Analgesic effects of nerve growth factor‐directed monoclonal antibody on diabetic neuralgia in an animal model. Issue 7 (3rd May 2022)

• Record Type: Journal Article
• Authors: Dong, Xingchen; Li, Huanhuan; Pei, Min; Tan, Jie; Chen, Ganjun; Li, Santai; Xie, Zuobin; Wang, Qi; Wang, Guifeng; Chen, Yi‐Li; Wang, Chunhe
• Is Part Of: FEBS open bio. Volume 12:Issue 7(2022)
• Page Start: 1325
• Page End: 1335
• Publication Date: 2022-05-03
• Subjects: diabetic neuralgia -- neuropathic pain -- nerve growth factor -- monoclonal antibody -- analgesia; Molecular biology -- Periodicals; Cytology -- Periodicals; Life sciences -- Periodicals; Biological Science Disciplines -- Periodicals; Molecular Biology -- Periodicals; Cell Biology -- Periodicals; Cytology; Life sciences; Molecular biology; Periodicals; 572.805
• DOI: 10.1002/2211-5463.13410
• Languages: English
• ISSNs: 2211-5463

Abstract

Abstract : Current treatment options for diabetic neuralgia are limited and unsatisfactory. Tanezumab, a monoclonal antibody that blocks nerve growth factor (NGF) signaling, has been shown to be effective in relieving the clinical symptoms of osteoarthritis pain, chronic low back pain, cancer pain induced by bone metastasis, and diabetic neuralgia. However, the clinical development of tanezumab has been terminated due to the risk of induction of rapidly progressive osteoarthritis (RPOA), and no other NGF antibodies have been examined for their ability to treat diabetic neuralgia in either animal models or clinical trials. In this study, a humanized high‐affinity NGF monoclonal antibody (mAb), huAb45 that could neutralize the interaction between NGF and its high‐affinity receptor TrkA. In a mouse diabetic neuralgia model, it effectively relieved neuropathic pain. This study may serve as the necessary foundation for future studies of huAb45 to potentially treat diabetic neuralgia. Abstract : NGF‐directed monoclonal antibody blocks the binding of NGF to its receptor, TrkA. Subsequently this blocks downstream signaling that interrupts diabetic neuralgia signaling.