Useful Links
Additional Resources
Information below provided by the Pharmaceutical Company.
Vemurafenib (RO5185426, PLX4032, ZELBORAF®)
Agent Description
Vemurafenib is a kinase inhibitor available as 240 mg tablets for oral use. Vemurafenib has the chemical name propane-1-sulfonic acid {3-[5-(4-chlorophenyl)-1H-pyrrolo[2,3-b]pyridine-3-carbonyl]-2,4-difluoro-phenyl}-amide. It has the molecular formula C23H18ClF2N3O3S and a molecular weight of 489.9.
Vemurafenib is a white to off-white crystalline solid. It is practically insoluble in aqueous media. Tablets are for oral administration. Each tablet contains 240 mg of vemurafenib. The inactive ingredients are: Tablet core: hypromellose acetate succinate, croscarmellose sodium, colloidal silicon dioxide, magnesium stearate, and hydroxypropyl cellulose. Coating: pinkish white: poly (vinyl alcohol), titanium dioxide, polyethylene glycol 3350, talc, and iron oxide red.
Mechanism of Action
Vemurafenib is a low molecular weight, orally available inhibitor of some mutated forms of BRAF serine-threonine kinase, including BRAF V600E. Vemurafenib also inhibits other kinases in vitro such as CRAF, ARAF, wild-type BRAF, SRMS, ACK1, MAP4K5, and FGR at similar concentrations. Some mutations in the BRAF gene including V600E result in constitutively activated BRAF proteins, which can cause cell proliferation in the absence of growth factors that would normally be required for proliferation. Vemurafenib has anti-tumor effects in cellular and animal models of melanomas with mutated BRAF V600E.
Classification
BRAF mutant v600 inhibitor
Molecular Targets
BRAF V600 mutant, CRAF, ARAF, wild-type BRAF, SRMS, ACK1, MAP4K5, and FGR
Monograph
Vemurafenib is indicated for the treatment of patients with unresectable or metastatic melanoma with BRAF V600E mutation as detected by an FDA-approved test.
Limitation of Use: Vemurafenib is not indicated for treatment of patients with wild-type BRAF melanoma.
Package insert: https://www.gene.com/download/pdf/zelboraf_prescribing.pdf
Studies of Interest
- Vemurafenib has been evaluated (ongoing/planned studies) in a broad number of BRAF-driven malignancies other than melanoma originating in a number of anatomic sites: colorectal, lung (non-small cell), thyroid, ovary (low grade serous), brain (gliomas, craniopharyngioma), histiocytic disorders (Erdheim-Chester Disease/Langerhan's Cell Histiocytosis), hairy cell leukemia, and multiple myeloma.
- Phase III Development in BRAF mutant metastatic melanoma continues with vemurafenib combined with cobimetinib plus atezolizumab vs. vemurafenib plus cobimetinib
Areas of interest:
- BRAF V600E-driven malignancies other than melanoma - vemurafenib plus cobimetinib with or without novel targeted or immune therapies to address known mechanisms of resistance to BRAFi+MEKi therapy and/or optimize response, respectively.
- BRAF V600 mutant melanoma: as above in patients with locally advanced disease accessible to biopsy, i.e. neo(adjuvant)
Areas not supported:
- Vemurafenib monotherapy in BRAF V600 mutant-driven malignancies
- Vemurafenib combinations with ipilimumab
Information collaborator would like included in investigator proposals
N/A
Genentech supports non-clinical research proposals through a separate mechanism. Please visit https://www.gene.com/gene/reagents-program/reagents-program.jsp
if you wish to submit a request for a Genentech agent for non-clinical work.