ArticleNature cardiovascular research2024
A bispecific antibody approach for the potential prophylactic treatment of inherited bleeding disorders.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Multi-step computational identification of small molecules targeting the TLT-1 stalk peptide: structural insights into platelet function and thrombosis.Journal of thrombosis and thrombolysis · 2026Article
- Efficacy and safety of recombinant activated factor VII for secondary prophylaxis in patients with Glanzmann thrombasthenia.Research and practice in thrombosis and haemostasis · 2026Observational
- HMB-002: a monovalent antibody that elevates circulating VWF and FVIII levels for treatment of von Willebrand disease.Blood advances · 2026Article
- Synthesis of Bispecific Conjugates by ADP-Ribosyl Cyclases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gynecologic and obstetric management of girls and women with von Willebrand disease.Haematologica · 2026Review
- Molecular Pathogenesis of Inherited Platelet Dysfunction.Biomolecules · 2025Review
- Therapeutic innovations in hemophilia: the essential role of a positive reinvestment cycle.Blood advances · 2025Review
- Functional characterization of a nanobody-based glycoprotein VI-specific platelet agonist.Research and practice in thrombosis and haemostasis · 2024Article
- Pregnancy and childbirth in patients with Glanzmann Thrombasthenia.British journal of haematology · 2024Review
- Considering future qualification for regulatory science in the early development of microphysiological systems: a case study of microthrombosis in a Vessel-on-Chip.Frontiers in toxicology · 2024Article
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19 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Inherited bleeding disorders such as Glanzmann thrombasthenia (GT) lack prophylactic treatment options. As a result, serious bleeding episodes are treated acutely with blood product transfusions or frequent, repeated intravenous administration of recombinant activated coagulation factor VII (rFVIIa). Here we describe HMB-001, a bispecific antibody designed to bind and accumulate endogenous FVIIa and deliver it to sites of vascular injury by targeting it to the TREM (triggering receptor expressed on myeloid cells)-like transcript-1 (TLT-1) receptor that is selectively expressed on activated platelets. In healthy nonhuman primates, HMB-001 prolonged the half-life of endogenous FVIIa, resulting in its accumulation. Mouse bleeding studies confirmed antibody-mediated potentiation of FVIIa hemostatic activity by TLT-1 targeting. In ex vivo models of GT, HMB-001 localized FVIIa on activated platelets and potentiated fibrin-dependent platelet aggregation. Taken together, these results indicate that HMB-001 has the potential to offer subcutaneous prophylactic treatment to prevent bleeds in people with GT and other inherited bleeding disorders, with a low-frequency dosing regimen.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.