Anti-CLEC12A / CD371 Reference Antibody (tepoditamab)
- Product Code: 139933
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Product Description:
Tepoditamab is an investigational monoclonal antibody designed to target CLEC12A (also known as CD371), a receptor expressed on myeloid cells, including acute myeloid leukemia (AML) blasts and myeloid-derived suppressor cells (MDSCs). Its primary application is in the treatment of AML, where it leverages immune-mediated mechanisms to eliminate malignant cells.
By binding to CLEC12A, tepoditamab activates antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), enabling immune effector cells like natural killer (NK) cells and macrophages to recognize and destroy leukemia cells. This makes it a promising candidate for immunotherapy in patients with relapsed or refractory AML.
Additionally, because CLEC12A is largely restricted to the myeloid lineage and has limited expression on hematopoietic stem cells, tepoditamab offers a favorable safety profile with reduced risk of targeting healthy stem cells. It is being evaluated both as a monotherapy and in combination with other agents to enhance anti-leukemic responses.
Tepoditamab may also help reduce immunosuppressive MDSCs in the tumor microenvironment, potentially improving the efficacy of other immunotherapies. Clinical development is ongoing to determine its full therapeutic potential in myeloid malignancies.
Sizes / Availability / Pricing:
| Size | Availability | Price | Quantity |
|---|---|---|---|
| 50μg | 10-20 days | ฿4,980.00 |
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Anti-CLEC12A / CD371 Reference Antibody (tepoditamab)
Tepoditamab is an investigational monoclonal antibody designed to target CLEC12A (also known as CD371), a receptor expressed on myeloid cells, including acute myeloid leukemia (AML) blasts and myeloid-derived suppressor cells (MDSCs). Its primary application is in the treatment of AML, where it leverages immune-mediated mechanisms to eliminate malignant cells.
By binding to CLEC12A, tepoditamab activates antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), enabling immune effector cells like natural killer (NK) cells and macrophages to recognize and destroy leukemia cells. This makes it a promising candidate for immunotherapy in patients with relapsed or refractory AML.
Additionally, because CLEC12A is largely restricted to the myeloid lineage and has limited expression on hematopoietic stem cells, tepoditamab offers a favorable safety profile with reduced risk of targeting healthy stem cells. It is being evaluated both as a monotherapy and in combination with other agents to enhance anti-leukemic responses.
Tepoditamab may also help reduce immunosuppressive MDSCs in the tumor microenvironment, potentially improving the efficacy of other immunotherapies. Clinical development is ongoing to determine its full therapeutic potential in myeloid malignancies.
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