1. Can you give us an outline of your role at Akari?
Scientific input and oversight to all areas of Akari’s work including strategic direction, regulatory interactions, clinical/preclinical and manufacturing programs, business development, and protection of intellectual property.
A typical day might involve drafting a response document to the FDA and liaising with regulatory advisors, planning preclinical testing, reviewing and signing off a preclinical report, agreeing the final version of a press release, talking to potential collaborators about a joint venture, and taking part in an internal meeting to discuss future clinical targets and trial designs.
2. What is the underlying science driving Akari’s pipeline?
Akari’s drugs are derived from parasites which have evolved to successfully exploit their hosts. Parasites do this by overcoming the hosts’ ability to sense and destroy the parasite, by secreting proteins, peptides and other molecules which regulate the immune, hemostatic and pain responses of the host.
Our lead Phase III drug nomacopan was originally derived from a tick. Nomacopan’s inhibitory bifunctional activity against complement C5 and leukotriene B4 (LTB4) was fully characterised, high resolution crystal structures obtained, and in vivo efficacy demonstrated in a number of animal models before it was considered worthy of further investment.
3. What makes Akari different from other companies in the sector?
Akari’s drugs are from a highly enriched source of biologicals that have been selected and perfected to manipulate the hosts immune and other defence systems by millions of years of co-evolution between host and parasite. The obvious benefits of this approach over other techniques are unique, ‘ready-to-go’ biological drugs that target key components of the immune system and have properties that may not be predicted by humans or artificial intelligence ‘AI’ which are both completely dependent on the quality of data inputs. Whereas coevolution depends on the actual efficacy and tolerability of the biological – since if it is non-efficacious or poorly tolerated coevolution ends with the death of the parasite.
A second difference is that our lead drug is bifunctional – it is not only a potent complement C5 inhibitor, but it also inhibits an unrelated proinflammatory mediator, LTB4. This differentiates nomacopan from all other drugs that only target the complement or leukotrine system.
4. Could you summarise the highlights of Akari’s clinical pipeline?
With a small core team we have successfully progressed our lead drug nomacopan through to Phase III clinical testing. Our initial work was in paroxysmal nocturnal hemoglobinuria (PNH), where nomacopan proved efficacious. We are now pursuing two indications in pivotal Phase III clinical studies. These are orphan, fast track programs for diseases with no approved treatments: bullous pemphigoid (BP) and thrombotic microangiopathy post stem cell transplant (HSCT – TMA). We also have earlier stage programs focused on the lung (direct delivery of nomacopan via inhalation) and eye diseases with large markets, most notably taking advantage of our detailed scientific understanding of nomacopan to develop an engineered long-acting form of nomacopan (PASylated-nomacopan) for treatment of geographic atrophy (GA).
5. Where do you see the company in 5 years?
I hope to see nomacopan marketed for the treatment of BP and/or HSCT-TMA which are both currently in phase 3 clinical testing. I also hope that we will be preparing to file for approval of long acting PASylated-nomacopan administered IVT at an interval of longer than 3 months for treatment of GA. and undertaking Phase III testing of an inhaled formulation of nomacopan. Given the broad potential of nomacopan in additional diseases, I would expect that a wide range of new clinical trials of nomacopan and long-acting nomacopan will be ongoing either alone or in partnership with other companies.