CEACAM5 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying CEACAM5 (carcinoembryonic antigen 5, CEA)'s role as the classical CEA tumor marker or modeling its applications in CEACAM5-targeted cancer therapy. The Knockout line is the standard tool for asking whether CEACAM5 is required for these processes — CEACAM5 is a GPI-anchored cell surface glycoprotein highly expressed on epithelial cancers (colorectal, lung, gastric, pancreatic, breast) with low normal-tissue expression except colon epithelium; CEACAM5 is the classical 'CEA' tumor marker for monitoring colorectal cancer recurrence by serum measurement, and is an emerging cancer therapy target. Overexpression is useful for studying CEACAM5 gain-of-function effects. For cancer therapy research, the EDITGENE CEACAM5 Knockout in HEK293 is uniquely valuable — HEK293 supports systematic structure-function studies of CEA and serves as a critical specificity control for CEACAM5-targeted compound development. Other CEACAM family member (CEACAM1, CEACAM6, CEACAM7, CEACAM8) expression analysis aids interpretation given some antibody cross-reactivity. Rescue with wild-type or GPI-anchor-deficient CEACAM5 enables structure-function studies. The knockout is a critical specificity tool for ⭐ tusamitamab ravtansine (anti-CEACAM5 ADC, in Phase III clinical development for NSCLC), CEACAM5-targeted CAR-T cells, anti-CEACAM5 × CD3 bispecific antibodies (cibisatamab/CEA-TCB), and labetuzumab govitecan (anti-CEACAM5 ADC) — CEACAM5 is one of the most validated solid tumor surface antigens for targeted therapy development.

Primary applications: • CEACAM5-targeted therapy specificity: critical genetic control for ⭐ tusamitamab ravtansine (Phase III NSCLC), cibisatamab (CEA-TCB, anti-CEACAM5×CD3 bispecific), labetuzumab govitecan, and other CEACAM5-targeted ADCs. • CEACAM5 CAR-T validation: critical specificity control for CEACAM5-CAR-T cells in solid tumor development. • Anti-CEA antibody specificity: critical genetic control for serum CEA detection antibodies — assessment of CEACAM family cross-reactivity (CEACAM6 in particular). • Cell-cell adhesion: in heterologous epithelial contexts, CEACAM5-mediated homophilic adhesion analysis. EDITGENE recommends this model as a critical specificity control for the entire CEACAM5-targeted cancer therapy field including ADCs, bispecifics, and CAR-T strategies.

Yes. CEACAM5 rescue experiments require attention to GPI anchor processing: • Construct design: use a codon-modified CEACAM5 sequence with a small N-terminal tag (FLAG, HA) — CEACAM5 is a GPI-anchored protein with C-terminal GPI signal sequence cleaved during processing; C-terminal tags are removed during GPI attachment. • Surface localization validation: confirm plasma membrane GPI-anchored expression by cell surface staining. • GPI-attachment-deficient rescue: C-terminal GPI signal mutations abolish GPI processing, generating secreted CEACAM5. • Domain-specific rescue: CEACAM5 has multiple Ig-like extracellular domains; specific tumor-targeting antibody epitopes can be analyzed by domain truncation. • Functional readout: rescue should restore CEACAM5-targeted compound (tusamitamab ravtansine, cibisatamab, labetuzumab govitecan) cellular binding. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation for systematic CEACAM5-targeted compound development.