Artery Therapeutics, Inc (Artery) is pleased to announce that the National Institute of Aging (NIA) of the National Institutes of Health (NIH) has awarded a Small Business Innovation Research (SBIR) fast-track grant to advance "CS6253 for the treatment of apoE4-driven dementia including Alzheimer’s disease".

Artery Therapeutics, Inc (Artery) is pleased to announce that the National Institute of Aging (NIA) of the National Institutes of Health (NIH) has awarded a Small Business Innovation Research (SBIR) fast-track grant to advance "CS6253 for the treatment of apoE4-driven dementia including Alzheimer’s disease". The phase I of this award, to be performed the next 6-9 months will focus on PK and PD assessment in cynomolgus monkey studies in preparation for IND enabling studies. If predefined milestones are met then the Phase II portion of the fast-track grant will focus on completing an IND submission for CS6253. ​ Dr. Johansson, Founder, Chief Executive Officer of Artery and Principal Investigator for the grant states “cynomolgus monkeys have an apoE with high homology to human apoE4 and already in the phase I part of the grant we hope to assess pharmacokinetics, pharmacodynamics and safety relevant to translation to studies in human apoE4 carriers." ApoE4 is the strongest genetic risk factor for Alzheimer’s disease and is also over-represented in many other dementias 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 60% of Alzheimer's patients and more than 2.5 million patients in the USA alone. The risk in apoE4 homozygote carriers is extra severe and increasing the likelihood to develop Alzheimer’s disease 12-fold. Recent data shows that apoE4 compared to apoE2 and apoE3 has impaired cooperation with its lipidation protein, the ATP Binding Cassette-A1 (ABCA1). Based on a discovery platform Artery’ has developed a lead molecule CS6253 targeting the ABCA1 transporter that improves the apoE - ABCA1 cooperation. Research reported in this publication was supported by the National Institute On Aging of the National Institutes of Health under Award Number R44AG060826. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. ​ ​

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