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Vemurafenib

SKU: orb1305565

Description

Vemurafenib

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Images & Validation

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Vemurafenib

Key Properties

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CAS Number918504-65-1
MW489.92
Purity99.65%
FormulaC23H18ClF2N3O3S
SMILESC(=O)(C=1C=2C(NC1)=NC=C(C2)C3=CC=C(Cl)C=C3)C4=C(F)C(NS(CCC)(=O)=O)=CC=C4F
TargetSrc,MAPK,Raf,ACK1,Autophagy
SolubilityEthanol:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:9 mg/mL (18.37 mM);H2O:< 1 mg/mL (insoluble or slightly soluble);DMSO:99 mg/mL (202.07 mM)

Bioactivity

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Target IC50
B-Raf (V600E):31 nM (cell free)|Ack1:19 nM (cell free)|SRMS:18 nM (cell free)|C-Raf1:48 nM (cell free)
In Vivo
METHODS: To assay anti-tumor activity in vivo Vemurafenib (12.5-75 mg/kg, suspended in an aqueous Vehicle containing 2% Klucel LF and adjusted to pH 4 with dilute HCl.) was orally administered to melanoma-carrying Athymic nude mice bearing LOX were administered orally twice daily for 11-13 days. Results: Vemurafenib significantly inhibited tumor growth and induced tumor regression. METHODS: In order to detec the anti-tumor activity in vivo Vemurafenib (60 mg/kg) was administered orally to athymic mice bearing melanoma Colo-205 twice a day for 14 days. Results: Vemurafenib effectively inhibited tumor growth in the Colo-205 xenograft mouse model.
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In Vitro
METHODS: Melanoma cells A375 and SK-Mel-28 were treated with Vemurafenib (0-8 μM) for 48 h. Cell viability was detected using CCK-8 assay. Results: Vemurafenib dose-dependently inhibite the proliferation of A375 and SK-Mel-28 cells with IC50 of 0.8 μM and 1.8 μM, respectively METHODS: Melanoma cell lines Colo829 and LOX expressing BRAF V600E were treated with Vemurafenib (0.05-30 μMol/L) for 2 h, an the expression levels of target proteins were detected by Western Blot. Results: Vemurafenib inhibite the phosphorylation of MEK and ERK in Colo829 and LOX cells.
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Cell Research
Cellular proliferation was evaluated by MTT assay. Briefly, cells were plated in 96-well microtiter plates at a density of 1,000 to 5,000 cells per well in a volume of 180 μL. Fo the assay, RG7204 was prepared at 10 time the final assay concentration in media containing 1% DMSO. Twenty-four hours after cell plating, 20 μL o the appropriate dilution were added to plates in duplicate the plates were assayed for proliferation 6 dayss afte the cells were plated according to the procedure originally described by Mosmann.
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Animal Research
All animal procedures were approved b the Ethical Commission o the Institute for Cancer Research and Treatment and b the Italian Ministry of Health. WiDr cells were injected Subcutaneously int the right posterior flanks of 7-week-old immunodeficient NODSCID f Male mice (6 mice per group). Tumour formation was monitored twice a week, and tumour volume based on caliper measurements was calculated b the modified ellipsoidal formula: tumour volume = 1/2 length × width. When tumours reached a volume of approximately 200–250 mm^3, mice were andomly assigned to treatment with Vehicle or drug(s).
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Storage & Handling

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StoragePowder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
DisclaimerFor research use only

Alternative Names

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Raf, Raf kinases, RG 7204, RG7204, RG-7204, RO 5185426, RO5185426, RO-5185426, SRMS, Vemurafenib, 1029872-54-5, ACK1, B-Raf (V600E), B-Raf, Autophagy, C-Raf, inhibit, PLX4032, PLX-4032, PLX 4032, Inhibitor, MAP4K5 (KHS1), FGR

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Compound Identifiers

PubChem CID
42611257 ↗

Key Properties

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No computed properties available.

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Vemurafenib (orb1305565)

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% DMSO +
%+
% Tween 80 +
%

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1 ml x 10 mM (in DMSO)
$ 90.00
10 mg
$ 90.00
50 mg
$ 120.00
100 mg
$ 140.00
200 mg
$ 220.00
500 mg
$ 350.00
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