Anisinia Announcement Comment

Anisina Announcement Comment


Written by Dr Graham Kelly on 25th June 2015
A few armchair critics have commented on the ‘ho-hum’ nature of yesterday’s announcement. The main comment being that if we had already announced that we were bringing Anisina into the clinic in 2016, then we must already have the required animal efficacy data. So, why the big deal about some animals carrying human melanoma tumors?
It’s true….we do already have animal data showing that Anisina provides a significant anti-cancer effect. But that is in animals bearing human neuroblastoma tumors. That is where a lot of our R&D effort has gone this past 6 months. That data identified Anisina as our lead candidate, proved that it delivered a significant anti-cancer effect in the whole animal (compared to cell culture) and that was what gave us the green light we needed to proceed into the clinic in 2016.
But neuroblastoma is a special case. It is the most common solid cancer in children. The anti-microtubule drug, vincristine, is standard of care for this tumor and delivers long-term remission in a proportion of children. But that comes at a significant cost to physical and mental development, leaving the child with a lifetime legacy of developmental problems.
The question that a group at a major US childrens’ hospital asked was whether by using Anisina in combination with vincristine (and thereby targeting both major components of a cancer cell’s cytoskeleton), that the vincristine dosage could be lowered to a much less toxic level without compromising its anti-tumor effect. Achieving that would represent a major step forward in pediatric oncology.
The results of those pre-clinical studies are being presented to a scientific conference in the US on July 13. I will talk about that data then.
That is how Anisina is being looked at in pediatric oncology.
In adults it is a different situation. Here the issue is less to do reducing toxicity than it is with making the commonly used anti-microtubule drugs work better, or finding something that on its own is a better option than them.
To answer this question, we are working with melanoma and prostate cancer. Melanoma, because it is a cancer that responds poorly to anti-microtubule drugs; prostate cancer because it does respond to anti-microtubule drugs, just not very well.
I’ll leave the discussion about prostate cancer to another day.
The studies we reported on yesterday with melanoma had two main objectives. The first was to decide whether we would be better using an oral dosage form or an intravenous dosage form in adults. In both cases the drug was suspended in the cyclodextrin carrier, Dexsolve. Both methods of treatment worked equally well, so on that basis we are proceeding into the clinic with the intravenous dosage form.
The second objective was to demonstrate that Anisina could deliver a potent anti-cancer effect in a tumor model notoriously difficult to treat with anti-microtubule drugs. As the graph below shows, it did this, with the mice tolerating the treatment with no evidence of any toxicity.


We now know we have a drug candidate that could go head-to-head with the most commonly-used cytotoxics in chemotherapy, but with the huge advantage of being highly on-target with no apparent toxicity.
With the dosage form determined, Anisina now will proceed on the path to a first-in-man (Phase 1) study in patients with solid cancers. Whether the next stage after that will be in patients with malignant melanoma, or late-stage prostate cancer, or some other cancer type that shows evidence of clinical response in the Phase 1 study, is a decision yet to be made.
Far from being ho-hum, yesterday’s announcement represented a key stepping stone in the development of Anisina.