Difference between revisions of "Vemurafenib (Zelboraf)"
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==General information== | ==General information== | ||
| − | Class/mechanism: Tyrosine kinase inhibitor of some mutated forms of BRAF | + | Class/mechanism: Tyrosine kinase inhibitor of some mutated forms of BRAF serine/threonine |
kinase, including BRAF V600E. Also has been observed to inhibit other tyrosine kinases such as CRAF, ARAF, wild-type BRAF, SRMS, ACK1, MAP4K5, and FGR. Certain BRAF mutations, such as V600E, result in constitutive activation of cell proliferation pathways and tumor growth.<ref name="insert">[http://www.gene.com/gene/products/information/zelboraf/pdf/pi.pdf Vemurafenib (Zelboraf) package insert]</ref><ref>[http://hemonc.org/docs/packageinsert/vemurafenib.pdf Vemurafenib (Zelboraf) package insert (locally hosted backup)]</ref><ref>[http://www.zelboraf.com Zelboraf manufacturer's website]</ref> | kinase, including BRAF V600E. Also has been observed to inhibit other tyrosine kinases such as CRAF, ARAF, wild-type BRAF, SRMS, ACK1, MAP4K5, and FGR. Certain BRAF mutations, such as V600E, result in constitutive activation of cell proliferation pathways and tumor growth.<ref name="insert">[http://www.gene.com/gene/products/information/zelboraf/pdf/pi.pdf Vemurafenib (Zelboraf) package insert]</ref><ref>[http://hemonc.org/docs/packageinsert/vemurafenib.pdf Vemurafenib (Zelboraf) package insert (locally hosted backup)]</ref><ref>[http://www.zelboraf.com Zelboraf manufacturer's website]</ref> | ||
<br>Route: PO | <br>Route: PO | ||
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==References== | ==References== | ||
<references/> | <references/> | ||
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| + | [[Category:Kinase inhibitors]] | ||
| + | [[Category:BRAF inhibitors]] | ||
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| + | [[Category:Melanoma medications]] | ||
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| + | [[Category:Drugs FDA approved in 2011]] | ||
Revision as of 03:50, 7 October 2014
FDA approved 8/17/2011. Also known as PLX4032, RG7204, and RO5185426.
General information
Class/mechanism: Tyrosine kinase inhibitor of some mutated forms of BRAF serine/threonine
kinase, including BRAF V600E. Also has been observed to inhibit other tyrosine kinases such as CRAF, ARAF, wild-type BRAF, SRMS, ACK1, MAP4K5, and FGR. Certain BRAF mutations, such as V600E, result in constitutive activation of cell proliferation pathways and tumor growth.[1][2][3]
Route: PO
Extravasation: n/a
For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as Micromedex, Lexicomp, UpToDate (courtesy of Lexicomp), or the prescribing information.[1]