Rheumatoid arthritis extends beyond merely aching joints. It is a chronic autoimmune disorder characterized by ongoing inflammation that can lead to swelling, pain, and gradual joint deterioration. While current medications can manage the condition, patient responses differ, highlighting the ongoing need for innovative methods to disrupt the biological mechanisms maintaining inflammation. A patent from Macau University of Science and Technology and Enoch Technology (Hong Kong) Limited identifies NAV2 (Neuron Navigator 2) as a potential target for rheumatoid arthritis therapy and suggests using an endogenous hydrogen sulfide donor, SPRC (S-propargyl-cysteine), to inhibit this pathway. The research shows that NAV2 levels are abnormally high in blood samples from rheumatoid arthritis patients and in fibroblast-like synovial cells from affected joints. The findings indicate that elevated NAV2 can activate the Wnt/β-catenin signaling pathway, promoting inflammatory responses as well as the proliferation, migration, and invasion of synovial cells, events that may contribute to disease progression. The patented strategy aims to interfere with this process using SPRC. In a rat arthritis model, SPRC reduced NAV2 expression and lowered levels of inflammatory proteins such as IL-6, ICAM-1, and MMP9, while also alleviating joint swelling and pain related to inflammation. The beneficial effects increased with higher doses of SPRC. By linking hydrogen sulfide signaling, NAV2, and Wnt/β-catenin activity, the patent proposes a novel approach for developing rheumatoid arthritis treatments: targeting a molecular pathway that may be responsible for driving inflammation, instead of merely addressing its symptoms.
A new target for tackling the inflammation behind rheumatoid arthritis
Patent number: CN 113181155 A
Inventor(s): Y. Zhu and R. Wang
Citation: Y. Zhu and R. Wang, “内源性硫化氢供体在制备治疗类风湿性关节炎药物中的用途 [Use of an endogenous hydrogen-sulfide donor in preparing a drug for rheumatoid arthritis],” China Patent CN 113181155 A, Jul. 30, 2021.
