Clinical

Mechanism of action through to specific applications

p300/CBP inhibition impacts

Inhibiting p300/CBP impacts androgen receptor expression and splice variants (AR-SV). It also affects MYC and IRF4, two other important genes in cancer progression.

The AR-axis is particularly important in the progression of late stage, drug resistant prostate cancer, where MYC plays a role as well. IRF4 is important in multiple myeloma, and in combination with MYC, p300/CBP inhibition has applications in other haematological malignancies too.

Tumours with either a p300 or CBP mutation are particularly susceptible to inhibition of both proteins (paralogue lethality). Tumours that over express AR or MYC can also be rationally targeted with a p300/CBP inhibitor.

Phase I/II clinical trials

CellCentric’s clinical programme reflects the mechanism of action of p300/CBP inhibition. CCS1477 is being evaluated in three parallel strands. Each represents significant and growing clinical unmet needs.

First-in-class p300/CBP

CellCentric’s first-in-class p300/CBP inhibitor is in patients with advanced, drug-resistant prostate cancer, as well as in patients with haematological malignancies (multiple myeloma, AML, lymphomas). CCS1477 will also be used to target tumours with specific drivers (p300 or CBP mutations, AR+, MYC over-expression). This includes small cell lung, bladder and breast cancers.

Patient enrolment

Potential suitability for enrolment in a CCS1477 clinical trial will be made by oncologists at our participating hospitals, and not by CellCentric. Any advice on clinical study options should come from your general practitioner and/or oncologist.