ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
Open Access

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Nilotinib Single-Dose Pharmacokinetics and Pharmacodynamics in Parkinson's Disease Patients

Hari Prasad Sonwani*, Pragya Sahu and Rashi Bandey
Department of Psychology, Apollo College of Pharmacy, Durg, Chhattisgarh, India
*Corresponding Author: Hari Prasad Sonwani, Department of Psychology, Apollo College of Pharmacy, Durg, Chhattisgarh, India, Email: harisonwani10@gmail.com

Received Date: Nov 14, 2023 / Published Date: Dec 14, 2023

Citation: Sonwani HP, Sahu P, Bandey R (2023) Nilotinib Single-Dose Pharmacokinetics and Pharmacodynamics in Parkinson's Disease Patients. J Alzheimers Dis Parkinsonism 13:586.DOI: 10.4172/2161-0460.1000586

Copyright: © 2023 Sonwani HP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

 

Abstract

With the strongest affinity for inhibiting Abelson (c-Abl) and Discoidal Domain Receptors (DDR1/2), nilotinib is a broad-based tyrosine kinase inhibitor. According to preclinical data, nilotinib lowers brain alpha-synuclein levels and lessens inflammation in Parkinson's Disease (PD) animals. As we previously demonstrated, nilotinib crosses the Blood-Brain Barrier (BBB) and may help patients with Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB) achieve better clinical outcomes. With a cohort of 75 PD subjects, we conducted a physiologically based Population Pharmacokinetic/Pharmacodynamic (popPK/PD) study to ascertain the effects of nilotinib. Five groups (n=15) were randomly assigned (1:1:1:1:1) and each group was given an open-label Random Single Dose (RSD) of 150:200:300:400 mg of nilotinib instead of a placebo. After taking nilotinib, samples of plasma and Cerebrospinal Fluid (CSF) were taken 1,2,3 and 4 hours later. The findings indicate that nilotinib penetrates the brain in a manner that is independent of dose and that nilotinib at a dose of 200 mg raises the levels of Homovanillic Acid (HVA) and 3,4-Dihydroxyphenylacetic Acid (DOPAC), which may indicate changes in dopamine metabolism. Both the CSF oligomeric: total alpha-synuclein ratio and plasma total alpha-synuclein are markedly decreased by nilotinib. Moreover, nilotinib dramatically raises the CSF concentration of TREM-2 activating receptors on myeloid cells, indicating an anti-inflammatory impact. When combined, 200 mg of nilotinib seems to be the ideal single dosage for reducing inflammation and activating alpha-synuclein and dopamine metabolism, two surrogate disease indicators.

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