Inobrodib affects less/different genes than JQ1 in 22Rv1 cells
In prostate cancer, inobrodib, unlike other agents, down-regulates not just the Androgen Receptor (AR), but also AR splice variants. These are important in the innate or acquired resistance to existing treatments.
Certain haematological cancers are highly susceptible to p300/CBP inhibition, and particularly in combination with IMiD agents, where certain pre-clinical models have shown that tumour cells can be eliminated. Being an orally delivered product, it has significant advantages over other new haematological treatments in development that can require extended intravenous infusion.
inobrodib has an unusual duration of effect in pre-clinical models. Tumour stasis is sustained far beyond cessation of drug administration, even though there is no drug remaining in circulation. Tumours are in effect, reprogrammed to a degree.
By targeting the bromodomain of p300/CBP, inobrodib has a different efficacy and tolerability profile from other agents in discovery that target the catalytic HAT or CH1 domain.