BIBW 2992 (Afatinib)

SKU: orb1306404

Description

Afatinib

Research Area

Cardiovascular Research, Cell Biology, Pharmacology & Drug Discovery, Signal Transduction

Key Properties

• CAS Number: 850140-72-6
• MW: 485.94
• Purity: >98%
• Formula: C₂₄H₂₅ClFN₅O₃
• SMILES: N(C=1C2=C(C=C(O[C@H]3CCOC3)C(NC(/C=C/CN(C)C)=O)=C2)N=CN1)C4=CC(Cl)=C(F)C=C4
• Target: Kinase
• Solubility: Soluble in DMSO (up to 25 mg/ml) or in Ethanol (up to 25 mg/ml).

Bioactivity

• Target IC50:
  EGFR (L858R/T790M):10 nM|EGFR (L858R):0.4 nM|EGFR:0.5 nM|HER2:14 nM
• In Vivo:
  METHODS: To assay antitumor activity in vivo, Afatinib (20 mg/kg, 1.8% HP-beta-CD + 5% acetic acid (10%) + aqueous Natrosol (0.5%)) was administered by gavage to NMRI-nu/nu mice bearing A431 xenografts once daily for 25 days. RESULTS: Afatinib resulted in significant tumor regression with a cumulative treatment/control tumor volume ratio (T/C ratio) of 2% and downregulation of EGFR and AKT phosphorylation.
• In Vitro:
  METHODS: NSCLC cells NCI-H1975, NCI-H1781, HCC827 and A549 were treated with Afatinib (0.0001-10 µM) for 72 h. Cell viability was measured by MTS assay. RESULTS: Afatinib inhibited the survival of tumor cell lines harboring wild-type (H1666) or L858R/T790M (NCI-H1975) EGFR. Afatinib is also effective against NSCLC cell lines expressing HER2 776insV (NCI-H1781) or EGFR E746_A750del (HCC827), but is inactive against A549 cells expressing wild-type EGFR and HER2 but also harboring the oncogenic Kras G12S point mutation. METHODS: BEAS-2B cells overexpressing wild-type or mutant HER2 were treated with Afatinib (0.1 µM) for 6 h, and target protein expression levels were measured by Western Blot. RESULTS: Afatinib treatment inhibited the phosphorylation of HER2, EGFR and AKT.

Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

BIBW2992

Compound Identifiers

PubChem CID

10184653