Artery receives NIH-NIA fast-track SBIR grant to open up IND and perform First in Human testing of the ABCA1 agonist CS6253 indicated for the treatment of hereditary APOE4 associated Alzheimer’s disease.

Artery receives NIH-NIA fast-track SBIR grant to open up IND and perform First in Human testing of the ABCA1 agonist CS6253 indicated for the treatment of hereditary APOE4 associated Alzheimer’s disease. ​ Artery Therapeutics, Inc (Artery) is pleased to announce that on the World Alzheimer’s Disease Day September 21, 2022 we received a fast-track development grant from National Institutes of Health (NIH) National Institute of Aging (NIA) to perform “first in human testing”. On the heels of successful toxicology studies with the ABCA1 agonist CS6253, also supported by a NIH-NIA grant, the Small Business Innovation Research (SBIR) fast-track grant was received for opening up the IND (part 1) and performing a Single Ascending Dose (SAD) study (part 2) in 32-40 men and women 50 years and older. “We are very pleased for the peer-review validation of our technology and its potential in the treatment of hereditary APOE4 associated AD”, Jan Johansson MD, PhD, CEO of Artery stated. “The first in human study will allow us to asses safety, pharmacokinetics, and instant lipoprotein and amyloid effects”, Dr. Johansson further stated. In mice AD models cholesterol-directed treatment with CS6253, ABCA1was upregulated, apoE4 lipidation increased, amyloid and tau levels decreased and AD reversed. Consistent with the mice studies multiple dosing in monkeys showed unique lipid changes which was associated with transfer of amyloid from brain to plasma. APOE4 is the strongest genetic risk factor for Alzheimer’s disease and is also over-represented in many other dementia conditions including Parkinson's dementia, fronto-temporal dementia and traumatic brain injury suggesting a general metabolic culprit - lipid transport. APOE4-driven dementia is found in approximately 65% of Alzheimer's patients and more than 3 million patients in the USA alone. In homozygote APOE4 carriers the likelihood of developing AD is increased 12-20 fold. Recent data shows that the apoE4 protein compared to apoE2 and apoE3 has impaired cooperation with its lipidation protein, the ABCA1 transporter. Based on a discovery platform Artery’ has developed a lead molecule CS6253 targeting the ABCA1 transporter that improves the apoE - ABCA1 protein-to-protein interaction and reverses AD. The content of this news release is solely the responsibility Artery and does not necessarily represent the official views of the National Institutes of Health. ​ ​

The release as fetched from its publisher. arterytx.com ↗