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Relevant bibliographies by topics / Apilimod

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Journal articles

Academic literature on the topic 'Apilimod'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Apilimod"

1

Baranov, Maksim V., Frans Bianchi, and Geert van den Bogaart. "The PIKfyve Inhibitor Apilimod: A Double-Edged Sword against COVID-19." Cells 10, no. 1 (2020): 30. http://dx.doi.org/10.3390/cells10010030.

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The PIKfyve inhibitor apilimod is currently undergoing clinical trials for treatment of COVID-19. However, although apilimod might prevent viral invasion by inhibiting host cell proteases, the same proteases are critical for antigen presentation leading to T cell activation and there is good evidence from both in vitro studies and the clinic that apilimod blocks antiviral immune responses. We therefore warn that the immunosuppression observed in many COVID-19 patients might be aggravated by apilimod.

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2

Gayle, Sophia, Sean Landrette, Neil Beeharry, et al. "Identification of apilimod as a first-in-class PIKfyve kinase inhibitor for treatment of B-cell non-Hodgkin lymphoma." Blood 129, no. 13 (2017): 1768–78. http://dx.doi.org/10.1182/blood-2016-09-736892.

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Key Points Apilimod has broad anticancer activity in vitro and in vivo across all subtypes of B-NHL. Apilimod induces B-NHL cytotoxicity through a unique mechanism of action that involves the disruption of lysosomal function.

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3

Kang, Yuan-Lin, Yi-ying Chou, Paul W. Rothlauf, et al. "Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2." Proceedings of the National Academy of Sciences 117, no. 34 (2020): 20803–13. http://dx.doi.org/10.1073/pnas.2007837117.

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Virus entry is a multistep process. It initiates when the virus attaches to the host cell and ends when the viral contents reach the cytosol. Genetically unrelated viruses can subvert analogous subcellular mechanisms and use similar trafficking pathways for successful entry. Antiviral strategies targeting early steps of infection are therefore appealing, particularly when the probability for successful interference through a common step is highest. We describe here potent inhibitory effects on content release and infection by chimeric vesicular stomatitis virus (VSV) containing the envelope pr

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4

Cinato, Mathieu, Laurie Guitou, Amira Saidi та ін. "Apilimod alters TGFβ signaling pathway and prevents cardiac fibrotic remodeling". Theranostics 11, № 13 (2021): 6491–506. http://dx.doi.org/10.7150/thno.55821.

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5

Nelson, Elizabeth A., Julie Dyall, Thomas Hoenen, et al. "The phosphatidylinositol-3-phosphate 5-kinase inhibitor apilimod blocks filoviral entry and infection." PLOS Neglected Tropical Diseases 11, no. 4 (2017): e0005540. http://dx.doi.org/10.1371/journal.pntd.0005540.

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6

Ring, Julian, Sarah Schlienkamp, Jil Haase, et al. "LBP-034 Evaluation of the PIKfyve kinase inhibitor Apilimod against hepatitis E virus infections." Journal of Hepatology 80 (June 2024): S94. http://dx.doi.org/10.1016/s0168-8278(24)00601-9.

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7

Wisniewski, Jasmine P., Caleb Cheng, Bailey Jackson, et al. "Abstract 3300: Dual inhibition of PIKfyve and KRAS/MAPK as a potential for therapeutic strategy for pancreatic ductal adenocarcinoma." Cancer Research 84, no. 6_Supplement (2024): 3300. http://dx.doi.org/10.1158/1538-7445.am2024-3300.

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Abstract Background: PIKfyve is a lipid kinase that serves as the single source for PI(3,5)P2, a critical molecule for lysosome functions, including autophagy. Pancreatic Ductal Adenocarcinoma (PDAC) is known to utilize autophagy as well as other lysosome functions to survive in its harsh microenvironment. Considering the role of PIKfyve in autophagy, we hypothesized that PIKfyve is important for PDAC pathophysiology. Indeed, we screened multiple cell lines of different cancer lineages and found that PDAC cell lines were highly sensitive to PIKfyve inhibitors apilimod and ESK981. Given these r

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8

Grenier, Shea, Cheska Galapate, Yijuan Zhang, et al. "Abstract A096: PIKfyve as a potential therapeutic target in pancreatic cancer." Cancer Research 84, no. 2_Supplement (2024): A096. http://dx.doi.org/10.1158/1538-7445.panca2023-a096.

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Abstract A lack of effective treatments beyond surgical resection and chemotherapy contributes to the 12% five-year survival rate of pancreatic ductal adenocarcinoma (PDAC), underscoring the need to identify novel therapeutic approaches. Pharmacological inhibition of phosphatidylinositol 3-phosphate 5-kinase (PIKfyve) with small molecules has been demonstrated to have therapeutic effects in tauopathies, viral infection, and cancer; however, these compounds have not been evaluated in PDAC. The PIKfyve lipid kinase generates PI5P and/or PI(3,5)P2 from phosphoinositol (PI) or PI3P, respectively,

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9

Wada, Yumiko, Irma Cardinale, Artemis Khatcherian, et al. "Apilimod Inhibits the Production of IL-12 and IL-23 and Reduces Dendritic Cell Infiltration in Psoriasis." PLoS ONE 7, no. 4 (2012): e35069. http://dx.doi.org/10.1371/journal.pone.0035069.

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10

DeLiberty, Jonathan M., Clint A. Stalnecker, Kristina Drizyte-Miller, et al. "Abstract 4851: Improving the efficacy of dual ERK-MAPK and autophagy inhibition as a therapeutic strategy for pancreatic ductal adenocarcinoma." Cancer Research 83, no. 7_Supplement (2023): 4851. http://dx.doi.org/10.1158/1538-7445.am2023-4851.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is characterized by KRAS- and autophagy-dependent growth. We and others recently demonstrated that inhibition of the RAF-MEK-ERK pathway resulted in upregulated autophagy, and that dual treatment with the autophagy inhibitor hydroxychloroquine (HCQ)/chloroquine (CQ) and MEK or ERK inhibitors (MEKi, ERKi) synergistically blocked PDAC growth. These findings provided rationale for our initiation of Phase I/II clinical trials evaluating the combination of MEKi (binimetinib; NCT04132505) or ERKi (LY3214996; NCT04386057) with HCQ in PDAC. However, HCQ

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