Erlotinib

Erlotinib (CP-358774) is a directly acting EGFR tyrosine kinase inhibitor, with an IC₅₀ of 2 nM for human EGFR. Erlotinib reduces EGFR autophosphorylation in intact tumor cells with an IC₅₀ of 20 nM. Erlotinib is used for the treatment of non-small cell lung cancer^[1]. Erlotinib is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups. IC50 & Target: IC50: 2 nM (EGFR)^[1] In Vitro: Erlotinib (CP-358774) is also a potent inhibitor of the recombinant intracellular (kinase) domain of the EGFR, with an IC₅₀ of 1 nM. The proliferation of DiFi cells is strongly inhibited by Erlotinib with an IC₅₀ of 100 nM for an 8-day proliferation assay^[1]. The combination of B-DIM and Erlotinib (2 μM) results in a significant inhibition of colony formation in BxPC-3 cells when compared with either agent alone. The combination of B-DIM and Erlotinib (2 μM) results in a significant induction of apoptosis only in BxPC-3 cells when compare with the apoptotic effect of either agent alone^[2]. In Vivo: Under the experimental conditions, the combination of B-DIM and Erlotinib (50 mg/kg, i.p.) treatment shows significant decrease (P <0.01) in tumor weight compared with untreated control^[2]. Erlotinib (20 mg/kg, p.o.) significantly attenuates Cisplatin (CP)-induced body weight (BW) loss when compared to the CP+vehicle (V) rats (P<0.05). Erlotinib treatment significantly improves renal function in CP-N(normal control group, NC) rats. The CP+Erlotinib (E) rats show significant reduction of the levels of Serum creatinine (s-Cr) (P<0.05), blood urea nitrogen (BUN) (P<0.05), urinary N-acetyl-β-D-glucosaminidase (NAG) index (P<0.05), and significant increase of urine volume (UV) (P<0.05) and Cr clearance (Ccr) (P<0.05) compare to the CP+V rats^[3]