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Tebentafusp (IMCgp100) is a bispecific fusion protein to target gp100 peptide-HLA-A*02:01 (a melanoma-associated antigen). Tebentafusp guides T cells to kill gp100 -expressing tumor cells via a high affinity T-cell receptor (TCR) binding domain and an anti-CD3 T-cell engaging domain. Tebentafusp leads to inflammatory cytokines and cytolytic proteins production, resulting in the direct lysis of tumour cells.
In Vitro
Tebentafusp is an ImmTAC recognizing a peptide derived from the melanoma-specific protein, gp100, presented by HLA-A*0201. Tebentafusp (31 pM, 82 pM, and 131 pM; 16 h) stimulates cytotoxic degranulation activity of PBMC against Mel526 cells rather than gp100-negative A375 cells. Tebentafusp (100 pM; 0-50 h) mediates CD8 + T cell killing despite the presence of regulatory T cells via monitoring caspase 3/7 activation during 40-48 hr. Tebentafusp (100 pM; 0-80 h) triggers cytolysis of melanoma cells by CD4 + T cell subpopulations. Tebentafusp (1, 12, 31, 82, and 131 pM; 24 h or 96 h) increases granzyme B amount, and induces broad cytokine and chemokine release including in both CD4 + and CD8 + cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Tebentafusp (10 μg/kg; i.v.) inhibits tumor growth in mouse melanoma model. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
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