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Nilotinib Effects on Safety, Tolerability, and Potential Biomarkers in Parkinson Disease: A Phase 2 Randomized Clinical Trial
Open accessAbstract
Importance: This study evaluated nilotinib safety and its effects on biomarkers as a potential disease-modifying drug in Parkinson disease. Objectives: To assess nilotinib effects on safety and pharmacokinetics and measure the change in exploratory biomarkers in patients with moderately severe Parkinson disease. Design, Setting, and Participants: This was a single-center, phase 2, randomized, double-blind, placebo-controlled trial with 300 patients approached in clinic; of these, 200 declined to participate, 100 were screened, 25 were excluded, and 75 were randomized 1:1:1 into placebo; nilotinib, 150-mg; or nilotinib, 300-mg groups. Recruitment started on May 17, 2017, and ended April 28, 2018, and follow-up ended August 10, 2019. Parkinson disease was confirmed according to the UK Brain Bank diagnostic criteria and symptoms were stabilized with use of optimal levodopa and/or dopamine agonists and other medications used in Parkinson disease. Interventions: Nilotinib vs placebo, administered orally once daily for 12 months followed by a 3-month washout period. Main Outcomes and Measures: It was hypothesized that nilotinib is safe and can be detected in the cerebrospinal fluid, where it alters exploratory biomarkers via inhibition of Abelson tyrosine kinase and potentially improves clinical outcomes. Results: Of the 75 patients included in the study, 55 were men (73.3%); mean (SD) age was 68.4 (8.2) years. Doses of 150 or 300 mg of nilotinib were reasonably safe, although more serious adverse events were detected in the nilotinib (150 mg: 6 [24%]; 300 mg: 12 [48%]) vs placebo (4 [16%]) groups. The 150-mg nilotinib group showed an increase in cerebrospinal fluid levels of the dopamine metabolites homovanillic acid (159.80nM; 90% CI, 7.04-312.60nM; P = .04) and 3,4-dihydroxyphenylacetic acid (4.87nM; 90% CI, 1.51-8.23nM; P = .01), and the 300-mg nilotinib group showed an increase in 3,4-dihydroxyphenylacetic acid (7.52nM; 90% CI, 2.35-12.69nM; P = .01). The nilotinib 150-mg but not the nilotinib 300-mg group demonstrated a reduction of α-synuclein oligomers (-0.04 pg/mL; 90% CI, -0.08 to 0.01 pg/mL; P = .03). A significant reduction of hyperphosphorylated tau levels was seen in the nilotinib 150-mg (-10.04 pg/mL; 90% CI, -17.41 to -2.67 pg/mL; P = .01) and nilotinib 300-mg (-12.05 pg/mL; 90% CI, -19.21 to -4.90 pg/mL; P = .01) groups. Conclusions and Relevance: In this study, nilotinib appeared to be reasonably safe and detectable in the cerebrospinal fluid. Exploratory biomarkers were altered in response to nilotinib. Taken together, these data will guide the development of a phase 3 study to investigate the effects of nilotinib therapy in patients with Parkinson disease. Trial Registration: ClinicalTrials.gov identifier: NCT02954978.
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“clinical trials showed that Nilotinib can reduce disease-related biomarkers in both AD and PD patients”
From Nilotinib restores memory function by preventing dopaminergic neuron degeneration in a mouse model of Alzheimer’s Disease (2021) · cites this paper as Pagan et al., 2019
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Cites
Cook, R. J., Dickens, B. M., & Fathalla, M. F. (2003) · Oxford University Press eBooks · doi:10.1093/acprof:oso/9780199241323.003.0025 · Cited by 10,825
Spillantini, M. G., Schmidt, M. L., Lee, V. M.-Y., Trojanowski, J. Q., Jakes, R., & Goedert, M. (1997) · Nature · doi:10.1038/42166 · Cited by 8,382
Spillantini, M. G., Crowther, R. A., Jakes, R., Hasegawa, M., & Goedert, M. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6469 · Cited by 2,868
Alpha-synuclein and neurodegenerative diseases
Goedert, M. (2001) · Nature reviews. Neuroscience · doi:10.1038/35081564 · Cited by 1,428
Catecholamine Metabolism: A Contemporary View with Implications for Physiology and Medicine
Eisenhofer, G., Kopin, I. J., & Goldstein, D. S. (2004) · Pharmacological Reviews · doi:10.1124/pr.56.3.1 · Cited by 1,072
El‐Agnaf, O. M. A., Salem, S. A., Paleologou, K. E., Curran, M. D., Gibson, M. J., Court, J. A., Schlossmacher, M. G., & Allsop, D. (2006) · The FASEB Journal · doi:10.1096/fj.03-1449com · Cited by 715
Catecholamine metabolism: basic aspects and clinical significance.
Kopin, I. J. (1985) · Pharmacological Reviews · doi:10.1016/s0031-6997(25)06859-0 · Cited by 582
Does levodopa slow or hasten the rate of progression of Parkinson’s disease?
Fahn, S., & and the Parkinson Study Group (2005) · Journal of Neurology · doi:10.1007/s00415-005-4008-5 · Cited by 348
Hebron, M. L., Lonskaya, I., & Moussa, C. (2013) · Human Molecular Genetics · doi:10.1093/hmg/ddt192 · Cited by 337
Flagged first, then by citations
3 of the 32 references couldn’t be matched to a known paper.
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Items 101–188 of 188
Cell Biology of Parkin: Clues to the Development of New Therapeutics for Parkinson’s Disease
Patel, J., Panicker, N., Dawson, V. L., & Dawson, T. M. (2022) · CNS Drugs · doi:10.1007/s40263-022-00973-7 · Cited by 9
Protein kinase inhibitors as therapeutics in neurodegenerative and psychiatric disorders
Tridente, G., Jana, A., Nath, A., & Ashraf, G. M. (2023) · Receptor Tyrosine Kinases in Neurodegenerative and Psychiatric Disorders · doi:10.1016/b978-0-443-18677-6.00015-4 · Cited by 8
Lewy Body Dementia: An Overview of Promising Therapeutics
Skylar‐Scott, I. A., & Sha, S. J. (2023) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-023-01292-0 · Cited by 8
Yang, Z., Ai, Y., Wan, S., Yang, Z., Li, H., Li, Z., Huang, C., Zhang, L., Li, M., Zhang, J., et al. (2022) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2022.117069 · Cited by 8
Pagán, F., Torres-Yaghi, Y. A., Hebron, M. L., Wilmarth, B., Turner, R. S., Matar, S., Liu, X., Ferrante, D., Esposito, G., Ahn, J., et al. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14124245 · Cited by 7
“…300 mg, once daily demonstrate a linearly proportional increase to dose in the brain of Alzheimer’s disease (AD) [4] and Parkinson’s disease (PD) [5] patients and reach a CNS concentration (1–5 nM) that directly inhibits DDR1 (IC 50 1 nM) [6], thus exhibiting an adequate pharmacokinetics and…”
InfluentialElucidating the molecular targets in Alzheimer's disease: Advances and therapeutic implications
Soni, U., & Pujari, R. (2026) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2026.111660 · Cited by 7
Werner, M. H., Olanow, C. W., McGarry, A. J., Meyer, C., Kruger, S., Klint, C., Pellecchia, J., Walaker, S., Ereshefsky, L., Blob, L. F., et al. (2024) · Journal of Parkinson s Disease · doi:10.3233/jpd-230319 · Cited by 7
c-KIT inhibitors reduce pathology and improve behavior in the Tg(SwDI) model of Alzheimer’s disease
Stevenson, M. E., Hebron, M. L., Liu, X., Balaraman, K., Wolf, C., & Moussa, C. (2024) · Life Science Alliance · doi:10.26508/lsa.202402625 · Cited by 8
“In addition, nilotinib, an Abl/DDR inhibitor, has been shown by to reduce pathological markers in AD and PD patients (Hebron et al, 2013a; Lonskaya et al, 2015; Turner et al, 2020; Fowler et al, 2021; Stevenson et al, 2023), and improve clinical outcomes in PD (Pagan et al, 2019, 2020, 2021).”
BackgroundRymbai, E., Roy, D., Jupudi, S., & Srinivasadesikan, V. (2024) · Molecular Diversity · doi:10.1007/s11030-023-10796-3 · Cited by 7
“Nilotinib is clinical approved drug for the treatment of chronic myeloid leukemia [29].”
Mouradian, M. M., Stoessl, A. J., & Lang, A. E. (2025) · Movement Disorders · doi:10.1002/mds.30259 · Cited by 6
Sarva, H., Pahwa, R., Hernández‐Vara, J., Goldstein, M. A., Borgohain, R., Factor, S. A., Inamdar, S., Love, D. K., Hames, C., Fu, Y., et al. (2026) · npj Parkinson s Disease · doi:10.1038/s41531-026-01275-1 · Cited by 6
Berton, G. G., Rodrigues, A. C. L. F., Borges, R. D. S., Cardoso, N. R., de Oliveira, T. A., & Marques, M. V. O. (2024) · Clinical Neuropharmacology · doi:10.1097/wnf.0000000000000597 · Cited by 6
Disease modifying therapies for Parkinson's disease: Novel targets
Vijiaratnam, N., & Foltynie, T. (2021) · Neuropharmacology · doi:10.1016/j.neuropharm.2021.108839 · Cited by 6
“(Pagan et al., 2020) A further concern in the study was a noted worsening in functional and cognitive assessments among participants using the 300mg dose.”
MethodEldik, L. J. V., Siemers, E., Collins, E. C., Gold, M., Henley, D. B., Johannsen, P., Möbius, H. J., Shulman, M. B., Zhou, J., Carrillo, M. C., et al. (2024) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.70014 · Cited by 5
Werner, M. H., McGarry, A. J., Meyer, C., Mancino, E., Klint, C., Pellecchia, J., Kieburtz, K. D., Levine, T., Bellaire, B., Gibbons, C. H., et al. (2026) · Nature Aging · doi:10.1038/s43587-026-01084-4 · Cited by 6
Ventorp, F., Asp, M., Olsson, S., Lindahl, J., Möller, S., Svensson, M., Ängeby, F., Pravdinske, A., Tjernberg, J., Schrey, S., et al. (2026) · Nature Medicine · doi:10.1038/s41591-026-04465-9 · Cited by 5
Lewy Body Dementias: Controversies and Drug Development
Chiu, S., Bowers, D., & Armstrong, M. J. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01161-z · Cited by 5
“Notably, recent trials of nilotinib in PD showed little efficacy in motor outcomes, with low CSF exposure and lack of biomarkers’ effect [64, 65].”
BackgroundSmerikarova, M., Bozhanov, S., & Maslarska, V. (2024) · Microchemical Journal · doi:10.1016/j.microc.2024.112220 · Cited by 5
The genetic background of Parkinson’s disease and novel therapeutic targets
Salamon, A., Zádori, D., Szpisjak, L., Klivènyi, P., & Vécsei, L. (2022) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2022.2153037 · Cited by 5
Erekat, N. S. (2025) · Clinical Anatomy · doi:10.1002/ca.70057 · Cited by 4
The Search for Disease Modification in Parkinson’s Disease—A Review of the Literature
Barber, D., Wijeratne, T., Singh, L., Barnham, K. J., & Masters, C. L. (2025) · Life · doi:10.3390/life15081169 · Cited by 5
“Unfortunately, multiple human trials on nilotinib have failed to demonstrate any meaningful clinical benefit over 12-month treatment periods [69,70].”
Köllő, Z., Garami, M., Vincze, I., Vásárhelyi, B., & Karvaly, G. (2023) · Pharmaceutics · doi:10.3390/pharmaceutics15010239 · Cited by 4
“Pagan, 2020 Nilotinib Registered clinical study(NCT02954978) 75 adults with Parkinson’s disease Blood: 75 PFS: 75 17 May 2017 to 28 April 2018 Nilotinib in CSF and in plasma [34]”
BackgroundMethodInfluentialGenetic modifiers of synucleinopathies—lessons from experimental models
Lee, R. M. Q., & Koh, T. (2023) · Oxford Open Neuroscience · doi:10.1093/oons/kvad001 · Cited by 4
Targeting α-synuclein and c-Abl in Parkinson’s disease
Xiao, B., & Tan, E. (2023) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2023.07.004 · Cited by 4
Dual-action kinase inhibitors influence p38α MAP kinase dephosphorylation
Stadnicki, E. J., Ludewig, H., Kumar, R. P., Wang, X., Qiao, Y., Kern, D., & Bradshaw, N. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2415150122 · Cited by 4
“…has been investigated as a treatment for neurodegenerative diseases including Lewy Body Dementias ( 67 ), Alzheimer’s disease ( 68 , 69 ), and Parkinson’s disease ( 70 ), with therapeutic benefit attributed to reduction of inflammation in the brain that could be due to p38 inhibition ( 71 ).”
Dopamine Metabolite Biomarkers and Testing for Disease Modification in Parkinson Disease—Reply
Moussa, C. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2020.1931 · Cited by 4
Song, J., Park, S. J., Kim, Y.-J., & Park, S. M. (2025) · Frontiers in Neurology · doi:10.3389/fneur.2025.1628876 · Cited by 3
Sahoo, S. K., Paidesetty, S. K., Sahu, P. K., Pattanaik, S., & Dandela, R. (2025) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2025.109129 · Cited by 4
Recent Developments in the Drug Treatment of Parkinson’s Disease
Leiter, S., Mahlknecht, P., & Poewe, W. H. (2026) · Drugs · doi:10.1007/s40265-026-02327-9 · Cited by 3
Nilotinib treatment outcomes in autosomal dominant spinocerebellar ataxia over one year
Lee, W., Moon, J., Jang, Y., Shin, Y.-W., Son, H., Shin, S., Jeon, D., Han, D., Lee, S., Park, K., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-67072-z · Cited by 3
“Recently, two randomized controlled studies demonstrated the effect of nilotinib in patients with PD and in patients with AD 17,18 , although another randomized controlled study in in patients with moderately advanced PD reported a negative result 19 .”
BackgroundMethodResultInfluentialNiazi, S. K. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms251810211 · Cited by 3
“Nilotinib [162] A tyrosine kinase inhibitor originally used in chronic myeloid leukemia, repurposed for Parkinson’s disease.”
Exploring the neuroprotective potential of immunosuppressants in Parkinson's disease
Mubarak, H., Racette, B. A., Killion, J. A., Faust, I. M., Laurido-Soto, O., Doddamreddy, S. A., & Nielsen, S. S. (2025) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2025.107294 · Cited by 4
Glutamate Receptors and C-ABL Inhibitors: A New Therapeutic Approach for Parkinson's Disease
Shejul, P. P., & Doshi, G. (2024) · Central Nervous System Agents in Medicinal Chemistry · doi:10.2174/0118715249268627231206115942 · Cited by 4
Lin, Y. M., Banoth, D., Wali, M. H., Bekova, K., Abdulla, N., Gurugubelli, S., & Khan, S. (2024) · Cureus · doi:10.7759/cureus.64766 · Cited by 4
“The 150-mg group did not show a significant change in this score; however, there was a 2.82 decrease in the UPDRS III score 15 months after baseline [16].”
InfluentialModern Pharmacological Treatment of Parkinson's Disease : Reviving Known Drugs and New Perspectives
Lastovetskyi, I., Cytlau, B., Marczyk, Ł., Zdrojewska, K., Łach, A., Krupa, J. K., Lorkowska-Zawicka, B., & Bujak-Giżycka, B. (2024) · International Journal Of Pharmaceutical Research And Allied Sciences · doi:10.51847/twysubd6pp · Cited by 3
Dopamine Metabolite Biomarkers and Testing for Disease Modification in Parkinson Disease
LeWitt, P. A. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2020.1928 · Cited by 3
c‐Abl Inhibitors as Disease‐Modifying Therapies for Parkinson's Disease: Gaps and Opportunities
Merchant, K., & Sullivan, J. (2022) · Movement Disorders · doi:10.1002/mds.28907 · Cited by 3
Targeting protein kinases in Parkinson’s disease: the emerging role of phytoconstituents
Joshi, D., Kulkarni, M., Parekh, P., Shah, S., Greig, N. H., & Acharya, S. P. (2025) · Nutritional Neuroscience · doi:10.1080/1028415x.2025.2531356 · Cited by 4
Pagán, F., Torres-Yaghi, Y. A., Hebron, M. L., Wilmarth, B., Liu, X., Ahn, J., & Moussa, C. (2025) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2025.108020 · Cited by 2
Receptor tyrosine kinases in Alzheimer's disease: Mechanistic insights and therapeutic implications
Zhao, P., Cao, Z., & Rozpędek‐Kamińska, W. (2026) · Neurochemistry International · doi:10.1016/j.neuint.2026.106117 · Cited by 2
Targeting of kinases to treat neurodegenerative diseases
Shomali, T., & Trempe, J.-F. (2026) · Pharmacological Reviews · doi:10.1016/j.pharmr.2026.100128 · Cited by 4
“188 Moreover, the heterogeneity in the trials might also be assigned to variable criteria and endpoints selected.”
Drug repurposing for disease-modifying effects in multiple system atrophy
Jeong, S. H., Shin, J. Y., & Lee, P. H. (2026) · Translational Neurodegeneration · doi:10.1186/s40035-026-00551-7 · Cited by 2
“In a Phase II PD trial, nilotinib failed to demonstrate clinical benefit and achieved only minimal CSF exposure, with brain-to-plasma concentration ratios of approximately 0.38% at 150 mg (0.94 nM CSF vs. 245.2 nM plasma) and 0.53% at 300 mg (1.6 nM CSF vs. 299.5 nM plasma) [37].”
InfluentialAutophagy and Parkinson’s Disease
Ryan, L., Rob, M., He, J., & Rubinsztein, D. C. (2022) · Springer eBooks · doi:10.1007/978-3-031-15080-7_242 · Cited by 2
Altered autophagy on the path to Parkinson's disease
Sanchez-Mirasierra, I., Hernández-Díaz, S., Ghimire, S., Main, P., & Soukup, S. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822003-0.00006-1 · Cited by 2
Autophagy Mechanisms for Brain Recovery. Keep It Clean, Keep It Alive
Nobili, A., Barbera, L. L., Mastrantonio, R., Palazzo, C., Molinari, M., D’Amelio, M., & Viscomi, M. T. (2023) · Contemporary clinical neuroscience · doi:10.1007/978-3-031-24930-3_2 · Cited by 1
Immunotherapy for Neurodegenerative Movement Disorders
Mosley, R. L., Saleh, M., & Olson, K. E. (2024) · Springer eBooks · doi:10.1007/978-3-031-68237-7_52 · Cited by 1
Current Drugs Used: Classification and Pharmacology
Swain, S. S., Mude, L., Roychowdhury, P., Karri, V. V. S. R., Kuppusamy, G., Gobinath, M., & Subramaniyan, V. (2024) · Springer eBooks · doi:10.1007/978-981-96-0259-9_8 · Cited by 1
Corticobasal Degeneration: A Review
Lopez, A. M., Johnson, S., Wax, N., Cutchin, C., May, D., Curtain, T., Bynum, Z., Galliher, M., Jones Diamond, A., Sudhakar, S., et al. (2025) · Journal of Neuroscience and Neurological Disorders · doi:10.29328/journal.jnnd.1001113 · Cited by 1
Pappu, M. A. A., Alamin, M., Noman, M. A., Sultana, M. H., Ahmed, M. F., Hossain, M. S., Latif, M. A., Faysal, M. F., Azad, A., Alyami, S. A., et al. (2025) · Genes · doi:10.3390/genes16121459 · Cited by 1
“This degeneration leads to a significant reduction in dopamine levels, resulting in the hallmark motor symptoms of PD, such as tremors, rigidity, and bradykinesia [1].”
Combination Disease‐Modifying Therapy for Neurodegenerative Diseases Using Repurposed Drugs
Shtilbans, A., & Lang, A. E. (2026) · Annals of Neurology · doi:10.1002/ana.78190 · Cited by 1
“62,105 These compounds enhance parkin activity within the central nervous system.”
Yang, Z., Ai, Y., Wu, G., Guo, F., Yang, Z., Cheng, B., Zhang, L., Li, M., Chen, J., Zhang, T., et al. (2023) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2023.117532 · Cited by 1
Revisiting Parkinson’s Disease Treatment: Exploring Established Medications and Emerging Therapies
Brooks, D., Carter, A., Moore, E., & Grant, O. (2024) · Journal of Applied Pharmaceutical Technologies and Systems · doi:10.68159/i340840675 · Cited by 1
Lee, M. T. W., Mahy, W., & Rackham, M. D. (2021) · RSC Medicinal Chemistry · doi:10.1039/d1md00113b · Cited by 1
Advances in clinical basic research: Performance, treatments, and mechanisms of Parkinson disease
Yang, T., Liu, Y., Li, J., Xu, H., Li, S., Xiong, L., & Wang, T. (2021) · Ibrain · doi:10.1002/ibra.12011 · Cited by 1
“An increase of 3,4‐dihydroxyphenylacetic acid and hyperphosphorylated tau levels in 300‐mg nilotinib group was observed by contraries, which indicate that nilotinib showed security and detectability in the CSF and exploratory biomarkers were changed after nilotinib.(65)”
BackgroundAutophagy and Parkinson’s Disease
Ryan, L., Rob, M., He, J., & Rubinsztein, D. C. (2021) · Springer eBooks · doi:10.1007/978-3-030-71519-9_242-1 · Cited by 1
Movement disorders in 2020: clinical trials, genetic discoveries, and COVID-19
Tan, E.-K. (2020) · The Lancet Neurology · doi:10.1016/s1474-4422(20)30448-8 · Cited by 1
Advances in Disease Modifying Therapies for Parkinson's Disease
Hassanzadeh, K., & Mouradian, M. M. (2025) · Wiley eBooks · doi:10.1002/9783527844678.ch2 · Cited by 1
Phase 2 Nilotinib Trials for Parkinson's Yield Conflicting Efficacy Results
Samson, K. (2020) · Neurology Today · doi:10.1097/01.nt.0000662128.13325.97
Reply to “Cardiovascular Safety of Nilotinib in Alzheimer's Disease”
Moussa, C. (2020) · Annals of Neurology · doi:10.1002/ana.25946
Blood-Brain Barrier Therapeutics for Neurological Diseases
Sahni, A., & Katchur, N. J. (2021) · Journal of Student Research · doi:10.47611/jsrhs.v10i3.1735
Development of autophagy enhancers for Parkinson’s disease therapy
Sasazawa, Y., Hattori, N., & Saiki, S. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-89906-2.00003-4
Simuni, T., & Merchant, K. (2023) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2023.105325
Novel therapeutics for diverse neurodegenerative disorders
Chaurasia, R. N., & Favas, T. T. (2024) · Elsevier eBooks · doi:10.1016/b978-0-323-95735-9.00051-6
Ayajuddin, M., Das, A., & Yenisetti, S. C. (2024) · Research Square · doi:10.21203/rs.3.rs-4645640/v1
REST API DAN ODOO 17 PADA APLIKASI TRACER ALUMNI UIN MAULANA MALIK IBRAHIM MALANG BERBASIS FLUTTER
Supriyono, S., Saputra, R. F. S., Zainuddin, A. H., Akbar, M., Habibillah, M. F., & Hasbulah, A. (2024) · Jurnal Manajemen Teknologi Informatika · doi:10.70038/jentik.v2i3.136
Pipeline of Pharmacotherapy in Parkinson’s Disease
Brugger, F., & Hägele-Link, S. (2025) · Cambridge University Press eBooks · doi:10.1017/9781108989855.026
Kim, J., Lee, H.-J., Park, J.-H., Cha, B.-Y., & Hoe, H.-S. (2022) · Figshare · doi:10.6084/m9.figshare.20329567
Stevenson, M. E., Varghese, R., Hebron, M. L., Liu, X., Ratliff, N., Smith, A., Turner, R. S., & Moussa, C. (2024) · Figshare · doi:10.6084/m9.figshare.26589822
Rodriguez‐Porcel, F. E., Wyman‐Chick, K. A., Ruiz, C. A., Toledo, J. B., Ferreira, D., Urwyler, P., Weil, R. S., Kane, J., Pilotto, A., Rongve, A., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19689331
Rodriguez‐Porcel, F. E., Wyman‐Chick, K. A., Ruiz, C. A., Toledo, J. B., Ferreira, D., Urwyler, P., Weil, R. S., Kane, J., Pilotto, A., Rongve, A., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19689334
Rodriguez‐Porcel, F. E., Wyman‐Chick, K. A., Ruiz, C. A., Toledo, J. B., Ferreira, D., Urwyler, P., Weil, R. S., Kane, J., Pilotto, A., Rongve, A., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19689340
Rodriguez‐Porcel, F. E., Wyman‐Chick, K. A., Ruiz, C. A., Toledo, J. B., Ferreira, D., Urwyler, P., Weil, R. S., Kane, J., Pilotto, A., Rongve, A., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19689343
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Peikert, K., Federti, E., Matte, A., Constantin, G., Pietronigro, E. C., Fabene, P. F., Defilippi, P., Turco, E., Gallo, F. D., Pucci, P., et al. (2021) · Figshare · doi:10.6084/m9.figshare.14532339
Stevenson, M. E., Varghese, R., Hebron, M. L., Liu, X., Ratliff, N., Smith, A., Turner, R. S., & Moussa, C. (2024) · Figshare · doi:10.6084/m9.figshare.26589819
Rodriguez‐Porcel, F. E., Wyman‐Chick, K. A., Ruiz, C. A., Toledo, J. B., Ferreira, D., Urwyler, P., Weil, R. S., Kane, J., Pilotto, A., Rongve, A., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19689337
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Talukder, P., Mohanta, S., Hazra, A., Dasgupta, M., Biswas, S., & Hore, S. (2026) · BENTHAM SCIENCE PUBLISHERS eBooks · doi:10.2174/9798898814533126010009
Majrashi, T. A., Alshahrani, M. Y., Asiri, M. A., Zia‐Ul‐Sabah, Abohassan, M., Kapoor, D. U., & Wahab, S. (2026) · Journal of Molecular Neuroscience · doi:10.1007/s12031-026-02511-2
“Together these findings provide a mechanistic rationale for exploring both agents in neurodegenerative settings (Pagan et al. 2020, Lee et al. 2018, Turner et al. 2020).”
Interaction entre autophagie et exosomes au niveau synaptique dans la maladie de Parkinson
Sanchez-Mirasierra, I. (2023) · theses.fr (ABES) · doi:10.70675/7104d6d5z945ez494eza917zda9e6be1eea6
A Systematic Review on Disease‐Modifying Therapies in Parkinsonian Disorders
Eijsvogel, P. P. N. M., Smits, L. M. G., Kremer, P. H. C., & Groeneveld, G. J. (2026) · Clinical Pharmacology & Therapeutics · doi:10.1002/cpt.70315 · Cited by 1
Novel treatments for Parkinson’s disease
Yin, Y., Gao, J., Zhang, K., Meng, F. D., & Feng, T. (2026) · Chinese Medical Journal · doi:10.1097/cm9.0000000000004163
Use of receptor and nonreceptor tyrosine kinase inhibitors and Parkinson disease risk
Malaty, G. R., Killion, J. A., Doddamreddy, S. A., Laurido-Soto, O., & Racette, B. A. (2026) · Neurotherapeutics · doi:10.1016/j.neurot.2026.e01040
Erdem, M., Erdem, Ş., & Karahan, S. C. (2026) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2026.579084
Kaur, R., Lang, D. K., Sood, A., Singh, T. G., Chandrasekaran, B., & Al-Sha’er, M. A. (2026) · RSC Advances · doi:10.1039/d6ra03269a
Wittström, F., Chen, E. Y., Blotenberg, I., & Dahlén, T. (2026) · Alzheimer s & Dementia · doi:10.1002/alz.71916
“12,36,37 Inameta-analysisoffivetrials( n = 197)nilotinibshowedan effect size of − 1.15 (95% CI, − 3.00 to 0.69) on Parkinson’s disease and Lewy body dementia symptom progression at a daily dose of 300 mg, unlike lower doses and other TKIs.”
Influential
Metadata
- Authors
- Pagan, F. L., Hebron, M. L., Wilmarth, B., Torres-Yaghi, Y., Lawler, A., Mundel, E. E., Yusuf, N., Starr, N. J., Anjum, M., Arellano, J., Howard, H. H., Shi, W., Mulki, S., Kurd-Misto, T., Matar, S., Liu, X., Ahn, J., & Moussa, C.
- Affiliations
- Translational Neurotherapeutics Program, Laboratory for Dementia and Parkinsonism, Department of Neurology, Georgetown University Medical Center, Washington, DC
- Georgetown University Medical Center (US)
- MedStar Georgetown University Hospital (US)
- Corresponding author
- Moussa, Charbel
- Venue
- JAMA Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2020-03-01
- Volume
- 77
- Issue
- 3
- Pages
- 309
- ISSN
- 2168-6149 (ISSN-L)
- PMC
- PMC6990742
- OpenAlex
- W2995537689
- Cited by
- 185
- References
- 32
- Citations by year
- 2026: 18 · 2025: 18 · 2024: 35 · 2023: 29 · 2022: 28 · 2021: 30 · 2020: 26
- FWCI
- 14.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- JAMA Neurology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- nilotinib, Parkinson's disease, disease-modifying therapy, safety and tolerability, pharmacokinetics, cerebrospinal fluid biomarkers, homovanillic acid, DOPAC, dopamine metabolism, adverse events, dose comparison, washout
- MeSH terms
- Aged, Dopamine, Double-Blind Method, Female, Humans, Male, Middle Aged, Parkinson Disease, Pyrimidines, Biomarkers, tau Proteins
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