Alzheimer's Association International Conference (AAIC) | July 14 - 18, 2019
Los Angeles, CA

  • Anti-inflammatory Effects of SM07883, a Novel, Potent, and Selective Oral DYRK1A Inhibitor in Neurodegenerative Mouse Models
    Abstract - Slides

Aging Cell | July 03, 2019

  • Tau pathology reduction with SM07883, a novel, potent, and selective oral DYRK1A inhibitor: A potential therapeutic for Alzheimer's disease

    Aging Cell.

    Benoît Melchior, Gopi Kumar Mittapalli, Carolyn Lai, Karen Duong‐Polk, Joshua Stewart, Bora Güner, Brian Hofilena, Amanda Tjitro, Scott D. Anderson, David S. Herman, Luis Dellamary, Christopher J. Swearingen, K.C. Sunil, Yusuf Yazici


Keystone Symposia - Neurodegenerative Diseases: New Insights and Therapeutic Opportunities | June 16 - 20, 2019
Keystone, CO

  • SM07883, a Novel Oral DYRK1A Kinase Inhibitor, Reduced Tau, Amyloid Pathology, and Related Inflammation in Preclinical Models
    Abstract - Poster

Alzheimer's Solutions Conference | June 02 - 03, 2019
Philadelphia, PA

  • Hitting 3 birds with one pill: How SM07883 may prevent tau, amyloid, and inflammation in Alzheimer’s disease
    Abstract - Slides

International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD) | March 26 - 31, 2019
Lisbon, Portugal

  • Cognitive Improvement and Protection Against Amyloid and Tau Pathology with SM07883, an Oral DYRK1A Inhibitor, in the 3xTG Mouse Model of Alzheimer’s Disease; Preliminary Results
    Abstract - Poster

New York Academy of Sciences (NYAS) Symposium on Alzheimer's Disease Therapeutics | December 11, 2018
New York, NY

  • Tau Pathology Reduction with SM07883, A Novel, Potent, and Selective Oral DYRK1A Inhibitor - Potential Therapeutic for Alzheimer’s Disease
    Abstract - Poster

International Conference on Frontotemporal Dementias | November 11 - 14, 2018
Sydney, Australia

  • SM07883, a Novel, Potent, and Selective Oral DYRK1A Inhibitor Reduced Tau Pathology in Preclinical Models
    Abstract - Poster

Clinical Trials on Alzheimer's Disease (CTAD) | October 24 - 27, 2018
Barcelona, Spain

  • SM07883, a novel DYRK1A inhibitor, reduced Tau pathology – discovery and preclinical development of a potential therapeutic for Alzheimer’s disease
    Abstract - Poster

Alzheimer’s Association International Conference (AAIC) | July 22 - 26, 2018
Chicago, IL

  • Tau Pathology Reduction with SM07883, a Novel, Potent, and Selective Oral DYRK1A Inhibitor - a Potential Therapeutic for Alzheimer’s Disease
    Abstract - Slides

Advances in Alzheimer's and Parkinson's Therapies (AAT-AD/PD) Focus Meeting 2018 | March 15 - 18, 2018
Turin, Italy

  • Tau Pathology Reduction with SM07883, a Novel, Potent, and Selective Oral DYRK1A Inhibitor – a Potential Therapeutic for Alzheimer’s Disease
    Abstract - Slides

Royal Society of Medicine's 13th Medical Innovations Summit | September 17, 2016
London, United Kingdom

  • Samumed's Regenerative Medicine Platform

Award Winning

Overview: Alzheimer’s Disease

Alzheimer’s disease (AD), the most common cause of dementia, is a chronic neurodegenerative disease affecting an estimated 5.8 million people in the United States (U.S.)1 and over 46 million people worldwide.2

  • Currently approved therapies help manage some symptoms but do not address the underlying causes or the progression of the disease, which is ultimately fatal.1
  • With the world’s aging population, AD is quickly becoming a global epidemic, and a socioeconomic burden impacting families, social services, and healthcare delivery systems.1

Symptoms of AD generally appear in patients in their mid-60s, though symptoms may occur earlier in patients with familial forms of AD stemming from a genetic predisposition. The disease is initially characterized by progressive memory loss followed by slow progression to severe difficulty in accessing basic brain functions and subsequent mental disorders.

Alzheimer’s disease is a multifactorial disorder that involves several different etiopathological mechanisms. These include aggregation and deposition of tau and amyloid that contribute to the neurodegeneration that characterizes AD.

The DYRK1A kinase is a promising target for Alzheimer’s disease research. DYRK1A contributes to the formation of amyloid plaques and may induce inflammation.3,4 In animal models of AD, upregulated DYRK1A activity also causes biochemical modification of tau protein structure in the brain.3-6 Inhibition of DYRK1A activity may reduce tau, amyloid, and related inflammatory pathology, thus providing a potential treatment modality for AD.


    1. Alzheimer’s Association. 2019 Alzheimer’s Disease Facts and Figures. Alzheimers Dement. 2019;15(3):321-87.
    2. Alzheimer’s Disease International. World Alzheimer’s Report 2015: The Global Impact of Dementia. Accessed 05/29/2019.
    3. Ryoo SR, Cho HJ, Lee HW, et al. Dual-specificity tyrosine(Y)-phosphorylation regulated kinase 1A-mediated phosphorylation of amyloid precursor protein: Evidence for a functional link between Down syndrome and Alzheimer's disease. J Neurochem. 2008;104(5):1333-44.
    4. Khor B, Gagnon JD, Goel G, et al. The kinase DYRK1A reciprocally regulates the differentiation of Th17 and regulatory T cells. Elife. 2015;4:1-27.
    5. Wegiel J, Gong CX, Hwang YW. The role of DYRK1A in neurodegenerative diseases. FEBS Journal. 2011;278(2):236-45.
    6. Ferrer I, Barrachina M, Puig B, et al. Constitutive Dyrk1A is abnormally expressed in Alzheimer disease, Down syndrome, Pick disease, and related transgenic models. Neurobiol Dis. 2005;20(2):392-400.