Antibodies targeting EOL-1-associated antigens are used for:
Phenotyping: Identifying surface markers (e.g., CD33, CD123) for leukemic blast characterization.
Therapeutic Targeting: Developing bispecific antibodies (BsAbs) to engage T cells against leukemia cells.
Differentiation Studies: Tracking changes in surface receptors during induced differentiation.
| Cell Line | CD33+/CD123+ (%) | CD34+/CD38+ (%) | FLT3 Expression |
|---|---|---|---|
| EOL-1 | 78.9 | 22.1 | High |
| MOLM-13 | 65.7 | 18.3 | Medium |
| KG1 | 58.8 | 41.2 | Low |
| Data source: |
| Antibody Target | E:T Ratio | % Cytotoxicity |
|---|---|---|
| CD33GOBi | 1:1 | 78% |
| CD123Bi | 1:1 | 56% |
| Dual (CD33/CD123) | 1:1 | 80% |
| Arming dose: 25 ng/10⁶ T cells; Data source: |
FLT3xCD3 BsAb (CLN-049): Induces T-cell-mediated lysis of FLT3-expressing EOL-1 cells, independent of soluble FLT3 ligand interference .
CD33/CD123 BsAbs: Redirect T cells to lyse EOL-1 blasts via dual antigen engagement, achieving >75% cytotoxicity at low effector-to-target (E:T) ratios .
Differentiation Markers: Anti-CD95 antibodies induce apoptosis, while differentiation agents (e.g., dbcAMP) upregulate CD11b and eosinophilic cationic protein (ECP) .
Targeted Therapy: Bispecific antibodies show promise for treating FLT3+ or CD33+/CD123+ acute myeloid leukemia (AML), with EOL-1 serving as a high-expression model .
Drug Resistance Insights: EOL-1’s sensitivity to kinase inhibitors (e.g., imatinib) highlights PDGFRα as a therapeutic target .