Cetuximab MMAE

Cetuximab MMAE (0.5-5 nM) specifically binds to EGFR⁺ tumor cell lines (CAL-27, SCC-61, A-549), induces G₂/M arrest across the 0.5-5 nM range, and restricts MMAE-mediated toxicity and radiosensitization to these EGFR⁺ cells^[1].
Cetuximab MMAE (2 nM; overnight) induces morphological changes consistent with G₂/M cell cycle arrest in CAL-27 cells^[8].
Cetuximab MMAE (2-5 nM; overnight) induces G₂/M cell cycle arrest in CAL-27 cells, but does not alter the cell cycle profile of OE19 cells^[8].
Cetuximab MMAE (0.000256-500 nM; 96 h) potently reduces viability of KRAS mutant MIA PaCa-2 and PANC-1 human pancreatic cancer cells in an EGFR-dependent manner, with IC₅₀ values of 1377 pM and 39 pM, respectively^[5].
Cetuximab MMAE (0.00005-50 nM; 8-14 days) suppresses colony formation of KRAS mutant MIA PaCa-2 and PANC-1 human pancreatic cancer cells in an EGFR-dependent manner^[5].
Cetuximab MMAE (0.5 nM; 72 h)-mediated cytotoxicity in PANC-1 human pancreatic cancer cells is dependent on EGFR expression, as EGFR knockdown significantly reduces cell death induced by 0.5 nM Cetuximab MMAE^[5].
Cetuximab MMAE (0.1-2 nM; 15 min on ice) binds to CAL-27 cells in a dose-dependent manner, but does not bind to OE19 cells^[8].
Cetuximab MMAE (0.01-10 nM; 72 h) potently kills CAL-27 cells across tested concentrations over 72 h, but has minimal cytotoxic effect on OE19 cells^[8].
Cetuximab MMAE (0.5 nM for CAL-27, 20 nM for LN229; overnight before 6 Gy irradiation) enhances ionizing radiation-induced DNA double-strand breaks in CAL-27 cells, but does not do so in low EGFR-expressing LN229 cells^[8].
Cetuximab MMAE (2 nM; overnight before 6 Gy irradiation) enhances ionizing radiation-induced DNA double-strand breaks in CALU3 cells, but does not do so in HER2-positive OE19 cells^[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.