Molecular Formula | C28H29ClFN5O7 |
Molar Mass | 602.02 |
Melting Point | >237oC (dec.) |
Solubility | DMSO: ≥ 35 mg/mL |
Appearance | Solid |
Color | White to Pale Yellow |
Storage Condition | Refrigerator |
In vitro study | In lung cancer cell lines expressing wild-type (H1666) or L858R/T790M (NCI-H1975) EGFR, Afatinib was more effective in inhibiting cell growth than erlotinib, ge fi tinib and lapatinib. Afatinib was also effective on NSCLC cell lines expressing HER 2 776insV (NCI-H1781) or EGFR E746_A750del (HCC827), but not on A549 cells expressing wild-type EGFR and HER2. Afatinib enhanced the cytotoxicity of topotecan and mitoxantrone on SP cells and enhanced the apoptosis-inducing effect of topotecan and mitoxantrone on SP cells. |
In vivo study | In a MDA-MB-453 xenograft model, Afatinib(20 mg/kg, P. O.) significantly induced tumor regression with a cumulative treated/control tumor volume ratio (T/C ratio). 2%, and down-regulation of EGFR and AKT phosphorylation levels. In A7, A431, FaDu, UT-SCC-14 and UT-SCC-15 xenograft models, Afatinib(30 mg/kg, oral administration) significantly prolonged tumor growth. In the HER2 amplified xenograft model, Afatinib(30 mg/kg, oral administration) significantly inhibited tumor growth and significantly prolonged survival. In the HER2 positive gastric cancer NCI-N87 xenograft model, oral administration of Afatinib(25 mg/kg) for 4 days significantly reduced the tumor volume and almost completely cured the tumor after 21 days of administration. |
HS Code | 29339900 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 1.393 ml | 6.963 ml | 13.926 ml |
5 mM | 0.279 ml | 1.393 ml | 2.785 ml |
10 mM | 0.139 ml | 0.696 ml | 1.393 ml |
5 mM | 0.028 ml | 0.139 ml | 0.279 ml |