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Tovorafenib: A novel B-RAF inhibitor for the treatment of pediatric low-grade glioma (Review)
de, Surya K.
de, Surya K.
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2026-07-01
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Article
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Adverse events,Drug metabolism,Pediatric glioma,Pharmacokinetics,Tovorafenib
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Citation
Mandapaka, H., & De, S.K. (2026). Tovorafenib: A novel B‑RAF inhibitor for the treatment of pediatric low‑grade glioma (Review). World Academy of Sciences Journal, 8, 65. https://doi.org/10.3892/wasj.2026.480
Abstract
The normal function of the RAF kinases (including BRAF and CRAF) is to relay signals from upstream activators (e.g., RAS) to the downstream effectors, MEK to ERK, thereby forming the RAF/MEK/ERK cascade (also known as the MAPK signaling pathway). This pathway regulates key cellular processes, such as proliferation, growth, differentiation and survival. In numerous types of cancer, including pediatric low‑grade gliomas, genetic alterations (mutations in BRAF, or BRAF fusions/rearrangements) lead to the constitutive activation of RAF, independent of upstream controls, resulting in uncontrolled cell proliferation and survival. Tovorafenib binds to RAF kinases (mutant or wild‑type, monomeric or dimeric) in their inactive DFG‑out state. Tovorafenib inhibits RAF kinase activity, prevents downstream MEK and ERK activation, disrupts MAPK signaling, resulting in the attenuation of inhibition of tumor cell growth; tumor regression or stabilization may thus occur. The present review discusses the efficacy of tovorafenib for the treatment of pediatric low‑grade glioma, as well as its association with RAF kinase activity and pharmacokinetics.
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This is an open access article under the CC BY license.
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Spandidos Publications
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26322900