Sutacimig (HMB-001) is a humanized antibody of the (H-γ4_L-κ)_(H-γ4_L-κ) format that targets FⅦa/TREML1. One arm of Sutacimig binds to endogenous FVIIa, thereby prolonging the half-life of FVIIa and increasing its accumulation in the bloodstream, while the other arm binds to TLT-1, which is exclusively expressed on the surface of activated platelets. This localizes endogenous FVIIa to activated platelets, further enhancing the activity of FVIIa. Sutacimig enhances Thrombin generation, fibrin formation, and the formation of stable fibrin-platelet networks at sites of vascular injury. Sutacimig can be used in studies related to Glanzmann thrombasthenia [1] [2] [3].
In Vitro, One arm of Sutacimig binds endogenous FVIIa, thereby extending the half-life of FVIIa and increasing its accumulation in the blood circulation. The other arm binds TLT-1, which is exclusively expressed on the surface of activated platelets, thus localizing endogenous FVIIa to activated platelets, enhancing the activity of FVIIa, boosting thrombin generation and fibrin formation downstream of platelet activation sites, and promoting the formation of a stable fibrin-platelet meshwork, which is essential for achieving hemostasis[2].
References:
[1]. Saultier P, et al. Sutacimig, a novel bispecific antibody for prophylactic treatment of glanzmann thrombasthenia: Analysis of a Phase 2 study[J]. 2025.
[2]. Saultier P, et al. A Phase 2 study to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and efficacy of sutacimig for prophylaxis in glanzmann thrombasthenia: A trial in progress[J]. Blood, 2025, 146: 8232.
[3]. INN Proposed List 131. 11 August 2024.
In Vitro, One arm of Sutacimig binds endogenous FVIIa, thereby extending the half-life of FVIIa and increasing its accumulation in the blood circulation. The other arm binds TLT-1, which is exclusively expressed on the surface of activated platelets, thus localizing endogenous FVIIa to activated platelets, enhancing the activity of FVIIa, boosting thrombin generation and fibrin formation downstream of platelet activation sites, and promoting the formation of a stable fibrin-platelet meshwork, which is essential for achieving hemostasis[2].
References:
[1]. Saultier P, et al. Sutacimig, a novel bispecific antibody for prophylactic treatment of glanzmann thrombasthenia: Analysis of a Phase 2 study[J]. 2025.
[2]. Saultier P, et al. A Phase 2 study to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and efficacy of sutacimig for prophylaxis in glanzmann thrombasthenia: A trial in progress[J]. Blood, 2025, 146: 8232.
[3]. INN Proposed List 131. 11 August 2024.