Vemurafenib

SKU: orb1305565

Description

Vemurafenib

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Key Properties

• CAS Number: 918504-65-1
• MW: 489.92
• Purity: 99.65%
• Formula: C₂₃H₁₈ClF₂N₃O₃S
• SMILES: C(=O)(C=1C=2C(NC1)=NC=C(C2)C3=CC=C(Cl)C=C3)C4=C(F)C(NS(CCC)(=O)=O)=CC=C4F
• Target: Src,MAPK,Raf,ACK1,Autophagy
• Solubility: Ethanol:< 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

• 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 detect 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.
• 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 inhibited 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, and the expression levels of target proteins were detected by Western Blot. RESULTS: Vemurafenib inhibited the phosphorylation of MEK and ERK in Colo829 and LOX cells.
• 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. For the assay, RG7204 was prepared at 10 times the final assay concentration in media containing 1% DMSO. Twenty-four hours after cell plating, 20 μL of the appropriate dilution were added to plates in duplicate. The plates were assayed for proliferation 6 days after the cells were plated according to the procedure originally described by Mosmann .
• Animal Research:
  All animal procedures were approved by the Ethical Commission of the Institute for Cancer Research and Treatment and by the Italian Ministry of Health. WiDr cells were injected subcutaneously into the right posterior flanks of 7-week-old immunodeficient NODSCID female mice (6 mice per group). Tumour formation was monitored twice a week, and tumour volume based on caliper measurements was calculated by the modified ellipsoidal formula: tumour volume = 1/2 length × width. When tumours reached a volume of approximately 200–250 mm^3, mice were randomly assigned to treatment with vehicle or drug(s) .

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

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

Compound Identifiers

PubChem CID

42611257