AlzeCure Pharma AB (publ) (FN STO: ALZCUR), a pharmaceutical company that develops a broad portfolio of drug candidates for diseases affecting the central nervous system, with projects in both Alzheimer’s disease and pain, today announced that the company has received a second abstract approved for poster presentation at the annual Alzheimer’s conference CTAD, Clinical Trials in Alzheimer’s Disease, which this year will be held completely digitally on November 4-7.
The abstract titled ACD856, a novel cognitive enhancer targeting neurotrophin signaling for the treatment of Alzheimer’s Disease shows that AlzeCure’s leading drug candidate, ACD856, in the company’s NeuroRestore platform has the potential for widespread use of various types of cognitive memory disorders. The abstract is based on the results that led to the selection of a drug candidate and the recent completion of a successful clinical microdose study; a work carried out in collaboration with Professor Bengt Winblad and Professor Maria Eriksdotter at Karolinska Institutet, as well as Pontus Forsell, Johan Sandin and Gunnar Nordvall at AlzeCure.
”It is very satisfactory that we have now received two abstracts approved for presentation at this leading Alzheimer’s conference. The results we have seen, and which are summarized in this abstract, show the possibilities with our main candidate ACD856 and support further clinical studies. I am very much looking forward to our upcoming clinical studies with the candidate, which we expect to be able to start before the end of the year”, said Martin Jönsson, CEO of AlzeCure Pharma AB.
The abstract and the poster will be available to registered participants online on CTAD’s website from November 4, 2020.
For more information, please contact
Martin Jönsson, CEO
Tel: +46 707 86 94 43
The information was submitted for publication, through the agency of the contact person set out above at 10:00am CET on October 13, 2020.
About AlzeCure Pharma AB (publ)
AlzeCure® is a Swedish pharmaceutical company that develops new innovative drug therapies for the treatment of severe diseases and conditions that affect the central nervous system, such as Alzheimer’s disease and pain – indications for which currently available treatment is extremely limited. The company is listed on Nasdaq First North Premier Growth Market and is developing several parallel drug candidates based on three research platforms: NeuroRestore®, Alzstatin® and Painless.
NeuroRestore consists of three symptomatic drug candidates where the unique mechanism of action allows for multiple indications, including Alzheimer’s disease, as well as cognitive disorders associated with traumatic brain injury, sleep apnea and Parkinson’s disease. Alzstatin comprises two disease-modifying and preventive drug candidates for early treatment of Alzheimer’s disease. Painless is the company’s research platform in the field of pain and contains two projects: ACD440, which is a clinical candidate for the treatment of neuropathic pain, and TrkA-NAM, which targets severe pain in conditions such as osteoarthritis. AlzeCure aims to pursue its own projects through preclinical research and development to an early clinical phase and is continuously working with business development to find suitable out-licensing solutions with other pharmaceutical companies.
FNCA Sweden AB, +46(0)8 528 00 399 email@example.com, is the company’s Certified Adviser. For more information, please visit www.alzecurepharma.se.
NeuroRestore is a platform of symptom-relieving drug candidates for disease states in which cognitive ability is impaired, e.g. Alzheimer’s Disease, sleep apnea, traumatic brain injury and Parkinson’s disease. NeuroRestore stimulates several important signaling pathways in the brain, which among other things leads to improved cognition. In preclinical studies with NeuroRestore we have been able to show that our drug candidates enhance communication between the nerve cells and improve cognitive ability. NeuroRestore stimulates specific signaling pathways in the central nervous system known as neurotrophins, the most well-known being NGF (Nerve Growth Factor) and BDNF (Brain Derived Neurotrophic Factor). The levels of NGF and BDNF are disturbed in several disease states and the signaling is reduced. The impaired function impairs communication betweenthe synapses, i.e. the contact surfaces of the nerve endings, as well as reducing the possibility of survival for the nerve cells, which gives rise to the cognitive impairments. Neurotrophins play a crucial role for the function of nerve cells, and a disturbed function of BDNF has a strong genetic link to impaired cognitive ability in several different diseases, such as Alzheimer’s, Parkinson’s disease, traumatic brain injury and sleep apnea.
About Alzheimer’s disease
Alzheimer’s disease is the most common form of dementia, affecting approximately 45 million people worldwide. Alzheimer’s disease is a lethal disorder that also has a large impact on both relatives and the society. Today, preventive and disease modifying treatments are missing. The main risk factors to develop Alzheimer’s are age and genetic causes. Even though the disease can start as early as between 40 and 65 years of age, it is most common after 65 years. Significant investments in Alzheimer research are being made because of the significant unmet medical need and the large cost of this disease for healthcare and society. The total global costs for dementia related diseases is estimated to about 1,000 billion USD globally in 2018. Given the lack of both effective symptomatic treatments and disease modifying treatments, the need for new effective therapies is acute.The few approved drugs on the market today have only a limited symptomatic effect and can produce dose limiting side effects. A disease modifying treatment for Alzheimer’s disease is estimated to reach more than 10 billion USD in annual sales. In Sweden, approximately 100,000 people suffer from Alzheimer’s disease with a healthcare cost of about 63 billion SEK yearly, which is more than for cancer and cardiovascular diseases combined.