Target intelligence / Profile preview

RAF kinase (RAF)

Target
RAF
Molecular classification
Enzyme, Serine/threonine protein kinase, Protein kinase, Oncogene family
01

Overview

Pan‑RAF refers to inhibitors that target all three members of the RAF kinase family—A‑Raf, B‑Raf, and C‑Raf—which are serine/threonine protein kinases involved in the RAS–RAF–MEK–ERK signal transduction cascade. This pathway is critical for regulating cell division, differentiation, and survival. Aberrant activation of this cascade—often through mutations or fusions involving BRAF—is a key driver in various cancers. Pan‑RAF inhibitors are designed to overcome limitations seen with earlier generation selective BRAF inhibitors by preventing paradoxical activation and targeting a broader range of oncogenic drivers within this family. These agents are under clinical investigation for several cancers including pediatric low-grade gliomas and melanomas[1][2][4][5].

Other names
Rapidly Accelerated Fibrosarcoma kinaseA-RafB-RafC-RafRaf-1 proto-oncogene serine/threonine-protein kinase (c-Raf)
02

Mechanism of action

Inhibition of all three RAF isoforms (A-Raf, B-Raf—including mutant forms—and C-Raf), blocking the RAS–RAF–MEK–ERK/MAPK signaling pathway to suppress tumor cell growth and survival[2][5][6].

03

Biological functions

Signal transductionCell proliferationCell differentiationApoptosis regulation
04

Disease associations

Cancer (notably melanoma and pediatric low-grade gliomas)Other malignancies
05

Safety considerations

Paradoxical activation of MAPK pathway with first-generation selective BRAF inhibitors in wild-type cells or non-V600E mutations[2]Potential for resistance mechanisms within the MAPK pathwayGeneral adverse effects associated with targeted cancer therapies
06

Interacting drugs

Tovorafenib (DAY101/TAK580/MLN2480)

4 more in the full profile.

07

Biomarkers

BRAF V600E mutation statusKIAA1549-BRAF fusionNeurofibromatosis type 1 loss in tumors[2]

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