Biological response modifiers
Biological response modifiers (BRMs) are substances that modify immune responses. They can be both endogenous (produced naturally within the body) and exogenous (as pharmaceutical drugs), and they can either enhance an immune response or suppress it. Some of these substances arouse the body's response to an infection, and others can keep the response from becoming excessive. Thus they serve as immunomodulators in immunotherapy (therapy that makes use of immune responses), which can be helpful in treating cancer (where targeted therapy often relies on the immune system being used to attack cancer cells) and in treating autoimmune diseases (in which the immune system attacks the self), such as some kinds of arthritis and dermatitis. Most BRMs are biopharmaceuticals (biologics), including monoclonal antibodies, interleukin 2, interferons, and various types of colony-stimulating factors (e.g., CSF, GM-CSF, G-CSF). "Immunotherapy makes use of BRMs to enhance the activity of the immune system to increase the body's natural defense mechanisms against cancer", whereas BRMs for rheumatoid arthritis aim to reduce inflammation.
Mechanism of action: A monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Clinical use: Acute coronary syndromes, percutaneous transluminal coronary angioplasty. Toxicity: Bleeding, thrombocytopenia.
Mechanism of action: A monoclonal antibody to TNF, proinflammatory cytokine. Clinical use: Crohn's disease, rheumatoid arthritis, ankylosing spondylitis. Toxicity: Respiratory infection, fever, hypotension. Predisposes to infections (reactivation of latent TB).
Mechanism of action: A monoclonal antibody to CD20 surface immunoglobulin. Clinical use: Lymphoma and a variety of autoimmune diseases, although it may be ineffective in treating IgA-mediated diseases.
Mechanism of action: A monoclonal antibody against HER2/neu (erb-B2). Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity. Clinical use: Metastatic breast cancer. Toxicity: Cardiotoxicity.
High dose intravenous ascorbate
- "Biological Response Modifiers (BRM)".
- He Y, Shimoda M, Ono Y, Villalobos IB, Mitra A, Konia T, Grando SA, Zone JJ, Maverakis E (2015). "Persistence of Autoreactive IgA-Secreting B Cells Despite Multiple Immunosuppressive Medications Including Rituximab". JAMA Dermatol 151 (6): 646–50. doi:10.1001/jamadermatol.2015.59. PMID 25901938.
- Tzianabos AO (2000). "Polysaccharide immunomodulators as therapeutic agents: structural aspects and biologic function.". Clin Microbiol Rev 13 (4): 523–33. doi:10.1128/CMR.13.4.523-533.2000. PMC 88946. PMID 11023954.
- "The Riordan IVC Protocol for Adjunctive Cancer Care: Intravenous Ascorbate as a Chemotherapeutic and Biological Response Modifying Agent" (PDF). Riordan Clinic Research Institut. February 2013. Retrieved 2 February 2014.
- "High-Dose Vitamin C (PDQ®): Human/Clinical Studies". National Cancer Institute. Retrieved 2 February 2014.