TPO-R

Thrombopoietin receptor (TPO-R) and its ligand (TPO) are the primary regulators of platelet production. TPO-R is found on the surface of megakaryocyte cells, hemangioblasts, and hematopoietic stem cells.1

Chemotherapy-induced thrombocytopenia (CIT) is a serious complication occurring when chemotherapy damages the bone marrow and lowers the production of platelets.2 Severely low platelet counts can negatively impact treatment outcomes and disrupt therapy, increasing the risk of bleeding and the need for platelet transfusions.3

Increasing platelet production by activating TPO-R represents a promising approach for CIT.

Learn more about modalities targeting TPO-R:
peptibody.

Search our clinical trials.

Download additional information from our resources section.

CD: cluster of differentiation.

References

1. Varghese LN, Defour JP, Pecquet C, Constantinescu SN. The thrombopoietin receptor: structural basis of traffic and activation by ligand, mutations, agonists, and mutated calreticulin. Front Endocrinol. 2017;8:59.2. American Society of Clinical Oncology. Low platelet count or thrombocytopenia. https://www.cancer.net/navigating-cancer-care/side-effects/low-platelet-count-or-thrombocytopenia. Accessed 4/9/2019.3. Vadhan-Raj S. Management of chemotherapy-induced thrombocytopenia: current status of thrombopoietic agents. Semin Hematol. 2009;26(1 suppl 2):S26-S32.