Erlotinib

Research use only, not for human use.

A potent, selective inhibitor of EGFR with IC50 of 2 nM; reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM.

A potent, selective inhibitor of EGFR with IC50 of 2 nM; reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM; inhibits the proliferation of DiFi human colon tumor cells at submicromolar concentrations in cell culture and blocks cell cycle progression at the G1 phase; 100mg/kg completely prevents EGF-induced autophosphorylation of EGFR in human HN5 tumors growing as xenografts in athymic mice and of the hepatic EGFR of the treated mice; orally active.Lung Cancer Approved(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. 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. (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. 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-尾-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.

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. 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.

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. 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

NSC-718781 | OSI-744 | R-1415 | CP-358774

Angiogenesis

EGFR

EGFR

Cancer

Lung Cancer

183321-74-6

393.4357

C22H23N3O4

>98% (HPLC)

10 mM in DMSO

COCCOC1=C(OCCOC)C=C2C(NC3=CC=CC(=C3)C#C)=NC=NC2=C1

4-Quinazolinamine, N-(3-ethynylphenyl)-6,7-bis(2-methoxyethoxy)-

(-20℃)

With Ice Pack

≥ 2 years