Analysis of whether tofacitinib (Shangjie) is an analgesic and why it can improve pain symptoms

Tofacitinib is not an analgesic in the traditional sense. It is an oral small moleculeJanuskinase (JAK) inhibitors are mainly used to treat autoimmune diseases, such as rheumatoid arthritis (RA), psoriatic arthritis and ulcerative colitis. Pain improvement is an important manifestation of its clinical efficacy, but this is not through direct analgesic mechanisms, but indirect pain relief through the regulation of immune-inflammatory pathways. Patients often report significant relief from joint pain, swelling, and morning stiffness after taking tofacitinib, which is a combination of its disease-modifying effects and symptom improvement.

The mechanism of action of tofacitinib is to selectively inhibit the activities of JAK1 and JAK3 and block JAK-STAT signaling pathway, thereby interfering with the signaling of pro-inflammatory cytokines (such as IL-6, IL-2, IFN-γ, etc.). This type of cytokine plays a central role in the inflammatory response and can activate the joint synovium and promote the release of inflammatory mediators, leading to tissue damage and pain. By inhibiting the JAK-STAT pathway, tofacitinib reduces inflammatory cell activity and inflammatory factor levels, fundamentally reducing joint inflammation and peripheral nerve ending stimulation, thereby improving patients' pain symptoms.

Clinical studies show that tofacitinib can quickly relieve pain in patients with rheumatoid arthritis. In multiple phase III randomized controlled trials, patients using tofacitinib reported significant decreases in pain scores, usually within 2 to 4 weeks, along with improvements in joint swelling and morning stiffness. This pain-relieving effect reflects both the drug's anti-inflammatory effects and its ability to control disease activity. Compared with nonsteroidal anti-inflammatory drugs (NSAIDs) or opioid analgesics, tofacitinib not only relieves pain, but also fundamentally delays the progression of the disease.

To sum up, tofacitinib is not a direct analgesic, and its pain improvement effect is due to its anti-inflammatory and immunomodulatory effects. By inhibiting the JAK-STAT pathway and reducing the levels of inflammatory mediators, it can significantly improve joint and tissue pain and have a long-term regulatory effect on disease activity. Therefore, the pain-relieving effect of tofacitinib in patients with autoimmune diseases is part of their disease-modifying treatment rather than a pure analgesic effect.

Reference materials:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7120274/