Watch: The competitive advantage of our immunotherapies explained

Dr Geoffrey Nichol, HaemaLogiX Non-executive director, explains in simple terms the difference between our targets and those of existing treatments for myeloma, and the competitive advantage this difference gives to our treatments.

Video: The competitive advantage of our immunotherapies explained

Transcript

Intro: You will start to fill this Gap of giving a treatment that gives you all the benefits of previous successful treatments without these really debilitating downsides. That's where the competitive differentiation and the competitive Advantage is.

Question: HaemaLogiX is developing three immunotechnologies: Monoclonal antibodies, CAR-Ts and bispecifics. How effective are these regarded to be for treatment of multiple myeloma?

There have been some major advances in the broad use of biologic agents in multiple myeloma:

• You can use an antibody like Kappamab, which persuades certain cell types to kill cancer cells,

• You can put that target onto T cells, which are the gorillas of the immune system -they will kill anything if you can activate them enough - and this we call a CAR-T,

• or you can use an antibody called a bi-specific which has one side that latches on to the T cell, the big gorilla again, and the other side that latches on to the cancer cell. When those two are brought together, the T cell will kill the cancer cell.

These are three great technologies and all three approaches have shown great efficacy in multiple myeloma to date.

Question: The targets in drug development are important especially when it comes to investment opportunity. Considering targets, can you explain the limitations of the drugs on the market?

When it comes to drug development, it comes down to two things:

• the target that is being used and

• whether that target has a good prospect of filling some gap in medical needs.

The problem has been the targets that we use, which currently are expressed both on the cancer cell and on a whole bunch of normal immune cells.  Unfortunately for the patient, although they get the benefit of the efficacy with the multiple myeloma, they often have very significant parts of their immune system knocked out and that eventually turns out to be a big problem for them because they get infections, and their quality of life is significantly decreased.

The other problem that happens is that the current targets that have been used successfully - as the disease becomes more severe and more progressive – the targets get progressively lost off the surface of the cancer cell which gives the target less to latch onto and so patients will relapse. While everyone tends to focus on the efficacy benefits, patients and the physicians who treat them, are certainly looking over their shoulders because they see this big gap in treatment.

Question: What makes our targets (KMA and LMA) and out KappaMab antibody and CAR-T treatments different?

HaemaLogiX’s targets - KMA and LMA - are different from the ones that have been used previously. They are only expressed on the cancer cell. They are not expressed on other bystander immune cells, so our targets can solve that first problem.

The other thing that's very interesting, is that the more you treat and the more the disease progresses, the more LMA and KMA are expressed on the surface of the cancer cell so we believe that we can have as much, if not better efficacy, that lasts for longer with these targets without this very consequential damage to the to the immune system, which is kind of the Achilles heel of the current approaches - yet you can use an antibody, you can build a CAR-T, and you can build a bispecific antibody to our targets, just as easily as you can build one to the others.

You then have a question - does this work and in drug development - coming back to the theory and practice of drug development - you then just have to come up with a development program which uses the least amount of time and investor money to come up with an answer. We already have some data from a Phase II study with KappaMab showing pretty interesting efficacy and we have some pre-clinical data with a CAR-T, showing the kind of efficacy that all the other CAR-T have shown in mice so we are feeling that there's a significant amount of de-risking already done and we just need to go to the next stage of development to get a definitive answer in patients.

You will have something that looks as effective, hopefully even a little bit more effective, because you know these targets are increasing in number on the cells rather than decreasing so that may improve efficacy and then have you will start to fill this gap of giving a treatment that gives you all the benefits of previous successful treatments without these really debilitating downsides. That's where the competitive differentiation and the competitive advantage is.

Question: If you succeed, how competitive do you expect the HaemaLogiX portfolio of products to be in the market?

It's going to be, to a degree, self-evident - why would you take something that gives you good efficacy, but in 2-3 years’ time could kill you with pneumonia because your immune system has been ripped to pieces because of collateral damage, versus a treatment that gives you all those treatments without that collateral damage.

There are plenty of examples commercially where drugs that have solved that collateral damage problem have come to dominate the market even though the previous drugs were kind of okay and some of them were really breakthroughs at the time.

END