The ‘next big thing’ comes along about every 10-15 years in oncology. The last ‘big things’ were the so-called immuno-oncology drugs (or checkpoint inhibitors) – Yervoy and Opdivo (Bristol-Myers Squibb) and Keytruda (Merck). These drugs were expected to turn cancer therapy on its head based on some early dramatic responses in patients with melanoma and lung cancer, with annual sales of US$100+ billion being projected.
But further experience unfortunately showed that they don’t work in most forms of cancer and in most patients. Although sales of all 3 drugs are still expected to reach US$15 billion this year, which is not bad for a therapy that appears to work in less than 5% of cancer patients when you include all forms of cancer.
Which is where the ‘next big thing’ comes in. Scientists have now discovered why the checkpoint inhibitors aren’t working in most patients, and a way to correcting that problem is what has created the ‘next big thing’, which is STING.
But first the problem. The problem lies in the way cancer cells survive by protecting themselves from the body’s immune cells. There are 2 main ways. One way is to erect a shield (called checkpoints) around themselves that prevents immune cells from being able to attach to them. This shield tricks the immune cells into ignoring them. The second way is to expel immune cells from the tumour, so that the cancer cells effectively live in an immune-free environment.
The aim of the checkpoint inhibitors is to remove the protective shield, thereby exposing the cancer cell to attack and elimination by immune cells. And that is where the problem appears to lie – only a small proportion of tumours have enough immune cells inside them to attack the exposed cancer cells. Hence the relatively low response rate to checkpoint inhibitors. The kind of tumours that do respond to the checkpoint inhibitor drugs are referred to as ‘HOT’ tumours, with the ‘hot’ referring to the presence of a strong level of immune activity.
However, the majority of cancers are not ‘HOT’ tumours. They either have expelled the immune cells to the edge of the tumour (referred to as ‘WARM’ tumours) or expelled them completely (‘COLD’) tumour. ‘WARM’ tumours respond partially to checkpoint inhibitors and ‘COLD’ tumours don’t respond at all. By way of example, in prostate cancer, which is a focus of Noxopharm’s efforts, most tumours appear to be ‘COLD’, accounting for the almost complete lack of response of prostate cancer to the so-called checkpoint inhibitors so far.
The solution. Converting ‘WARM’ and ‘COLD’ tumours to ‘HOT’ has become the latest goal of a lot of pharma and biotech companies. And the way they are trying to do this is by something called STING.
STING stands for Stimulating Interferon Genes. It is exactly what it says --- the aim is to get a tumour to make interferon (a protein that the human body uses to activate immune calls) which then goes on to pull immune cells into the tumour and activates them, with the result that you now have a ‘HOT’ tumour.
We believe we know of about 10 companies actively working in this field. Each is using a different way of activating STING. Whoever first comes up with an effective and safe way of doing this will have a very valuable piece of property, given the potential to be the means for the checkpoint inhibitors to meet their US$100-plus billion market size.
We believe that Noxopharm is potentially one of those 10 companies, and we have a high degree of confidence in our position.
You will be hearing a lot more about our STING program over the coming months.
ASX April 29th, 2019; https://www.noxopharm.com/site/PDF/1947_0/VeyondaandImmunoOncologyEffectExplained