Mycophenolic acid
|
|
| Systematic (IUPAC) name |
|
(4E)-6-(4-Hydroxy-6-methoxy-7-methyl-3-oxo-1,3-dihydro-2-benzofuran-5-yl)-4-methylhex-4-enoic acid
|
| Clinical data |
| Trade names |
CellCept, Myfortic |
| AHFS/Drugs.com |
Multum Consumer Information |
| MedlinePlus |
a601081 |
| Licence data |
EMA:Link, US FDA:link |
Pregnancy
category |
- AU: D
- US: D (Evidence of risk)
|
| Legal status |
- AU: Prescription Only (S4)
- CA: ℞-only
- UK: Prescription-only (POM)
- US: ℞-only
|
Routes of
administration |
Oral, intravenous |
| Pharmacokinetic data |
| Bioavailability |
72% (sodium),
94% (mofetil)[1] |
| Protein binding |
82–97%[1] |
| Metabolism |
Hepatic[1] |
| Biological half-life |
17.9±6.5 hours[1] |
| Excretion |
Urine (93%),
faeces (6%)[1] |
| Identifiers |
| CAS Registry Number |
24280-93-1 Y |
| ATC code |
L04AA06 |
| PubChem |
CID: 446541 |
| IUPHAR/BPS |
6832 |
| DrugBank |
DB01024 Y |
| ChemSpider |
393865 Y |
| UNII |
HU9DX48N0T N |
| KEGG |
D05096 Y |
| ChEBI |
CHEBI:168396 Y |
| ChEMBL |
CHEMBL866 Y |
| Chemical data |
| Formula |
C17H20O6 |
| Molecular mass |
320.34 g/mol |
SMILES
-
O=C1OCc2c1c(O)c(c(OC)c2C)C\C=C(/C)CCC(=O)O
|
InChI
-
InChI=1S/C17H20O6/c1-9(5-7-13(18)19)4-6-11-15(20)14-12(8-23-17(14)21)10(2)16(11)22-3/h4,20H,5-8H2,1-3H3,(H,18,19)/b9-4+ Y
-
Key:HPNSFSBZBAHARI-RUDMXATFSA-N Y
|
| N (what is this?) (verify) |
Mycophenolate mofetil
|
|
| Systematic (IUPAC) name |
|
2-Morpholin-4-ylethyl (E)-6-(4-hydroxy-6-methoxy-7-methyl-3-oxo-1H-2-benzofuran-5-yl)-4-methylhex-4-enoate
|
| Clinical data |
| Trade names |
CellCept |
| AHFS/Drugs.com |
monograph |
| Licence data |
EMA:Link, US FDA:link |
| Legal status |
|
| Identifiers |
| CAS Registry Number |
128794-94-5 Y |
| ATC code |
L04AA06 |
| PubChem |
CID: 5281078 |
| DrugBank |
DB00688 Y |
| ChemSpider |
4444535 Y |
| KEGG |
C07908 Y |
| ChEBI |
CHEBI:8764 N |
| ChEMBL |
CHEMBL1456 Y |
| Chemical data |
| Formula |
C23H31NO7 |
| Molecular mass |
433.49474 g/mol |
SMILES
-
CC1=C(C(=C(C2=C1COC2=O)O)CC=C(C)CCC(=O)OCCN3CCOCC3)OC
|
InChI
-
InChI=1S/C23H31NO7/c1-15(5-7-19(25)30-13-10-24-8-11-29-12-9-24)4-6-17-21(26)20-18(14-31-23(20)27)16(2)22(17)28-3/h4,26H,5-14H2,1-3H3/b15-4+ Y
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Key:RTGDFNSFWBGLEC-SYZQJQIISA-N Y
|
| N (what is this?) (verify) |
Mycophenolic acid (INN, BAN and USAN) (less accurately called mycophenolate) is an immunosuppressant drug used to prevent rejection in organ transplantation. It inhibits an enzyme needed for the growth of T cells and B cells. It was initially marketed as the prodrug mycophenolate mofetil (MMF) to improve oral bioavailability. More recently, the salt mycophenolate sodium has also been introduced. Mycophenolate mofetil is commonly marketed under the trade name CellCept (Roche), and mycophenolate sodium as Myfortic (Novartis).
Discovered by an Italian medical scientists Bartolomeo Gosio in 1893, mycophenolic acid was the first antibiotic to be synthesised in pure and crystalline form. But its medical application was forgotten until two American scientists C.L. Alsberg and O.M. Black resynthesied it in 1912, and gave its chemical name. It was eventually found to be a broad-spectrum acting drug having antiviral, antifungal, antibacterial, anticancer, and antipsoriasis properties.[2] The clinically usable drug Cellcept was developed by a South African geneticist Anthony Allison and his wife Elsie M. Eugui. It was first approved by the US Food and Drug Administration on 3 May 1995 for use in Kidney transplantation.[3]
Contents
- 1 Discovery and development
- 2 Clinical use
- 2.1 Indications
- 2.2 Comparison to other agents
- 2.3 Potential future uses
- 3 Adverse effects
- 4 Pharmacology
- 5 Chemistry
- 6 References
Discovery and development
Mycophenolic acid was discovered by an Italian medical scientist Bartolomeo Gosio. Gosio collected a fungus from spoiled corn and named it Penicillium glaucum. (The species is now called P. brevicompactum.) In 1893 he found that the fungus had antibacterial activity. In 1896 he could isolate the crystals of the compound, which he successfully demonstrated as the active antibacterial compound against the anthrax bacterium.[2] This was the first antibiotic that was isolated in pure and crystalline form. But the discovery was forgotten.[4] It was rediscovered by two American scientists C.L. Alsberg and O.M. Black in 1912, and gave the name mycophenolic acid. The compound was eventually demonstrated to have antiviral, antifungal, antibacterial, anticancer, and antipsoriasis activities.[5] Although it is not commercialised as antibiotic due to its adverse effects, its modified compound (ester derivative) is an approved immunosuppressant drug in kidney, heart, and liver transplantations, and is marketed under the brands CellCept (mycophenolate mofetil by Roche) and Myfortic (mycophenolate sodium by Novartis).[6]
Cellcept was developed by a South African geneticist Anthony Allison and his wife Elsie M. Eugui. In the 1970s while working at the Medical Research Council, Allison investigated the biochemical causes of immunune deficiency in children. He discovered the metabolic pathway involving an enzyme, inosine monophosphate dehydrogenase, which is responsible for undersirable immune response in autoimmune diseases, as well as for immune rejection in organ transplantation. He conceived an idea that if a molecule that could block the enzyme is discovered, then, it would become an immunosuppressive drug that could be used for autoimmune diseases and in organ transplantation. In 1981 he decided to go for drug discovery and approached several pharmaceutical companies, which turned him down one by one as he had no primary knowledge on drug research. However, Syntex liked his plans and asked him to join the company with his wife.[7] He became Vice President for the research. In one of their experiments the Allisons used an antibacterial compound, mycophenolate mofetil, which was abandoned in clinical use due to its adverse effects. They discovered that the compound had immunosuppressive activity.[8][9] They synthesised a chemical variant for increased activity and reduced adverse effects.[10][11][12][13][14] They subsequently demonstrated that it was useful in organ transplantation in experimental rats.[15][16] After successful clinical trials,[17] the compound was approved for use in kidney transplant by the US Food and Drug Administration on 3 May 1995,[3] and was commercialised under the brand name CellCept.[18][19]
Clinical use
Indications
Mycophenolate is used for the prevention of organ transplant rejection. Mycophenolate mofetil is indicated for the prevention of organ transplant rejection in adults and renal transplant rejection in children over 2 years; whereas mycophenolate sodium is indicated for the prevention of renal transplant rejection in adults. Mycophenolate sodium has also been used for the prevention of rejection in liver, heart, and/or lung transplants in children older than two years.[20]
An immunosuppressant that has drastically decreased the incidence of acute rejection in solid transplant recipients, mycophenolate is increasingly utilized as a steroid sparing treatment in autoimmune diseases and similar immune-mediated disorders including Behçet's disease, pemphigus vulgaris, refractory incomplete systemic lupus erythematosus,[21] immunoglobulin A nephropathy, small vessel vasculitides, and psoriasis.[22]
Its increasing application in treating lupus nephritis has demonstrated more frequent complete response and less frequent complications[22] compared to cyclophosphamide bolus therapy, a regimen with risk of bone marrow suppression, infertility, and malignancy.[23] Further work addressing maintenance therapy demonstrated mycophenolate superior to cyclophosphamide, again in terms of response and side-effects.[23] Walsh et al. even propose that mycophenolate should be considered as a first-line induction therapy for treatment of lupus nephritis in patients without renal dysfunction,[24] suggesting that mycophenolate will be encountered more frequently in medical practice.
Comparison to other agents
Compared with azathioprine it has significantly higher incidence of diarrhea, and no difference in risk of any of the other side effects.[25] Mycophenolic acid is 15 times more expensive than azathioprine.[26] The exact role of mycophenolate vs azathioprine has yet to be conclusively established. In long-term immunosuppression, it may be used to avoid calcineurin inhibitors or steroids.
Potential future uses
|
|
This section is outdated. Please update this article to reflect recent events or newly available information. (November 2014) |
Mycophenolate mofetil is beginning to be used in the management of auto-immune disorders such as idiopathic thrombocytopenic purpura (ITP), systemic lupus erythematosus (SLE), scleroderma (systemic sclerosis or SSc), and pemphigus vulgaris (PV) with success for some patients.[27]
It is also currently being used as a long-term therapy for maintaining remission of granulomatosis with polyangiitis, though thus far, studies have found it inferior to azathioprine.[citation needed] A combination of mycophenolate and ribavirin has been found to stop infection by and replication of dengue virus in vitro.[28][29]
Takayasu arteritis, ANCA associated vasculitides and all medium vessel vasculitic conditions do respond to it. However, due to its slow onset of action, initial aggressive disease may be managed with high dose steroids and other immunosuppressants. Maintenance of remission is much better with mycophenolate, especially due to lower infection rate with this agent. After persistent remission, dose can be reduced to 1000 mg per day, but not lower as relapses more common in doses lower than this.[citation needed]
Adverse effects
Common adverse drug reactions (≥1% of patients) associated with mycophenolate therapy include diarrhea, nausea, vomiting, joint pain; infections, leukopenia, and/or anemia reflect the immunosuppressive and myelosuppressive nature of the drug. Mycophenolate sodium is also commonly associated with fatigue, headache, cough and/or breathing issues. Intravenous (IV) administration of mycophenolate mofetil is also commonly associated with thrombophlebitis and thrombosis. Infrequent adverse effects (0.1–1% of patients) include esophagitis, gastritis, gastrointestinal tract hemorrhage, and/or invasive cytomegalovirus (CMV) infection.[20] More rarely, pulmonary fibrosis or various neoplasia occur: melanoma, lymphoma, other malignancies having an occurrences of 1 in 20 to 1 in 200, depending on the type, with neoplasia in the skin being the most common site.[30][31] Several cases of pure red cell aplasia (PRCA) have also been reported.[32]
The U.S. Food and Drug Administration (FDA) has issued an alert that patients on mycophenolate mofetil and mycophenolic acid are at increased risk of opportunistic infections, such as activation of latent viral infections, including shingles, other herpes infections, cytomegalovirus, and BK virus associated nephropathy. In addition the FDA is investigating 16 patients that developed a rare neurological disease while taking the drug. This is a viral infection known as progressive multifocal leukoencephalopathy; it attacks the brain and is usually fatal.[33]
Mycophenolic acid is associated with miscarriage and congenital malformations when used during pregnancy, and should be avoided whenever possible by women trying to conceive.[34][35]
GI intolerance in about 10% of patients taking mycophenolate mofetil can be overcome largely by replacing it with mycophenolate sodium or azathioprine.[citation needed]
Blood tests
Among the most common effects of this drug is increased blood cholesterol levels. Other changes in blood chemistry such as hypomagnesemia, hypocalcemia, hyperkalemia, and an increase in BUN are regularly noted.
Pharmacology
Mycophenolate is derived from the fungus Penicillium stoloniferum or in P. echinulatum.[36] Mycophenolate mofetil is metabolised in the liver to the active moiety mycophenolic acid. It reversibly inhibits inosine monophosphate dehydrogenase,[37] the enzyme that controls the rate of synthesis of guanine monophosphate in the de novo pathway of purine synthesis used in the proliferation of B and T lymphocytes.[38] Other cells are able to recover purines via a separate salvage pathway and are thus able to escape the effect.
Mycophenolate is potent and can, in many contexts, be used in place of the older anti-proliferative azathioprine. It is usually used as part of a three-compound regimen of immunosuppressants, also including a calcineurin inhibitor (ciclosporin or tacrolimus) and prednisolone.
Chemistry
Mycophenolate mofetil is the morpholinoethyl ester of mycophenolic acid; the ester masks the carboxyl group. Mycophenolate mofetil is reported to have a pKa values of 5.6 for the morpholino moiety and 8.5 for the phenolic group.[39]
References
- ^ a b c d e "CellCept®" (PDF). TGA eBusiness Services. Roche Products Pty Limited. 13 December 2012. Retrieved 25 February 2014.
- ^ a b Silverman Kitchin, Jennifer E.; Pomeranz, Miriam Keltz; Pak, Grace; Washenik, Ken; Shupack, Jerome L. (1997). "Rediscovering mycophenolic acid: A review of its mechanism, side effects, and potential uses". Journal of the American Academy of Dermatology 37 (3): 445–449. doi:10.1016/S0190-9622(97)70147-6.
- ^ a b "Risk Evaluation and Mitigation Strategy (REMS) Under Review for CellCept and Myfortic". U.S. Food and Drug Administration. Retrieved 23 July 2014.
- ^ Zhang, Lixin; Demain, Arnold L. (2005). Natural Products: Drug Discovery and Therapeutic Medicine. Totowa, N.J.: Humana Press. p. 14. ISBN 9781592599769.
- ^ Regueira, T. B.; Kildegaard, K. R.; Hansen, B. G.; Mortensen, U. H.; Hertweck, C.; Nielsen, J. (2011). "Molecular Basis for Mycophenolic Acid Biosynthesis in Penicillium brevicompactum". Applied and Environmental Microbiology 77 (9): 3035–3043. doi:10.1128/AEM.03015-10. PMC 3126426. PMID 21398490.
- ^ Bentley, Ronald (2000). "Mycophenolic Acid: A One Hundred Year Odyssey from Antibiotic to Immunosuppressant". Chemical Reviews 100 (10): 3801–3826. doi:10.1021/cr990097b. PMID 11749328.
- ^ Watts, Geoff (2014). "Anthony Clifford Allison". The Lancet 383 (9925): 1290. doi:10.1016/S0140-6736(14)60635-8.
- ^ Allison, Anthony C (2000). "Immunosuppressive drugs: the first 50 years and a glance forward". Immunopharmacology 47 (2-3): 63–83. doi:10.1016/S0162-3109(00)00186-7. PMID 10878284.
- ^ Allison, AC; Kowalski, WJ; Muller, CD; Eugui, EM (1993). "Mechanisms of action of mycophenolic acid.". Annals of the New York Academy of Sciences 696 (1): 63–87. doi:10.1111/j.1749-6632.1993.tb17143.x. PMID 7906496.
- ^ Nelson, PH; Eugui, E; Wang, CC; Allison, AC (1990). "Synthesis and immunosuppressive activity of some side-chain variants of mycophenolic acid.". Journal of Medicinal Chemistry 33 (2): 833–838. doi:10.1021/jm00164a057. PMID 1967654.
- ^ Eugui, Elsie M.; Allison, Anthony C. (1993). "Immunosuppressive Activity of Mycophenolate Mofetil". Annals of the New York Academy of Sciences 685 (1): 309–329. doi:10.1111/j.1749-6632.1993.tb35881.x. PMID 8363235.
- ^ Allison, AC; Eugui, EM (1996). "Purine metabolism and immunosuppressive effects of mycophenolate mofetil (MMF).". Clinical Transplantation 10 (1 Pt 2): 77–84. PMID 8680053.
- ^ Allison, AC; Eugui, EM (1993). "The design and development of an immunosuppressive drug, mycophenolate mofetil.". Springer Seminars in Immunopathology 14 (4): 353–80. doi:10.1007/bf00192309. PMID 8322167.
- ^ Allison, AC; Eugui, EM (1993). "Immunosuppressive and other effects of mycophenolic acid and an ester prodrug, mycophenolate mofetil". Immunological Reviews 136 (1): 5–28. doi:10.1111/j.1600-065x.1993.tb00652.x. PMID 7907572.
- ^ Bechstein, WO; Suzuki, Y; Kawamura, T; Jaffee, B; Allison, A; Hullett, DA; Sollinger, HW (1992). "Low-dose combination therapy of DUP-785 and RS-61443 prolongs cardiac allograft survival in rats". Transplant International 5 (Suppl 1): S482–3. PMID 14621853.
- ^ Kawamura, T; Hullett, DA; Suzuki, Y; Bechstein, WO; Allison, AM; Sollinger, HW (1993). "Enhancement of allograft survival by combination RS-61443 and DUP-785 therapy". Transplantation 55 (4): 691–4; discussion 694–5. doi:10.1097/00007890-199304000-00001. PMID 8475537.
- ^ Taylor, DO; Ensley, RD; Olsen, SL; Dunn, D; Renlund, DG (1994). "Mycophenolate mofetil (RS-61443): preclinical, clinical, and three-year experience in heart transplantation". The Journal of Heart and Lung Transplantation 13 (4): 571–82. PMID 7947873.
- ^ Donlon, Diane M (15 June 1995). "New Agent to Prevent Kidney Transplant Rejection Now Available". Stanford University. Retrieved 23 July 2014.
- ^ "CellCept registry data demonstrated superior long-term organ transplant outcomes". Roche.com. F. Hoffmann-La Roche Ltd. Retrieved 23 July 2014.
- ^ a b Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3[page needed]
- ^ Boehm I et al. Chilblain lupus erythematosus Hutchinson: successful treatment with mycophenolate mofetil. Arch Dermatol 2001;137:235 – 236 http://archderm.jamanetwork.com/article.aspx?articleid=478189
- ^ a b Moore RA, Derry S (2006). "Systematic review and meta-analysis of randomised trials and cohort studies of mycophenolate mofetil in lupus nephritis". Arthritis Research & Therapy 8 (6): R182. doi:10.1186/ar2093. PMC 1794528. PMID 17163990.
- ^ a b D'Cruz DP, Khamashta MA, Hughes GR (February 2007). "Systemic lupus erythematosus". Lancet 369 (9561): 587–96. doi:10.1016/S0140-6736(07)60279-7. PMID 17307106.
- ^ Walsh M, James M, Jayne D, Tonelli M, Manns BJ, Hemmelgarn BR (September 2007). "Mycophenolate mofetil for induction therapy of lupus nephritis: a systematic review and meta-analysis". Clinical Journal of the American Society of Nephrology 2 (5): 968–75. doi:10.2215/CJN.01200307. PMID 17702723.
- ^ Knight SR, Russell NK, Barcena L, Morris PJ (March 2009). "Mycophenolate mofetil decreases acute rejection and may improve graft survival in renal transplant recipients when compared with azathioprine: a systematic review". Transplantation 87 (6): 785–94. doi:10.1097/TP.0b013e3181952623. PMID 19300178.
- ^ Remuzzi G, Lesti M, Gotti E et al. (2004). "Mycophenolate mofetil versus azathioprine for prevention of acute rejection in renal transplantation (MYSS): a randomised trial". Lancet 364 (9433): 503–12. doi:10.1016/S0140-6736(04)16808-6. PMID 15302193.
- ^ Mimouni D, Anhalt GJ, Cummins DL, Kouba DJ, Thorne JE, Nousari HC (June 2003). "Treatment of pemphigus vulgaris and pemphigus foliaceus with mycophenolate mofetil". Archives of Dermatology 139 (6): 739–42. doi:10.1001/archderm.139.6.739. PMID 12810504.
- ^ Diamond MS, Zachariah M, Harris E (2002). "Mycophenolic acid inhibits dengue virus infection by preventing replication of viral RNA". Virology 304 (2): 211–21. doi:10.1006/viro.2002.1685. PMID 12504563.
- ^ Takhampunya R, Ubol S, Houng HS, Cameron CE, Padmanabhan R (July 2006). "Inhibition of dengue virus replication by mycophenolic acid and ribavirin". The Journal of General Virology 87 (Pt 7): 1947–52. doi:10.1099/vir.0.81655-0. PMID 16760396.
- ^ http://reference.medscape.com/drug/cellcept-myfortic-mycophenolate-343209#4
- ^ http://www.bnf.org
- ^ "CellCept (mycophenolate mofetil) August 2009". U.S. Food and Drug Administration. August 14, 2009. Retrieved 2009-08-21.
- ^ "CellCept (mycophenolate mofetil) August 2009". U.S. Food and Drug Administration. August 14, 2009. Retrieved 2009-08-21.
- ^ "FDA Issues Second CellCept Warning". newsinferno.com. 2008-05-18. Retrieved 2010-10-26.
- ^ "MedWatch Safety Alerts for Human Medical Products". fda.gov. May 2008. Retrieved 2010-10-26.
- ^ Anderson, HA; Bracewell, JM; Fraser, AR; Jones, D; Robertson, GW; Russell, JD (December 1988). "5-Hydroxymaltol and mycophenolic acid, secondary metabolites from Penicillium echinulatum" (PDF). Transactions of the British Mycological Society 91 (4): 649–651. doi:10.1016/S0007-1536(88)80040-8.
- ^ Fulton B, Markham A. "Mycophenolate mofetil : a review of its pharmacodynamic and pharmacokinetic properties and clinical efficacy in renal transplantation." Drugs. 1996, 51(2):278-98.
- ^ Ransom JT (December 1995). "Mechanism of action of mycophenolate mofetil". Therapeutic Drug Monitoring 17 (6): 681–4. doi:10.1097/00007691-199512000-00023. PMID 8588241.
- ^ http://www.rocheusa.com/products/cellcept/pi.pdf
|
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
|
|
|
