SynAct Pharma announced positive data from preclinical study in nephrotic syndrome with candidate drug AP1189

SynAct Pharma AB (“SynAct”) today announced that the company received positive data from a preclinical study in nephrotic syndrome (NS). The study shows that daily dosing for four weeks with candidate drug AP1189 (currently in clinical phase I) provided a significant reduction in proteinuria (protein loss via the kidneys) in a trial model for nephrotic syndrome. This data is the basis of a patent application filed by the company to ensure the protection of AP1189 as a potential treatment of proteinuria in patients with nephrotic syndrome and other conditions characterized by protein loss from the kidneys.

AP1189 is a biased agonist against melanocortin type 1 and 3 receptors, currently in clinical development with the primary purpose of taking the candidate drug into clinical phase II development as adjunctive therapy to methotrexate in active arthritis (rheumatoid and psoriatic arthritis). In parallel with the clinical development, SynAct has, as an integral part of its research activities, initiated a program in which AP1189 is tested in animal models for diseases with an “unmet medical need”, including studies in an animal model on NS.

Nephrotic Syndrome (NS) is a disease characterised by the loss of plasma protein by the kidneys (proteinuria), decreased levels of plasma protein and oedema development. Untreated, the disease leads to chronic renal failure, where dialysis and transplantation are the only treatment options. Chronic renal failure leads to a markedly increased risk of cardiovascular diseases, including high blood pressure and myocardial infarction. NS can in many cases be considered an autoimmune disease and is often seen as manifestation of systemic inflammatory diseases. Approximately 40% of all patients with systemic lupus erythematosus (SLE) have symptoms of impaired renal function with proteinuria. NS is primarily treated with glucocorticoids, cytostatics, ACTH and ACE inhibitors.

SynAct Pharma now has preclinical data showing that AP1189 in a therapeutic dosage significantly reduces the excretion of albumin in urine (proteinuria). Treatment with AP1189 of rats with immunologically induced proteinuria, given from the time when the degree of proteinuria was greatest, resulted in a significant decrease in proteinuria (approximately 50%) in relation to the maximum proteinuria level that the animals had before treatment began, and compared to animals treated with the placebo. The degree of reduction in proteinuria is comparable to the effect that can be achieved with ACTH treatment, which is used under the ACTHAR-gel brand to treat NS. The pharmacological effect of ACTHAR gel, like the Synact drug candidate AP1189, is mediated via stimulation of melanocortin receptors, but also has undesirable effects including stimulation of glucocorticoid release from the adrenal glands leading to a wide range of side effects. Another side effect is induction of skin pigmentation. The use of ACTHAR gel is therefore restricted to difficult-to-treat patients, but despite this, the annual sales for the treatment of NS alone are approximately USD 300 million.

CEO Jeppe Øvlesen comments:

“This new preclinical data, which showed that AP1189 has a good effect in a model of nephrotic syndrome, indicates that our candidate drug also has potential in the treatment of nephrotic syndrome where there is a significant need for Improved treatment”. We will continue our preclinical studies, including further studies of AP1189 ‘s potential in nephrology, in parallel with completing the Phase I study and making AP1189 ready for Phase II clinical development.”

For further information about SynAct Pharma AB, please contact:

Jeppe Øvlesen
CEO, SynAct Pharma AB
Telephone: +45 28 44 75 67
E-mail: [email protected]

Thomas Jonassen
CSO, SynAct Pharma AB
Telephone: +45 40 15 66 69
E-mail: [email protected]

This is information that SynAct Pharma AB is obliged to disclose under the EU’s market abuse regulation. The information was submitted by the above contact person for publication on 20th August 2018.