| Name | EGFR-IN-2 |
| Description | EGFR-IN-2 is a non-covalent, orally available and mutation-selective EGFR inhibitor for the treatment of non-small cell lung cancer (NSCLC), with high selectivity for resistant single and double mutant T790M with IC50 = 27 nm to 33 nM, and low inhibitory activity for wild-type H292 (IC50 = 218 nM). |
| In vitro | EGFR-IN-2 (Compound 21) demonstrated excellent inhibitory activity in various EGFR-mutant NSCLC cell lines. Inhibition of EGFR autophosphorylation was evaluated in H1975 (T790M/L858R), PC9-ER (T790M/del746–750), and PC9 (del746–750) cell lines, with IC₅₀ values of 0.027 μM, 0.008 μM, and 0.033 μM respectively. In a kinase panel of 225 kinases, only 12 were inhibited >70% at 0.1 μM, demonstrating high target specificity. EGFR-IN-2 exhibited low clearance in human liver microsomes and hepatocytes (3.8 and 2.7 mL/min/kg, respectively), and good predicted oral bioavailability [1]. |
| In vivo | In a H1975 xenograft mouse model, EGFR-IN-2 was evaluated for in vivo target engagement and pharmacokinetics. After oral administration at 50 mg/kg, free plasma concentrations remained above the in vitro IC₅₀ (0.027 μM) for up to 8 hours; at 100 mg/kg, this duration extended to 16 hours. Corresponding suppression of phosphorylated EGFR, ERK1/2, and AKT confirmed effective target inhibition in vivo. The EGFR-IN-2 exhibited moderate plasma clearance in mice (104 mL/min/kg) with 19% oral bioavailability, and in dogs, clearance was 13 mL/min/kg with 30% bioavailability[1]. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Keywords | EGFRIN2 | EGFR IN 2 | EGFR |
| Inhibitors Related | (S)-Afatinib | Osimertinib | Lidocaine Hydrochloride hydrate | Lapatinib | Erlotinib hydrochloride | Erlotinib | Neratinib | Afatinib | Chalcone | Brigatinib | Genistein | Gefitinib |
| Related Compound Libraries | Anti-Lung Cancer Compound Library | Bioactive Compound Library | Kinase Inhibitor Library | JAK-STAT Compound Library | Multi-Target Compound Library | Post-Translational Modification Compound Library | Immunology/Inflammation Compound Library | Bioactive Compounds Library Max | Anti-Cancer Compound Library |
United States
