BiTE® technology: designed to ENGAGE T CELLS TO FIGHT CANCER

The need for new therapeutic approaches remains high

Despite recent advances in immuno-oncology, not enough patients benefit from current treatments and additional options are needed to address both hematologic malignancies and solid tumors.

  • Certain immuno-oncology therapies and chemotherapies do not specifically target cancer cells through tumor-associated antigens1,2
  • Not enough patients experience long-term benefits while managing the potential cost of high toxicity2,3
BiTE® technology is designed to engage the natural power of T cells

Cytotoxic T cells play an important role in the body’s immune defense by identifying and eliminating cancer cells; however, cancer cells can develop mechanisms to evade T-cell recognition and destruction.4-6

Bispecific T-cell Engager (BiTE®) technology is designed to overcome cancer cells’ evasion of the immune system by engaging patients’ own T cells to directly target cancer cells. BiTE® molecules comprise of two flexibly linked, single-chain antibodies, with one designed to bind specifically to a selected tumor-associated antigen and the other to bind CD3 found on T cells.4,7,8

This versatile technology is engineered with the goal of delivering off-the-shelf therapies that direct patients’ own T cells to tumor cells, activating their cytotoxic potential.4,7 Currently being investigated in multiple solid and hematological malignancies, BiTE® technology aims to close the space between tumors and T cells.4

Download a copy of BiTE The Engager™, an educational resource on BiTE® technology.


Search our clinical trials.

Visit our resources section for further information on modalities currently under investigation.

Click here for more information on the BiTE® immuno-oncology platform     

BiTE® technology is designed to fight cancer


The BiTE® molecule is designed to recruit a T cell to bind to a cancer cell, leading to the formation of a cytolytic synapse4,10


The T cell becomes activated, releasing perforin and granzymes; fusion of perforin with the cancer cell membrane allows granzymes to enter the cancer cell to induce apoptosis9,10


T-cell activation also causes the release of cytokines and production of additional perforin and granzymes that may allow T cells to target surrounding cancer cells; this potentially results in the serial lysis of multiple cancer cells by a single T cell4,10,11


Sustained activation of a single activated cytotoxic T cell can result in local proliferation of T cells4,10,12

BiTE® technology has the potential to be ready when patients need it

  • Engineered with the goal of delivering off-the-shelf therapies to enable patients, including those with aggressive tumors, to initiate treatment immediately4,7
  • Does not depend on ex vivo manipulation of patients’ cells4,7
  • Investigated for use as monotherapies and in combination with other treatments8,9
BiTE® molecules are under investigation to target:
Clinical trials are underway in several cancers, including13,14:

Amgen is committed to bringing T-cell innovation to more patients

Amgen is a pioneer in the development of immuno-oncology therapies. The BiTE® immuno-oncology platform continues to be investigated across multiple different hematologic malignancies and solid tumors.8

BiTE: Bispecific T-cell Engager; CD: cluster of differentiation; PSMA: prostate-specific membrane antigen.


1. Ok CY, Young KH. J Hematol Oncol. 2017;10(1):103. 2. Baudino TA. Curr Drug Discov Technol. 2015;12(1):3-20. 3. Shekarian T, Valsesia-Wittmann S, Caux C, Marabelle A. Mutagenesis. 2015;30(2):205-211. 4. Baeuerle PA, Kufer P, Bargou R. Curr Opin Mol Ther. 2009;11(1):22-30. 5. Ferrone S, Whiteside TL. Surg Oncol Clin N Am. 2007;16(4):755-774. 6. Rabinovich GA, Gabrilovich D, Sotomayor EM. Annu Rev Immunol. 2007;25(4):267-296. 7. Frankel SR, Baeuerle PA. Curr Opin Chem Biol. 2013;17(3):385-392. 8. Yuraszeck T, Kasichayanula S, Benjamin JE. Clin Pharmacol Ther. 2017;101(5):634-645. 9. Baeuerle PA, Reinhardt C. Cancer Res. 2009;69(12):4941-4944. 10. Nagorsen D, Baeuerle PA. Exp Cell Res. 2011;317(9):1255-1260. 11. Ross SL, Sherman M, McElroy PL, et al. PLoS One. 2017;12(8):e0183390. 12. Brischwein K, Schlereth B, Guller B, et al. Mol Immunol. 2006;43(8):1129-1143. 13. Accessed 4/13/2022. 14. Accessed 4/13/2022.