A poor IDO1 function has been involved in the pathophysiology of IBD. Recently, we made the ground-breaking discovery that N-acetylserotonin (NAS) binds to IDO1 and acts as positive allosteric ligand, enhancing the enzymatic catalytic activity. We were then able to design a first-in-class candidate (VIS329) that act as positive allosteric IDO1 modulator by boosting the enzymatic catalytic activity. VIS319 may have great untapped potential for developing disease modifying therapies for IBD.
Patent Status
PENDING
Priority Number
102022000017703
Priority Date
29/08/2022
License
ITALY
Market
The prevalence of IBD in EU and USA has been estimated at 3.5 million patients. The market size is €19,5 billion, with a 5.1% Compounded Average Growth Rate (CAGR).
There is an unmet need for: (i) consistent drugs with less non-responses; (ii) improved second and third line drugs with regard to cost and efficacy; (iii) novel targets improving mucosal barrier healing as a better long-term treatment strategy.
Problem
IBD is a highly prevalent disease in western society and a growing problem in emerging countries. It includes a group of disorders that cause chronic inflammation in the intestines such as Crohn’s disease (CD) and ulcerative colitis (UC). Although the underlying cause of IBD is multifactorial and remains largely unknown, it is attributed to an inappropriate immune response against environmental factors (e.g. dietary or microbial antigens) and genetic susceptibility. As such, so far, no long-lasting disease modifying therapies exist for IBD. Although multiple treatment strategies are available for IBD, all of them show indeed varying efficacy and safety. For example, aminosalicylates are well established for UC, but not for CD. Most critically, long term clinical remission of IBD is hardly reached. Patients have frequent relapses and remain sensitive to triggers. The thrust of our invention idea stems from the observations that (i) IDO1 is highly upregulated in the gut mucosa in response to IBD; (ii) several Trp metabolites have been involved in the pathophysiology of IBD; (iii) genetic polymorphisms of IDO1 have been associated with a severe clinical course of CD, suggesting lower IDO1 functions during the disease. These observations suggest that VIS329, acting as positive allosteric modulator of IDO1, may represent a disease modifying therapy for IBD.
Current Technology Limits
Although multiple treatment strategies are available for IBD, they have varying efficacy and safety. Aminosalycilates are effective in 90% of mild to severe UC patients yet have limited effectiveness in CD. Corticosteroid courses result in adverse side effects. Third-line treatments are expensive, have more side effects and are only effective in specific subsets of patients. These observations pose the following problems of unmet needs:
Our novel candidate VIS329 presents a better, cheaper and safer treatment for severe autoimmune diseases, including IBD. VIS329 boosts IDO1 activation which unlocks a positive feedback loop that sustains immune tolerance and restores immune homeostasis. This unique mechanism of action provides VIS329 with high specificity and selectivity that may reduce non-responses and lead to longer remission in treated IBD patients. Moreover, the relatively cheap and simple synthesis of VIS329 will drastically reduce the cost of treatment for IBD.
Killer Application
Main applications of our patented compounds (e.g. VIS329) are:
Our Technology and Solution
The novel allosteric immunotolerogenic candidate VIS329 presents a better, cheaper and safer treatment for the severe autoimmune diseases, including IBD. The relatively cheap and simple synthesis of VIS329 will drastically reduce the cost of treatment for IBD. Moreover, VIS329’s unique mechanism of action provides it with high specificity and selectivity, reducing non-responses and leading to longer remission in treated patients.
Advantages
Roadmap
The following hurdles need to be overcome for commercialization of VIS329:
The proposed roadmap includes: (i)advancing the technology further in collaboration with industry partners; (ii)selling current IP in exchange for up-front fees, milestone payments, royalties.
TRL
Team
