Peer-reviewed veterinary case report
RNAi treatment helps blood clotting in dogs with acquired hemophilia
By Zhang, Yuyang et al.·Published in Gene therapy·2025·Institute of Hematology, China·View original on PubMed →
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Original publication title: RNAi targeting heparin cofactor II promotes hemostasis in a canine model of acquired hemophilia A.
- Species:
- dog
Plain-English summary
A group of Beagle dogs with acquired hemophilia A were observed for spontaneous bleeding and prolonged bleeding times. Researchers tested a new treatment called GalNAc-HCII, which showed promising results in improving blood clotting. After receiving the treatment, the dogs had significantly shorter times for blood clot formation and experienced less bleeding in their joints. This suggests that GalNAc-HCII could be a helpful new option for dogs suffering from hemophilia, especially those with specific inhibitors that complicate treatment.
People also search for: dog bleeding problems · hemophilia treatment for dogs · Beagle joint bleeding · GalNAc-HCII for dogs
Abstract
Heparin cofactor II (HCII) is a critical anticoagulant protein that inactivates thrombin. In our previous mouse studies, we demonstrated that GalNAc-HCII, a small interfering RNA (siRNA) targeting HCII conjugated with N-acetylgalactosamine (GalNAc), exhibited promising therapeutic effects in hemophilia A mouse models. Further evaluation in large animal models, especially with FVIII inhibitors, is essential before GalNAc-HCII can proceed to clinical trials. In this study, we successfully established, for the first time, an acquired hemophilia A canine model by multiple intravenous injections of a rabbit-dog chimeric neutralizing anti-canine FVIII antibody. In the control group, the Beagle dogs exhibited spontaneous bleeding symptoms accompanied by prolonged activated partial thromboplastin time (APTT). After administration, GalNAc-HCII (0.8 and 1.6 mg/kg) demonstrated potent, dose-dependent, and durable HCII inhibitory effects. After 5 days, in normal dogs, GalNAc-HCII reduced HCII levels to 32.67% ± 3.07% and 10.62% ± 1.74% with 0.8 and 1.6 mg/kg GalNAc-HCII, respectively. In hemophilic dogs, GalNAc-HCII treatment significantly improved hemostatic function. Specifically, in the carotid artery thrombosis model, the thrombus formation time was shortened [29.7 ± 2.08 min (0.8 mg/kg) and 18.0 ± 1.0 min (1.6 mg/kg) vs. 40 min (control), P < 0.01]; in the knee joint puncture-induced bleeding model, joint bleeding and synovitis were alleviated; and in the saphenous vein bleeding model, the number of hemostatic events increased. Furthermore, repeated administration of GalNAc-HCII effectively reduced the prolonged APTT. This study demonstrates the efficacy of GalNAc-HCII in hemophilic dogs, suggesting it as a promising novel therapeutic option for patients with hemophilia, including those with FVIII inhibitors.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/40413293/