Hemab shares clinical data on HMB-002, unveils HMB-003 program
Hemab Therapeutics (Nasdaq: COAG) presented clinical data from its HMB-002 program in Von Willebrand disease (VWD) and announced a new drug candidate, HMB-003, at the International Society on Thrombosis and Haemostasis (ISTH) 2026 Congress in Paris, France.
HMB-002, a monovalent human antibody administered subcutaneously, is designed to elevate the body's endogenous levels of Von Willebrand Factor (VWF) and Factor VIII (FVIII) rather than infusing exogenous factor. In its highest tested dose cohort of 150 mg, the drug produced at least a 2.4-fold increase in both VWF and FVIII, along with normalization of thrombin generation and activated partial thromboplastin time. The pharmacokinetic profile observed is said to support potential monthly dosing.
In the single ascending dose portion of the study, which was not designed to measure efficacy, 8 of 9 evaluable patients reported zero treated bleeds in the 28 days following dosing. The baseline mean annualized treated bleed rate before treatment was 20.1, compared to a mean of 1.6 following dosing. Most treatment-emergent adverse events were mild to moderate, with no serious adverse events, no thromboembolic events, no injection site reactions, and no study discontinuations reported.
Hemab also introduced HMB-003, a subcutaneously administered fatty-acid-conjugated peptide that directly inhibits plasmin. The company said preclinical data show potent antifibrinolytic activity across both tPA- and uPA-driven pathways, with no observed effect on thrombin generation, platelet function, or coagulation. In minipig studies, a single subcutaneous dose sustained antifibrinolytic activity for approximately one week. Hemab said HMB-003 is initially being developed for heavy menstrual bleeding, with potential applications in hereditary hemorrhagic telangiectasia and peri-operative bleeding management.
HMB-003 is currently in preclinical development. HMB-002 is in clinical-stage development, with trial information registered under NCT06610201 and NCT06754852.
