Osteoarthritis Pain Drug Discovery Service
Creative Biolabs is an experienced service provider in the field of life sciences. As neuroscience evolves, and the growing demand for drug research and development, we consolidate global resources and are committed to providing customized one-stop solutions to facilitate the progression of osteoarthritis pain from mechanism to clinical translational research.
Background of Osteoarthritis Pain
Osteoarthritis is a prevalent joint disorder. Chronic joint pain is the main clinical symptom, which tends to be frequent and worsen as the disease progresses. Currently, there are no effective therapeutics that can delay the progression of this chronic disease. The available medications for osteoarthritis pain are inadequate for pain treatment and poorly tolerated. For example, the most common non-steroidal anti-inflammatory drugs (NSAIDs) used in osteoarthritis pain are not sufficient for pain relief and have health risks in the gastrointestinal tract and thrombotic cardiovascular disease with long-term medication.
The severity and symptoms of the patients with osteoarthritis pain present significant heterogeneity. The pathogenesis of osteoarthritis pain is commonly considered to be driven by abnormal excitability in the pain pathways of both peripheral and central nervous systems as well as nociceptive and neuropathic mechanisms. Identifying the sources and mechanisms of osteoarthritis pain may facilitate targeted and rational treatment and help develop alternative therapies to help reduce pain symptoms and improve joint function. Creative Biolabs is dedicated to providing one-stop solutions to help researchers to develop novel non-opioid agents acting on the central nervous system along with purely peripherally acting antibody therapy against nerve growth factor (NGF) to modulate musculoskeletal pain.
Mechanism Studies of Osteoarthritis Pain
Osteoarthritis pain is generally caused by sensitization of the central nervous system and peripheral tissues around the joint. The nociceptor has an axonal stalk extending in the dorsal root ganglia (DRG) and separates into two terminals, which innervates peripheral tissues and extends to the dorsal horn of the spinal cord, respectively. Nociceptors are thus able to receive and send signals through both terminals. When the sensory receptors located on the peripheral terminal detect stimuli, they will be activated to trigger sodium and potassium channels. The action potentials are generated and propagated as pain signals along the nociceptor axons to the dorsal horn of the spinal cord. The signal is further transmitted by neurons to the brain. Creative Biolabs has established a pain research platform equipped with advanced technologies, such as patch clamp, calcium imaging, and fine glass electrode extracellular recordings, which is able to assist in the mechanism of action (MoA) studies of osteoarthritis pain.
Fig.1 Neuroanatomy of the pain pathway and analgesic targets in OA. (Malfait, 2013)
Osteoarthritis Pain Solutions at Creative Biolabs
Creative Biolabs provides one-stop solutions for osteoarthritis pain drug discovery, including services for the MoA studies and development of targeting agents. We offer a variety of neuron cultures, induced pluripotent stem cells (iPSCs), and spinal cord slices as well as exprimantal mice, rats, dogs, and monkeys. Our advanced electrophysiology tools with a wide range of in vitro, in vivo, and ex vivo assays allow researchers and developers to grasp the mystery of osteoarthritis pain MoA, and thus explore promising targeting therapeutics. More detailed information about our platform and services for translational research and integrated research in osteoarthritis pain is as follows.
If you have the intention to design your customized preclinical osteoarthritis pain solution program at Creative Biolabs, please don't hesitate to contact us for more information.
Reference
- Malfait, A. M.; Schnitzer, T. J. Towards a mechanism-based approach to pain management in osteoarthritis. Nature Reviews Rheumatology. 2013, 9(11), 654-664.
