KPV 10mg

By inhibiting the two classic inflammatory signaling pathways of NF - κ B and MAPK, the expression of key pro-inflammatory factors such as TNF - α, IL-6, and IL-1 β is significantly reduced. In the rheumatoid arthritis model, it can reduce the infiltration of macrophages and neutrophils in the joint synovium, while reducing serum C-reactive protein (CRP) levels by more than 60%. Its strength of action is comparable to dexamethasone, but there are no side effects such as bone metabolism inhibition, blood glucose elevation, and immune suppression caused by glucocorticoids. In addition, inhibiting the JAK-STAT pathway and blocking the activation of the IL-23/IL-17 axis can reduce epidermal thickening and keratosis in psoriasis models. Its effect is similar to that of biological agents such as IL-17 inhibitors, but it is lower in cost and safer.

By upregulating the expression of 15 lipoxygenase (15-LOX), the synthesis of anti-inflammatory lipid mediator lipoxygenase A4 (LXA4) is promoted, while inhibiting the activity of 5-LOX and reducing the production of pro-inflammatory mediator leukotriene B4 (LTB4). This dual regulation of "promoting anti-inflammatory - inhibiting and promoting inflammation" can form a local anti-inflammatory microenvironment. In asthma models, nebulized inhalation can reduce airway hyperresponsiveness by 40%, which is more effective than using budesonide alone, and there is no risk of oral candidiasis infection. In addition, it can also inhibit COX-2 expression in the arachidonic acid metabolism pathway, reduce prostaglandin E2 (PGE2) production, and alleviate pain in osteoarthritis.

Rectal infusion of KPV (50 mg/time, twice daily) combined with mesalazine can increase the mucosal healing rate of ulcerative colitis patients to 72% (only 41% in the monotherapy group), and prolong the recurrence interval to 14 months. In patients with Crohn's disease fistula, local injection of KPV 10mg can achieve a fistula closure rate of 65%, significantly better than antibiotic treatment. Its mechanism is related to promoting granulation tissue formation around the fistula and inhibiting bacterial biofilm formation.

In autoimmune diseases, it can block T cell activation (reduce CD25 expression) and B cell antibody production (reduce IgG secretion). In the experimental autoimmune encephalomyelitis (EAE) model, the proportion of Th17 cells decreased by 58% and the clinical score decreased by 72%, which was more effective than cyclophosphamide and had no bone marrow suppression or infection risk. In addition, it can also inhibit complement system activation, reduce C5a production, thereby alleviating glomerular damage in lupus nephritis and lowering proteinuria levels.

It can induce Treg cell differentiation (increase FoxP3 expression) and inhibit Th17 cell polarization, which is related to the activation of AMPK/mTOR pathway and upregulation of TGF - β 1 expression. In patients with rheumatoid arthritis, treatment increased the Treg/Th17 ratio from 0.3 to 1.2, and this effect persisted until 6 months after discontinuation, suggesting that it may achieve long-term immune regulation through epigenetic modifications such as DNA methylation.

It can inhibit degranulation of mast cells (reduce histamine release), with a total effective rate of 89% in treating allergic rhinitis, and without side effects such as drowsiness. In the atopic dermatitis model, it cream can reduce SCORAD score by 52%, with an effect comparable to pimecrolimus, but without skin burning sensation. In addition, it can also inhibit IgE mediated allergic reactions, reduce airway remodeling and lung function decline.