An Update on Targets for Treating Osteoarthritis Pain: NGF and TRPV1
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Osteoarthritis (T Appleton, Section Editor)
An Update on Targets for Treating Osteoarthritis Pain: NGF and TRPV1 Alia M. Obeidat, PhD Anita Donner, BS Rachel E. Miller, PhD* Address * Division of Rheumatology, Rush University Medical Center, 1735 W Harrison St, Room 714, Chicago, IL, 60612, USA Email: [email protected]
* Springer Nature Switzerland AG 2020
This article is part of the Topical Collection on Osteoarthritis Keywords Osteoarthritis I Pain I NGF I TrkA I Capsaicin I TRPV1
Abstract Purpose of review Osteoarthritis (OA) is the most common form of arthritis, and pain is the primary symptom of the disease, yet analgesic options for treating OA pain remain limited. In this review, we aimed to give an update on the current clinical and preclinical studies targeting two pathways that are being investigated for treating OA pain: the nerve growth factor (NGF) pathway and the transient receptor potential vanilloid-1 (TRPV1) pathway. Recent findings Antibodies against NGF, small molecule inhibitors of TrkA, TRPV1 agonists, and TRPV1 antagonists are all in different stages of clinical and pre-clinical testing for the treatment of OA pain. NGF antibodies have shown efficacy in the primary endpoints tested compared with placebo; however, rapidly progressive OA has been consistently observed in a subset of patients and the cause remains unclear. TRPV1 agonists have also demonstrated reduced pain with no serious adverse events—the most common adverse events include a burning or warming sensation upon administration. Summary Targeting the NGF and TRPV1 pathways appears effective for reducing OA pain, but further work is needed to better understand which patients may benefit most from these treatments. The anti-NGF antibody tanezumab and the TRPV1 agonist CNTX-4975 have both received fast-track designation from the FDA for the treatment of OA pain.
Osteoarthritis (T Appleton, Section Editor)
Introduction Osteoarthritis (OA) is the most common form of arthritis, affecting an estimated 303 million people globally in 2017 [1], and pain is the predominant symptom associated with this disease. OA is a degenerative disease of the synovial joints including the knee, hip, facet joints of the spine, and hand. Risk factors for OA include aging, prior joint injury, obesity, female sex, and genetics [2]. These risk factors are related to the underlying pathogenesis of OA, which is a complex process impacted by altered biomechanics, chronic low-level inflammation, and aging. All of these processes can promote degradation and remodeling of the joint tissues, which ultimately results in failure of the structural integrity of the joint. OA is a slowly developing, chronic disease with no known cure or strategies for reducing or stopping the progression of joint damage [3]. Management of symptoms is also limited—NSAIDs are one of the few strongly recommended pharmacological therapies for OA [4], yet the efficacy of oral NSAIDs declines with time and these drugs are associated with adverse gastrointestinal and cardiac effects th
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