You have got a new drug that’s an anti-oestrogen drug. Let me ask you why did we need an anti-oestrogen drug and what is the reason for the study that you’re talking about here at San Antonio?

It’s not a classic anti-oestrogen, it targets the oestrogen receptor. So it works in a fundamentally different way than other drugs that currently work. It is intended for patients who are oestrogen receptor positive. So currently we already have drugs that work some for patients who are oestrogen receptor positive, however those drugs initially work and then afterwards those drugs stop working.

What’s different about this one, about the mechanism then?

The mechanism, it’s a fundamentally different mechanism from the other drugs that are commercially available, that are FDA approved. This targets the way the oestrogen receptor functions. So in order for the oestrogen receptor to function it functions by binding to certain coregulator proteins and what this does is it blocks the interaction between the oestrogen receptor and critical coregulators. So it’s a fundamentally different mechanism than other drugs that are commercially available.

We’ve been hearing here in San Antonio about the way that anti-oestrogen therapies can modulate the environment and perhaps influence the development of the disease. How would yours differ, is it just another agent?

One of the key things is in order for resistance to happen, resistance happens by mutations, alterations in the oestrogen receptor, but at the same time one of the key ways all those mutant receptors work is that they interact with coregulators. This cuts the legs out from underneath the oestrogen receptor, it prevents the oestrogen receptor from interacting, whether mutant or wildtype, from interacting with the coregulators so it’s fundamentally different.

It sounds a great idea, what did you do in practice in your preclinical work?

We first developed an agent and we’ve tested it in a variety of breast cancer cell lines first. Then we tested it in animal models and interesting we also tested it in primary breast cancer tissues, so tumour tissues from patients with breast cancer, those are exactly the patients who would benefit from the therapy, and we showed that in the tumour tissues that this drug has activity.

Activity, what about potential toxicities too?

That’s a great question, any time you develop these drugs there’s a question of toxicity. So we try to establish what’s called a toxicity to therapeutic ratio, so you go a hundred times higher dose than what you would give the animal for therapeutic efficacy and try to see this toxicity. Even at that higher dose we did not see toxicity in the animal.

So what do you think is the big advantage of going for the coregulators?

When you target coregulators resistance is a little harder to come by. So you’re targeting a broad panel of interactions. In order for resistance to develop the receptor must change in a fundamentally different way than what we’ve seen it develop so far in order to avoid the activity of this drug.

So what has come out of the study so far that is pointing in a clinical direction?

We have a lead candidate that we are funded to take it forward to IND or investigational new drug status. We’re currently performing the IND enabling studies and bringing it forward to clinical trials.

What do you think doctors should take home from this sort of promising but, as yet, unproven research?

This is a novel way to target the oestrogen receptor and I think this highlights additional ways to target the oestrogen receptor. We’re still targeting the oestrogen receptor but in a more effective manner.

So the status of ECBI at the moment is what?

It’s preclinical, rapidly heading towards final testing for IND status and then trying to move it forward to the clinic.