Masitinib for the Treatment of Alzheimer’s Disease

Abstract

The actual standard treatment for mild-to-moderately severe Alzheimer’s disease only attacks its symptoms. Masitinib is a potent and selective phenylaminothiazole-type tyrosine kinase inhibitor which is currently in Phase III studies for the treatment of Alzheimer’s disease (AD) with the aim of modifying its evolution and with multiple pharmacological targets such as inhibition of mast cells activity, inhibition of microglia activation, modulation of Aβ and Tau protein signaling pathway and prevention of synaptic damage. Here, we review the preclinical and clinical studies that investigated the administration of masitinib treatment in monotherapy in AD. All research studies revealed positive effects concerning the cognitive functions in AD and generally with good safety and tolerability.

Lay abstract

In the 21st century, life expectancy has increased a lot in developed countries but so has the number of people who are diagnosed with Alzheimer’s disease (AD). AD causes a decline in brain function over time and is the main cause of death and disability in elderly people. Current treatments only improve the symptoms of the disease but do not cure or stop the disease getting worse. For this reason, new treatments are being developed including the drug masitinib which is in Phase III in clinical trials. Masitinib protects specific brain and nervous system cells from being damaged by the disease. Results from current research into masitinib suggest that it can improve cognitive processes in AD patients. This article summarizes results from masitinib clinical and preclinical studies.

Graphical abstract

Keywords:

• Alzheimer’s disease
• clinical trials
• masitinib
• mechanism of action

Author contributions

M Ettcheto and A Camins equally performed the conceptualization, methodology, validation, formal analysis, bibliographic search and writing of the original draft. A. Cano, E Sanchez-López, E Verdaguer, J Folch and C Auladell contributed in the bibliographic search and writing of an original draft section. A Cano contributed in the supervision, writing/review and editing, project administration, resources and funding acquisition. All authors have made a substantial contribution to the work. All authors have read and agreed to the published version of the manuscript.

Financial & competing interests disclosure

A Cano acknowledges the support of the Spanish Ministry of Science, Innovation and Universities under the grant Juan de la Cierva (FJC2018-036012-I). Authors acknowledge the support of Spanish Ministry of Economy and Competitiveness under project SAF2017-84283-R, and Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED) under the project CB06/05/0024. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.