Polycythemia Vera (PV)
Polycythemia vera (PV) is a rare myeloproliferative neoplasm. With our pioneering efforts in polycythemia vera research, we are at the forefront of developing cutting-edge diagnostic tools and therapeutics to facilitate the effective management of polycythemia vera. As your reliable partner in polycythemia vera research, we offer unmatched support to fulfill your scientific research needs.
Overview of Polycythemia Vera
Polycythemia vera is a rare, chronic blood disorder characterized by an abnormal overproduction of red blood cells in the bone marrow. Too many red blood cells can cause the blood to thicken, increasing the risk of complications such as blood clots, heart disease, and stroke. Polycythemia vera progresses slowly and is more common in older people. The prevalence of polycythemia vera is estimated to be around 0.6-1.6 cases per million individuals.
Fig. 1 JAK2 signaling. (Ginzburg, Yelena Z., et al., 2018)Pathogenesis of Polycythemia Vera
The pathogenesis of polycythemia vera revolves around the dysregulation of signaling pathways involved in blood cell production. The causes include the following processes.
JAK2 Mutation
Janus kinase 2 (JAK2) mutations occur in approximately 95% of polycythemia vera cases. This results in sustained activation of JAK-STAT signaling.
Abnormal Proliferation
This abnormal signaling drives the expansion of hematopoietic stem cells and their progenitor cells, leading to the overproduction of red blood cells.
Disease Occurrence
The abnormal increase in red blood cells causes the blood to thicken, causing a series of health problems related to polycythemia vera disease.
Strategies of Polycythemia Vera Therapy Development
Inhibit JAK2 Pathway
The JAK2 pathway is a primary focus for polycythemia vera therapy development. The JAK2 gene mutation, specifically the JAK2V617F mutation, is present in the majority of polycythemia vera individuals. Ruxolitinib, a JAK1/2 inhibitor, effectively normalizes blood counts, alleviates symptoms, and reduces spleen size in individuals with polycythemia vera.
Inhibit Erythropoietin (EPO)
EPO is a hormone that regulates red blood cell production. Inhibiting the action of EPO can help red blood cell levels return to normal. For example, erythropoietin receptor (EPOR) antagonists are effective in reducing red blood cell production and improving disease symptoms.
Our Services
Our company leads the way in rare disease research and therapeutic development. Our experienced team of scientists and researchers is committed to unraveling the intricacies of polycythemia vera and other rare diseases through the creation of advanced research platforms.
Research Platforms of Polycythemia Vera
Utilizing cutting-edge technology, our goal is to strategize and develop diagnostics for polycythemia vera to promote early identification and accurate diagnosis of the disease. With the establishment of polycythemia vera animal models and comprehensive investigations into disease mechanisms and targets, we possess the capacity to develop therapeutic drugs for polycythemia vera, thereby facilitating safety evaluation and pharmacokinetic studies of drug candidates.
Animal Models of Polycythemia Vera
| Genetically Engineered Models | ||
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| Our company excels in utilizing cutting-edge gene manipulation technologies, including CRISPR/Cas9, to introduce the JAK2 V617F mutation into animal models. With this method, our researchers successfully replicated the overproduction of red blood cells observed in human polycythemia vera individuals in an animal model, which provides a powerful tool for the study of polycythemia vera mechanisms and therapies. | ||
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| Optional Species | Mice, Rats, Zebrafish, Non-human Primates (Baboons and Macaques), Others | |
If you are interested in our services, please don't hesitate to contact us for more information and a detailed quotation regarding the specific services you require.
References
- Ginzburg, Yelena Z., et al. "Dysregulated iron metabolism in polycythemia vera: etiology and consequences." Leukemia 32.10 (2018): 2105-2116.
- Parsons, Tyler M., et al. "Engineering a humanized animal model of polycythemia vera with minimal JAK2V617F mutant allelic burden." Haematologica 109.3 (2024): 968.
All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.