Pegg7, W. West7, N. Brooks7, A. Hughes7, J. de Bono8

Author affiliations

  • 1 University Hospital Southampton, NHS Foundation Trust, 000 - Southampton/GB
  • 2 Newcastle University, Newcastle Hospitals NHS Foundation Trust, NE7 7DN - Newcastle-upon-Tyne/GB
  • 3 University Of Manchester, The Christie NHS Foundation Trust, Manchester/GB
  • 4 Department Of Oncology And Cancer Research Uk, Cambridge Centre, Cambridge/GB
  • 5 University Of Leicester, University Hospitals, Leicester/GB
  • 6 Patrick G. Johnston Centre For Cancer Research, Queens University Belfast, BT9 7AE - Belfast/GB
  • 7 Cellcentric Ltd, Chesterford Research Park, CB10 1XL - Cambridge/GB
  • 8 Institute Of Cancer Research, Royal Marsden NHS Foundation Trust, SM2 5PT - Sutton/GB

Resources

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Abstract 560TiP

Background

CCS1477 is a potent, selective, orally bioavailable inhibitor of the bromodomains of p300 and CBP, two closely related histone acetyl transferases with oncogenic roles in cancer. In vitro and in vivo models demonstrate molecular alterations that increase sensitivity to p300/CBP inhibition with CCS1477. Tumours with loss of function mutations in either p300 or CBP become dependent on the corresponding non-mutated paralogue (twin) protein. When the non-mutated twin is inhibited, this drives synthetic lethality leading to apoptosis/cell death. Recently, loss of function mutations in ARID1A have also demonstrated functional dependence upon p300/CBP.

Trial design

This Ph I/IIa study sponsored by CellCentric, evaluates the clinical activity of CCS1477 in patients with advanced solid tumours harbouring molecular alterations indicating sensitivity to p300/CBP inhibition. Specifically, potential markers determined by local testing, include loss of function mutations in p300, CBP or ARID1A; myc and AR amplification or over expression. Acceptable tests are next generation sequencing or equivalent, in archival or fresh tumour biopsies or in cell free DNA from a pre treatment blood sample. IHC may be used for over expression of proteins such as myc or AR. Patients with cancers where there is strong molecular rationale for a potential response to CCS1477 (e.g. myc over expression in Small Cell Lung Cancer and Radiation induced breast sarcoma) may be entered following discussion with sponsor. The trial is in 2 parts. Part 1 commenced Dec 2020 in the UK, and is opening in US & EU mid 2021, recruiting 20 patients to receive CCS1477 at a dose and schedule previously declared tolerated from the rising dose tolerability arm of the trial being separately conducted in men with metastatic castrate resistant prostate cancer (NCT03568656). In Part 2, up to 30 patients will receive CCS1477 at the recommended phase 2 dose and schedule. Anti-tumour activity will be determined by standard imaging according to RECIST guidelines. Paired tumour biopsies for biomarker assessment are being collected.

Clinical trial identification

2018-000285-10.

Editorial acknowledgement

Legal entity responsible for the study

CellCentric Ltd.

Funding

CellCentric Ltd.

Disclosure

T. Knurowski: Financial Interests, Personal, Full or part-time Employment: CellCentric Ltd. K. Clegg: Financial Interests, Personal, Full or part-time Employment: CellCentric Ltd. F. Ashby: Financial Interests, Personal, Full or part-time Employment: CellCentric Ltd. N. Pegg: Financial Interests, Personal, Member of the Board of Directors: CellCentric Ltd. W. West: Financial Interests, Personal, Member of the Board of Directors: CellCentric Ltd. N. Brooks: Financial Interests, Personal, Full or part-time Employment: CellCentric Ltd. A. Hughes: Financial Interests, Personal, Full or part-time Employment: CellCentric Ltd. J. de Bono: Financial Interests, Institutional, Research Grant: CellCentric Ltd. All other authors have declared no conflicts of interest.

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