Anticomplement Therapy
A substance that neutralizes the action of a complement by combining with it and preventing its union with an antibody.
Anticomplement therapy is used to treat health conditions where the complement system—a part of the immune system—becomes overactive or dysregulated, leading to tissue damage or disease. The complement system normally helps fight infections and clear damaged cells, but when it malfunctions, it can attack healthy tissues. Below are some key conditions where anticomplement therapy is either established or being explored:
- PNH is a rare blood disorder where the complement system destroys red blood cells due to a lack of protective proteins on their surface. Drugs like eculizumab and ravulizumab, which block the C5 protein in the complement cascade, are standard treatments to prevent hemolysis (red blood cell destruction).
- aHUS is a rare condition causing blood clots in small blood vessels, often due to uncontrolled complement activation. This can lead to kidney failure. Eculizumab is commonly used to inhibit complement activity and protect kidney function.
- C3G involves excessive complement protein C3 deposition in the kidneys, causing inflammation and damage to the glomeruli (kidney filters). Recently, therapies targeting the complement system, like the FDA-approved iptacopan (announced in March 2025), have been used to reduce proteinuria and slow disease progression.
- Glomerulonephritis (e.g., Membranoproliferative Glomerulonephritis - MPGN):
- Certain types of glomerulonephritis, especially those linked to complement dysregulation (like MPGN), can benefit from anticomplement therapy. These conditions involve kidney inflammation, and drugs targeting complement components (e.g., C5 or C3 inhibitors) are being studied or applied.
- In systemic lupus erythematosus (SLE), complement overactivation can contribute to kidney damage (lupus nephritis). While not yet standard, anticomplement therapies are under investigation to reduce inflammation and preserve kidney function.
- Myasthenia Gravis (Generalized):
- For patients with generalized myasthenia gravis (gMG) who have anti-acetylcholine receptor antibodies, complement activation damages the neuromuscular junction. Eculizumab is approved to reduce this damage and improve muscle strength.
- CAD is an autoimmune hemolytic anemia where complement activation destroys red blood cells in cold temperatures. Sutimlimab, a C1s inhibitor, is approved to block this process and reduce the need for transfusions.
- Ischemia-Reperfusion Injury (e.g., in Myocardial Infarction or Transplant):
- During events like heart attacks or organ transplants, restoring blood flow can trigger complement-mediated damage. Anticomplement therapies have been tested in trials to limit this injury, though they’re not yet standard care.
- Other Emerging Uses:
- Conditions like sepsis, antibody-mediated rejection in kidney transplants, and certain neurodegenerative diseases (e.g., where complement affects the brain) are being studied for potential anticomplement therapy. These are still experimental but show promise based on complement’s role in inflammation.
These therapies work by targeting specific parts of the complement cascade (e.g., C5, C3, or C1) to stop the destructive immune response. The choice of therapy depends on the condition and how complement is involved—whether it’s overactivation, genetic mutations, or autoantibody-driven damage. Research is ongoing, so this list may grow as new evidence emerges. Always consult a healthcare provider for individual cases, as these treatments are specialized and often tailored.
Herbs
Meadowsweet: One study showed F. ulmaria extracts inhibit complement activation and T-cell proliferation, and interfere with ROS or ROS production by PMNs in vitro which may explain the effective use of F. ulmaria preparations in inflammatory diseases. Strong anticomplementary activities of root, herb, and flower extracts of F. ulmaria were found towards the classical pathway of the complement system. The EA extracts of the roots and flowers, all MeOH extracts, and the AQ extract of the roots were found to be most effective (IC50<15 mg/mL).
Olive Leaf Extract: Oleuropein is converted into elenoic acid in the body which may prevent viruses and bacteria from replicating . The antihypertensive and vasodilating effects of olive leaf occurred independently of the integrity of the vascular endothelium . Constituents of olive leaf have been shown to strongly inhibit the complement system, although it is unknown what effect this has on the body.
Rough Osbeckia ; In vitro studies on the immunomodulatory effects of extracts of Osbeckia aspera The extract has been shown to have hepatoprotective effects in vitro and in vivo, and to have inhibitory effects on the complement system and on in vitro phagocytosis by polymorphonuclear cells.
Anticomplement and Antimicrobial Activities of Flavonoids from Entada phaseoloides
Anticomplement activity of terpenoids from the spores of Ganoderma lucidum
Steroids from herbs of Reineckia carnea and their anticomplement activities
Plant Mucilages : An Anti-complementary Mucilage from the Leaves of Malva sylvestris var. mauritiana
Anticomplementary principles of a Chinese multiherb remedy for the treatment and prevention of SARS contains five ingredients of Herba Houttuyniae, Flos Chrysanthemi Indici, Herba Artemisiae Scopariae, Herba Eupatorii and Fructus Tsaoko.