A bispecific, TCR-based biologic (TCER) that uses a high-affinity soluble TCR to bind a PRAME-derived peptide presented by HLA class I on tumor cells and an anti-CD3 moiety to engage and activate T cells, redirecting cytotoxicity against PRAME-positive solid tumors.
IMA402 is a TCR-based bispecific T-cell engager (TCER) that uses a high-affinity soluble TCR to bind a PRAME-derived peptide presented by HLA class I on tumor cells and an anti-CD3 moiety to recruit and activate T cells, forming an immune synapse and redirecting perforin/granzyme-mediated cytotoxicity against PRAME-positive tumors.
YES
DIRECT
The TCER binds the PRAME peptide–HLA class I complex on tumor cells and CD3 on T cells, forming an immune synapse that activates T cells to kill target-expressing cells via perforin/granzyme-mediated cytotoxicity.
A bispecific, TCR-based biologic (TCER) that uses a high-affinity soluble TCR to bind a PRAME-derived peptide presented by HLA class I on tumor cells and an anti-CD3 moiety to engage and activate T cells, redirecting cytotoxicity against PRAME-positive solid tumors.
IMA402 is a TCR-based bispecific T-cell engager (TCER) that uses a high-affinity soluble TCR to bind a PRAME-derived peptide presented by HLA class I on tumor cells and an anti-CD3 moiety to recruit and activate T cells, forming an immune synapse and redirecting perforin/granzyme-mediated cytotoxicity against PRAME-positive tumors.
NO
INDIRECT
The drug binds CD3 on T cells to recruit and activate them; activated T cells then kill PRAME/HLA-positive tumor cells via perforin/granzyme. CD3+ cells are not targeted for killing.
Base-edited, allogeneic anti-CD33 chimeric antigen receptor (CAR) T-cell therapy. Donor T cells are engineered with a CD33-specific CAR and base edits to enable function after chemotherapy and reduce alloreactivity/off-tumor effects (e.g., lower GVHD risk). Administered as a single IV infusion prior to allo-HSCT to target CD33+ AML blasts.
Base-edited, allogeneic T cells expressing a CD33-specific chimeric antigen receptor bind CD33 on AML blasts and induce targeted cytotoxicity via T-cell activation (perforin/granzyme release, cytokines, and death-receptor pathways). Base edits reduce TCR-driven alloreactivity and off-tumor effects and are intended to enable persistence/function after conditioning chemotherapy. Administered as a single IV infusion prior to allo-HSCT.
YES
DIRECT
CD33-specific CAR T cells bind CD33 on target cells and induce T-cell cytotoxicity via perforin/granzyme release and death-receptor signaling (e.g., Fas/TRAIL), leading to apoptosis.
An allogeneic, CD70-directed CAR T-cell therapy engineered ex vivo with CRISPR-Cas9; administered by IV infusion after lymphodepleting chemotherapy to recognize and kill CD70-expressing tumor cells via CAR-mediated T-cell activation and cytotoxicity.
Allogeneic T cells engineered ex vivo with CRISPR-Cas9 to knock out endogenous TCR and MHC class I and to express a CD70-specific chimeric antigen receptor. After IV infusion following lymphodepletion, the CAR binds CD70 on tumor cells, activating the T cells to release cytokines and perforin/granzyme, leading to targeted cytotoxic killing of CD70-positive malignant cells while reducing GVHD risk and enhancing persistence.
YES
DIRECT
CD70-directed CAR T cells bind CD70 on target cells, triggering T-cell activation and immune synapse formation, leading to perforin/granzyme-mediated cytolysis (and related T-cell effector mechanisms).