Infliximab?
|
| Monoclonal antibody |
| Type |
Whole antibody |
| Source |
Chimeric (mouse/human) |
| Target |
TNF |
| Clinical data |
| Trade names |
Remicade, Remsima, Inflectra |
| AHFS/Drugs.com |
monograph |
Pregnancy
category |
- AU: C
- US: B (No risk in non-human studies)
|
| Legal status |
- AU: Prescription Only (S4)
- CA: ℞-only
- UK: Prescription-only (POM)
- US: ℞-only
|
Routes of
administration |
IV |
| Pharmacokinetic data |
| Bioavailability |
92% (IV, if 8% left in the syringe) |
| Metabolism |
reticuloendothelial system |
| Biological half-life |
9.5 days |
| Identifiers |
| CAS Registry Number |
170277-31-3 Y |
| ATC code |
L04AB02 |
| DrugBank |
DB00065 Y |
| UNII |
B72HH48FLU Y |
| KEGG |
D02598 Y |
| ChEMBL |
CHEMBL1201581 N |
| Chemical data |
| Formula |
C6428H9912N1694O1987S46 |
| Molecular mass |
144190.3 g/mol |
| N (what is this?) (verify) |
Infliximab (INN; trade names Remicade, Remsima, Inflectra) is a chimeric monoclonal antibody against tumour necrosis factor alpha (TNF-α) used to treat autoimmune diseases.
Infliximab was approved by the U.S. Food and Drug Administration (FDA) for the treatment of psoriasis, Crohn's disease, ankylosing spondylitis, psoriatic arthritis, rheumatoid arthritis, and ulcerative colitis. Infliximab won its initial approval by the FDA for the treatment of Crohn's disease in August 1998.[1]
Infliximab works by binding to TNF-α. TNF-α is a chemical messenger (cytokine) and a key part of the autoimmune reaction. The role of TNF as a key player in the development of rheumatoid arthritis was originally demonstrated by Kollias and colleagues in proof of principle studies in transgenic animal models.[2][3] In rheumatoid arthritis, infliximab seems to work by preventing TNF-α from binding to its receptor in the cell.
Infliximab is an artificial antibody. It was originally developed in mice as a mouse antibody. Because humans have immune reactions to mouse proteins, the mouse common domains were replaced with similar human antibody domains. They are monoclonal antibodies and have identical structures and affinities to the target. Because they are a combination of mouse and human antibody amino acid sequences, they are called a "chimeric monoclonal antibody".
Infliximab was developed by Junming Le and Jan Vilcek at New York University School of Medicine and developed by Centocor, (now Janssen Biotech, Inc.)[4]
Remicade is marketed by Janssen Biotech, Inc. (formerly Centocor Biotech, Inc.) in the USA, Mitsubishi Tanabe Pharma in Japan, Xian Janssen in China, and Schering-Plough (now part of Merck & Co) elsewhere.[5] In 2013, two biosimilars were submitted for approval in Europe, by Hospira and Celltrion Healthcare.[6] European Medicines Agency’s (EMA) Committee for Medicinal Products for Human Use (CHMP) had given positive opinion[7] for Celltrion-developed Remsima for sale in the European Union (EU). Celltrion obtained marketing authorization approval (MAA) from 27 EU countries and 3 EEA (European Economic Area) countries.[8] The company has received marketing authorization for Remsima from the Japan's Ministry of Health, Labour and Welfare (MHLW) in July 2014. In India, Epirus Biopharmaceuticals has obtained approval to produce infliximab under the brand name "Infimab" (trail name BOW015).[9]
In the United States, Infliximab can cost $19,000 to $22,000 a year per patient wholesale, according to Centocor.[10]
Other monoclonal antibodies targeting TNF-α are golimumab (Simponi), adalimumab (Humira), and certolizumab pegol (Cimzia). Etanercept also binds and inhibits the action of TNF-α, but is not a monoclonal antibody (it is instead a fusion of TNF-receptor and an antibody constant region).[11]
Infliximab is administered by intravenous infusion, typically at six- to eight-week intervals, at a clinic or hospital. It cannot be administered orally because the digestive system would destroy the drug.[12]
Contents
- 1 Medical uses
- 1.1 Crohn's disease
- 1.1.1 Fistulizing disease
- 1.1.2 Inflammatory disease
- 1.2 Ulcerative colitis
- 1.3 Other
- 2 Adverse effects
- 3 Pharmacology
- 4 Availability/affordability
- 5 See also
- 6 References
- 7 External links
Medical uses
Crohn's disease
Three phenotypes, or categories of disease, are present in Crohn's disease: stricturing disease (which causes narrowing of the bowel), penetrating disease (which causes fistulae or abnormal connections of the bowel), and inflammatory disease (which causes primarily inflammation).[13]
Fistulizing disease
Infliximab was first used for closure of fistulae in Crohn's disease in 1999. In a 94-patient, phase II clinical trial, the researchers showed Infliximab was effective in closing fistulae between the skin and bowel in 56-68% of patients.[14] A large, 296-patient, Phase III clinical trial called the ACCENT 2 trial, showed infliximab was additionally beneficial in maintaining closure of fistulae, with almost two-thirds of all patients treated with the three initial doses of infliximab having a fistula response after 14 weeks, and 36% of patients maintaining closure of fistulae after a year, compared with 19% who received placebo therapy. This final trial resulted in the FDA approval of the drug to treat fistulizing disease.[15]
Inflammatory disease
Inflammatory Crohn's disease, seen here as ulcers on colonoscopy, can be treated with infliximab
Infliximab has been used to induce and maintain remission in inflammatory Crohn's disease. The ACCENT 1 trial, a large, multicentre trial, found 39 to 45% of patients treated with infliximab, who had an initial response to it, maintained remission after 30 weeks, compared with 21% who received placebo treatment. It also showed a mean maintenance of remission from 38 to 54 weeks compared with 21 weeks for patients who received placebo treatment.[16]
Crohn's patients have flares of their disease between periods of disease quiescence. Severe flares are usually treated with steroid medications to obtain remission, but steroids have many undesirable side effects, so some gastroenterologists are now advocating the use of infliximab as the first drug to try to get patients into remission. This has been called the top-down approach to treatment.[17]
Ulcerative colitis
Infliximab targets TNF, thought to be more related to Th1 cytokines. Ulcerative colitis was thought to be a Th2 disease, and infliximab would be of limited use. However, patients with ulcerative colitis have begun to be treated with infliximab on the basis of two large clinical trials conducted in 2005 by Paul Rutgeerts and William Sandborn. The Acute ulcerative Colitis Treatment trials (ACT1 and ACT2) to evaluate the utility of infliximab in ulcerative colitis showed 44-45% of patients treated with infliximab for a year maintained a response to the medication, compared with 21% of patients who were treated with placebo medication. At two months, the response was 61-69% for patients treated with infliximab, and 31% for those treated with placebo.[18]
Other
Infliximab has been tested in COPD but there was no evidence of benefit with the possibility of harm.[19]
It was approved for treating ankylosing spondylitis, psoriatic arthritis, psoriasis, rheumatoid arthritis. Infliximab is also prescribed (out of indication) for the treatment of Behçet's disease.[20]
Infliximab is the most frequently used biological agent in treating relapsing polychondritis.[21] Half of the patients saw benefit from this treatment, and a few other patients experienced infections that in some cases lead to death.[21][22]
There have been numerous case reports of the efficacy of infliximab in various inflammatory skin conditions diseases; the FDA approved infliximab for chronic severe plaque psoriasis in adults in September 2006.[23]
In psoriatic arthritis, inhibitors of TNF, such as infliximab, improve the signs and symptoms. Several therapies with modest efficacy have been studied in nail psoriasis. Among available agents, higher quality data are available to support the efficacy of cyclosporine and infliximab. Based on studies in AS, the results suggest infliximab, etanercept, and adalimumab have the potential to reduce the signs and symptoms of moderate to severely active axial involvement in PsA in patients who have had an inadequate response to NSAID (level 1a, grade A). The anti-TNF agents (infliximab and etanercept; level 1b, grade A) are more effective for the treatment of enthesitis than traditional agents. Results suggest infliximab is effective for the treatment of dactylitis in PsA.[24]
Adverse effects
|
|
This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2009) |
Infliximab has adverse effects, some life-threatening, common to drugs in the class of immunosuppressants (which also includes etanercept (Enbrel) and adalimumab (Humira)). Some of the most severe are:
- serious infections
- reactivation of hepatitis B
- reactivation of tuberculosis[25]
- lethal hepatosplenic T-cell lymphoma (generally only when combined with 6-mercaptopurine)
- drug-induced lupus
- demyelinating central nervous system disorders
- psoriasis and psoriasiform skin lesions
- new-onset vitiligo
Cases of leukopenia, neutropenia, thrombocytopenia, and pancytopenia (some fatal) have been reported with infliximab.[26] The FDA issued a warning to doctors appearing in the respective product labeling of infliximab instructing them to screen and monitor potential patients more carefully.[27] The FDA issued a warning to doctors that there is an increased risk of lymphoma and other cancers associated with the use of infliximab and other tumor necrosis factor blockers in children and adolescents.[28]
Maintenance therapy with the drug (versus intermittent or sporadic therapy) lessens the likelihood of developing antibodies to infliximab which are known to reduce the efficacy of the drug. Combination treatment with methotrexate (an antifolate drug which suppresses the immune system) has been shown to reduce the formation of these antibodies in patients with rheumatoid arthritis[29] and combination therapy with other immunosuppressants has been shown to reduce the likelihood of these antibodies being formed in Crohn's disease.[16] The use of immunosuppressants may not be necessary in all diseases for which infliximab is indicated, and indiscriminant uses of these other immunosuppressants carry their own risks. Infliximab was studied in monotherapy (without concomitant immunosuppressants such as methotrexate or azathioprine) in psoriasis, psoriatic arthritis, and ankylosing spondylitis. Only its use in rheumatoid arthritis requires the concomitant use of methotrexate by FDA product labeling; however, the concomitant use of methotrexate in other disease states may help to reduce the body's immune response to the infliximab and increase its duration of efficacy.
Pharmacology
Infliximab neutralizes the biological activity of TNF-α by binding with high affinity to the soluble (free floating in the blood) and transmembrane (located on the outer membranes of T cells and similar immune cells) forms of TNF-α, and inhibits or prevents the effective binding of TNF-α with its receptors. Infliximab and adalimumab (another TNF antagonist) are in the subclass of "anti-TNF antibodies" (they are in the form of naturally occurring antibodies), and are capable of neutralizing all forms (extracellular-, transmembrane-, and receptor-bound) TNF-α.[30] Etanercept, a third TNF antagonist, is in a different subclass (receptor-construct fusion protein), and, because of its modified form, cannot neutralize receptor-bound TNF-α.[31] Additionally, the anti-TNF antibodies adalimumab and infliximab have the capability of lysing cells involved in the inflammatory process, whereas the receptor fusion protein apparently lacks this capability.[32] Although the clinical significance of these differences have not been absolutely proven, etanercept, has been shown to perform worse than placebo for Crohn's disease. These differences may account for the differential actions of these drugs in both efficacy and side effects.
Infliximab has high specificity for TNF-α, and does not neutralize TNF beta (TNFβ, also called lymphotoxin α), an unrelated cytokine that uses different receptors from TNF-α. Biological activities attributed to TNF-α include induction of proinflammatory cytokines (such as interleukins IL-1 and IL-6), enhancement of leukocyte movement or migration from the blood vessels into the tissues (by increasing the permeability of endothelial layer of blood vessels), and increasing the release of adhesion molecules. Infliximab prevents disease in transgenic mice (a special type of mice biologically engineered to produce a human form of TNF-α and which are used to test the results of these drugs that might be expected in humans). These experimental mice develop arthritis as a result of their production of human TNF-α, and when administered after disease onset, infliximab allows eroded joints to heal.
Availability/affordability
Like all of the TNF inhibitors, infliximab is an expensive medication, costing about US$900 for a 100 mg dose, and within the United States is covered by almost every medical insurance plan (though caps on many plans make it possible to be covered for only a subset of treatments in the course of a year).[citation needed] Infliximab is supplied as a sterile, white, lyophilized (freeze-dried) powder,[33] so must be reconstituted and administered by a health care professional, usually in a hospital or office setting.[5] For this reason, it is usually covered under major medical insurance rather than prescription drug coverage. The loading regimen for all approved indications occurs at weeks 0, 2, and 6 at the above dosages.[5]
Infliximab is available from the NHS in the UK for Crohn's disease treatment provided three criteria are met.[34] Patients should have severe active Crohn's disease with a CDAI score of 300 or more, have not responded to immunomodulating drugs and corticosteroids, and for whom surgery is inappropriate. Since February 2015 it is also approved for the treatment of ulcerative colitis where other treatments have not worked.[35]
Infliximab is available through the PBS in Australia for Crohn's disease treatment provided the patient has not responded to conventional treatment and is suffering from a severe case of the condition.[36]
Infliximab is available in the Republic of Ireland through the HSE's Medical Card and Drug Payment Scheme.
Johnson & Johnson reported in its 2013 annual report, "REMICADE® (infliximab), accounted for approximately 9.4% of the Company's total revenues for fiscal 2013." [37]
See also
- Biological therapy for inflammatory bowel disease
References
- ^ "Infliximab Product Approval Information - Licensing Action". Drugs@FDA. U.S. Food and Drug Administration (FDA). Retrieved 2009-11-14.
- ^ Keffer J, Probert L, Cazlaris H, Georgopoulos S, Kaslaris E, Kioussis D, Kollias G (December 1991). "Transgenic mice expressing human tumour necrosis factor: a predictive genetic model of arthritis". The EMBO Journal 10 (13): 4025–31. PMC 453150. PMID 1721867.
- ^ Brenner D, Blaser H, Mak TW (May 2015). "Regulation of tumour necrosis factor signalling: live or let die.". Nat Rev Immunol 15 (6): 362–74. PMID 26008591.
- ^ Knight DM, Trinh H, Le J, Siegel S, Shealy D, McDonough M, Scallon B, Moore MA, Vilcek J, Daddona P (November 1993). "Construction and initial characterization of a mouse-human chimeric anti-TNF antibody". Mol. Immunol. 30 (16): 1443–53. doi:10.1016/0161-5890(93)90106-L. PMID 8232330.
- ^ a b c "Remicade Becomes First Anti-TNF Biologic Therapy to Treat One Million Patients Worldwide" (Press release). Johnson & Johnson. November 6, 2007. Retrieved 2009-11-14.
- ^ George, John (June 28, 2013). "Billion-dollar biotech drug may soon have biosimilar competition". Philadelphia Business Journal. Retrieved June 27, 2013.
- ^ "European Medicines Agency recommends approval of first two monoclonal-antibody biosimilars", European Medicines Agency, June 28, 2013
- ^ "European Commission Approves Biosimilar of J&J and Merck's Remicade", Jonathan D. Rockoff, The Wall Street Journal, September 10, 2013
- ^ Serebrov, Mari. "Epirus racks up its first biosimilar approval in India". BioWorld. Retrieved 26 October 2014.
- ^ "Priced out of pain relief; Insurers balk at high costs of promising new treatments", Victoria Colliver, San Francisco Chronicle, May 8, 2007
- ^ Peppel K, Crawford D, Beutler B (1991). "A tumor necrosis factor (TNF) receptor-IgG heavy chain chimeric protein as a bivalent antagonist of TNF activity". J. Exp. Med. 174 (6): 1483–9. doi:10.1084/jem.174.6.1483. PMC 2119031. PMID 1660525.
- ^ Steinhilber, D; Schubert-Zsilavecz, M; Roth, HJ (2005). "Molekülstruktur und biologische Eigenschaften". Medizinische Chemie (in German) (1 ed.). Stuttgart: Deutscher Apothekerverlag. p. 5. ISBN 3-7692-3483-9.
- ^ Dubinsky MC, Fleshner PP (June 2003). "Treatment of Crohn's Disease of Inflammatory, Stenotic, and Fistulizing Phenotypes". Curr Treat Options Gastroenterol 6 (3): 183–200. doi:10.1007/s11938-003-0001-1. PMID 12744819.
- ^ Present DH, Rutgeerts P, Targan S, Hanauer SB, Mayer L, van Hogezand RA, Podolsky DK, Sands BE, Braakman T, DeWoody KL, Schaible TF, van Deventer SJ (May 1999). "Infliximab for the treatment of fistulas in patients with Crohn's disease". The New England Journal of Medicine 340 (18): 1398–405. doi:10.1056/NEJM199905063401804. PMID 10228190.
- ^ Sands BE, Anderson FH, Bernstein CN, Chey WY, Feagan BG, Fedorak RN, Kamm MA, Korzenik JR, Lashner BA, Onken JE, Rachmilewitz D, Rutgeerts P, Wild G, Wolf DC, Marsters PA, Travers SB, Blank MA, van Deventer SJ (February 2004). "Infliximab maintenance therapy for fistulizing Crohn's disease". The New England Journal of Medicine 350 (9): 876–85. doi:10.1056/NEJMoa030815. PMID 14985485.
- ^ a b Hanauer SB, Feagan BG, Lichtenstein GR, Mayer LF, Schreiber S, Colombel JF, Rachmilewitz D, Wolf DC, Olson A, Bao W, Rutgeerts P (May 2002). "Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial". Lancet 359 (9317): 1541–9. doi:10.1016/S0140-6736(02)08512-4. PMID 12047962.
- ^ Hanauer SB (February 2003). "Crohn's disease: step up or top down therapy". Best Pract Res Clin Gastroenterol 17 (1): 131–7. doi:10.1053/bega.2003.0361. PMID 12617888.
- ^ Rutgeerts P, Sandborn WJ, Feagan BG, Reinisch W, Olson A, Johanns J, Travers S, Rachmilewitz D, Hanauer SB, Lichtenstein GR, de Villiers WJ, Present D, Sands BE, Colombel JF (2005). "Infliximab for induction and maintenance therapy for ulcerative colitis". The New England Journal of Medicine 353 (23): 2462–76. doi:10.1056/NEJMoa050516. PMID 16339095.
- ^ Rennard SI, Fogarty C, Kelsen S, Long W, Ramsdell J, Allison J, Mahler D, Saadeh C, Siler T, Snell P, Korenblat P, Smith W, Kaye M, Mandel M, Andrews C, Prabhu R, Donohue JF, Watt R, Lo KH, Schlenker-Herceg R, Barnathan ES, Murray J (May 2007). "The safety and efficacy of infliximab in moderate to severe chronic obstructive pulmonary disease". Am. J. Respir. Crit. Care Med. 175 (9): 926–34. doi:10.1164/rccm.200607-995OC. PMID 17290043.
- ^ Sfikakis PP (November 2002). "Behçet's disease: a new target for anti-tumour necrosis factor treatment". Ann. Rheum. Dis. 61 Suppl 2 (Suppl 2): ii51–3. doi:10.1136/ard.61.suppl_2.ii51. PMC 1766720. PMID 12379622.
- ^ a b Puéchal X, Terrier B, Mouthon L, Costedoat-Chalumeau N, Guillevin L, Le Jeunne C (March 2014). "Relapsing polychondritis". Joint, bone, spine : revue du rhumatisme 81 (2): 118–24. doi:10.1016/j.jbspin.2014.01.001. PMID 24556284.
- ^ Kemta Lekpa F, Kraus VB, Chevalier X (April 2012). "Biologics in relapsing polychondritis: a literature review". Seminars in arthritis and rheumatism 41 (5): 712–9. doi:10.1016/j.semarthrit.2011.08.006. PMID 22071463.
- ^ Gupta AK, Skinner AR (2004). "A review of the use of infliximab to manage cutaneous dermatoses". J Cutan Med Surg 8 (2): 77–89. doi:10.1007/s10227-004-0115-7. PMID 15685387.
- ^ Kavanaugh AF, Ritchlin CT (July 2006). "Systematic review of treatments for psoriatic arthritis: an evidence based approach and basis for treatment guidelines". J. Rheumatol. 33 (7): 1417–21. PMID 16724373.
- ^ Keane J, Gershon S, Wise RP, Mirabile-Levens E, Kasznica J, Schwieterman WD, Siegel JN, Braun MM (2001). "Tuberculosis associated with infliximab, a tumor necrosis factor α–neutralizing agent". N Engl J Med 345 (15): 1098–1104. doi:10.1056/NEJMoa011110. PMID 11596589.
- ^ Remicade for Healthcare Professionals
- ^ [1][dead link]
- ^ "Tumor Necrosis Factor (TNF) Blockers (marketed as Remicade, Enbrel, Humira, Cimzia, and Simponi) August 2009". MedWatch. U.S. Food and Drug Administration (FDA). August 31, 2009. Retrieved 2009-11-15.
- ^ Maini R, St Clair EW, Breedveld F, Furst D, Kalden J, Weisman M, Smolen J, Emery P, Harriman G, Feldmann M, Lipsky P (Dec 4, 1999). "Infliximab (chimeric anti-tumour necrosis factor alpha monoclonal antibody) versus placebo in rheumatoid arthritis patients receiving concomitant methotrexate: a randomised phase III trial. ATTRACT Study Group". Lancet 354 (9194): 1932–9. doi:10.1016/s0140-6736(99)05246-0. PMID 10622295.
- ^ Choy EH, Panayi GS (March 2001). "Cytokine pathways and joint inflammation in rheumatoid arthritis". The New England Journal of Medicine 344 (12): 907–16. doi:10.1056/NEJM200103223441207. PMID 11259725.
- ^ Etanercept product labeling
- ^ Etanercept, Adalimumab and Infliximab product labeling
- ^ http://www.rxlist.com/remicade-drug.htm
- ^ "Guidance on the use of infliximab for Crohn’s disease (TA40)"
- ^ "Infliximab, adalimumab and golimumab for treating moderately to severely active ulcerative colitis after the failure of conventional therapy (including a review of TA140 and TA262)"
- ^ "Section 100 arrangements; only for infliximab"
- ^ JNJ annual report, downloaded April 22, 2014. http://www.sec.gov/Archives/edgar/data/200406/000020040614000033/a2013122910-k.htm
External links
- Remicade Centocor Ortho Biotech
- National Rheumatoid Arthritis Society (NRAS) Information on anti-TNF drugs such as Infliximab
- Remicade Drug Label
- Full Prescribing Information and Medication Guide Centocor Ortho Biotech
|
Immunosuppressive drugs / Immunosuppressants (L04)
|
|
Intracellular
(initiation) |
| Antimetabolites |
- purine synthesis inhibitors: Azathioprine
- Mycophenolic acid
- pyrimidine synthesis inhibitors: Leflunomide
- Teriflunomide
|
|
Macrolides/
other IL-2 inhibitors |
- FKBP/Cyclophilin/Calcineurin: Tacrolimus
- Ciclosporin
- Pimecrolimus
|
|
| IMiDs |
- Lenalidomide
- Pomalidomide
- Thalidomide
|
|
|
Intracellular
(reception) |
| IL-1 receptor antagonists |
|
|
| mTOR |
- Sirolimus
- Everolimus
- Ridaforolimus
- Temsirolimus
- Umirolimus
- Zotarolimus
|
|
|
| Extracellular |
| Antibodies |
| Monoclonal |
Serum target
(noncellular) |
- Complement component 5 (Eculizumab)
- TNF (Adalimumab
- Afelimomab
- Certolizumab pegol
- Golimumab
- Infliximab
- Nerelimomab)
- Interleukin 5 (Mepolizumab)
- Immunoglobulin E (Omalizumab)
- IL-12 and IL-23 (Lebrikizumab
- Ustekinumab)
|
|
| Cellular target |
- CD3 (Muromonab-CD3
- Otelixizumab
- Teplizumab
- Visilizumab)
- CD4 (Clenoliximab
- Keliximab
- Zanolimumab)
- CD11a (Efalizumab)
- CD18 (Erlizumab)
- CD20 (Obinutuzumab
- Rituximab
- Ocrelizumab
- Pascolizumab)
- CD23 (Gomiliximab
- Lumiliximab)
- CD40 (Teneliximab
- Toralizumab)
- CD62L/L-selectin (Aselizumab)
- CD80 (Galiximab)
- CD147/Basigin (Gavilimomab)
- CD154 (Ruplizumab)
- BLyS (Belimumab
- Blisibimod)
- CTLA-4 (Ipilimumab
- Tremelimumab)
- CAT (Bertilimumab
- Lerdelimumab
- Metelimumab)
- Integrin (Natalizumab)
- Interleukin-6 receptor (Tocilizumab)
- LFA-1 (Odulimomab)
- IL-2 receptor/CD25 (Basiliximab
- Daclizumab
- Inolimomab)
- T-lymphocyte (Zolimomab aritox)
|
|
| Unsorted |
- Atorolimumab
- Cedelizumab
- Fontolizumab
- Maslimomab
- Morolimumab
- Pexelizumab
- Reslizumab
- Rovelizumab
- Siplizumab
- Talizumab
- Telimomab aritox
- Vapaliximab
- Vepalimomab
|
|
|
| Polyclonal |
- Anti-thymocyte globulin
- Anti-lymphocyte globulin
|
|
|
| -cept (Fusion) |
- CTLA-4 (Abatacept
- Belatacept)
- TNF inhibitor (Etanercept
- Pegsunercept)
- Aflibercept
- Alefacept
- Rilonacept
|
|
|
|
Index of the immune system
|
|
| Description |
- Physiology
- cells
- autoantigens
- autoantibodies
- complement
- surface antigens
- IG receptors
|
|
| Disease |
- Allergies
- Immunodeficiency
- Immunoproliferative immunoglobulin disorders
- Hypersensitivity and autoimmune disorders
- Neoplasms and cancer
|
|
| Treatment |
- Procedures
- Drugs
- antihistamines
- immunostimulants
- immunosuppressants
- monoclonal antibodies
|
|
|
