Identification
- Summary
Alemtuzumab is a monoclonal anti-CD52 antibody used in the treatment of B-cell chronic lymphocytic leukemia and relapsing forms of multiple sclerosis.
- Brand Names
- Campath, Lemtrada, MabCampath
- Generic Name
- Alemtuzumab
- DrugBank Accession Number
- DB00087
- Background
Alemtuzumab is a humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein, CD52. The Campath-1H antibody is an IgG1 kappa with the human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Alemtuzumab is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin.4
Alemtuzumab was approved by the FDA in 2001.4 It is marketed as LEMTRADA for multiple sclerosis (MS) treatment and CAMPTAH for B-cell chronic lymphocytic leukemia (B-CLL). The dose of alemtuzumab used for B-CLL is much higher than that for MS, and also at more frequent dosing.4,5
- Type
- Biotech
- Groups
- Approved, Investigational
- Biologic Classification
- Protein Based Therapies
Monoclonal antibody (mAb) - Protein Structure
- Protein Chemical Formula
- C6468H10066N1732O2005S40
- Protein Average Weight
- 145453.8 Da
- Sequences
>1CE1:H CAMPATH-1H:Heavy Chain 1 QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTT EYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVS SASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLG GPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQY NSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRD ELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSR WQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
>1CE1:L CAMPATH-1H:Light Chain 1 DIQMTQSPSSLSASVGDRVTITCKASQNIDKYLNWYQQKPGKAPKLLIYNTNNLQTGVPS RFSGSGSGTDFTFTISSLQPEDIATYYCLQHISRPRTFGQGTKVEIKRTVAAPSVFIFPP SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT LSKADYEKHKVYACEVTHQGLSSPVTKSFNR
>1CE1:H CAMPATH-1H:Heavy Chain 2 QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTT EYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVS SASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLG GPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQY NSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRD ELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSR WQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
>1CE1:L CAMPATH-1H:Light Chain 2 DIQMTQSPSSLSASVGDRVTITCKASQNIDKYLNWYQQKPGKAPKLLIYNTNNLQTGVPS RFSGSGSGTDFTFTISSLQPEDIATYYCLQHISRPRTFGQGTKVEIKRTVAAPSVFIFPP SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT LSKADYEKHKVYACEVTHQGLSSPVTKSFNR
>1bey_H|CAMPATH-1H|Humanized||VH-CH1 (VH(1-121)+CH1(122-210))|||||||219||||MW 23397.3|MW 23397.3| QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTT EYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVS SASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKV
>1bey_L|CAMPATH-1H|Humanized||L-KAPPA (V-KAPPA(1-107)+C-KAPPA(108-214))|||||||214||||MW 23571.3|MW 23571.3| DIQMTQSPSSLSASVGDRVTITCKASQNIDKYLNWYQQKPGKAPKLLIYNTNNLQTGVPS RFSGSGSGTDFTFTISSLQPEDIATYYCLQHISRPRTFGQGTKVEIKRTVAAPSVFIFPP SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT LSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC
>8005_H|alemtuzumab|||H-GAMMA-1 (VH(1-121)+CH1(122-219)+HINGE-REGION(220-220)+CH2(221-330)+CH3(331-437))|||||||437||||MW 47976.2|MW 47976.2| QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTT EYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVS SASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEAPELLGGPSVFLFPPKPKDT LMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLH QDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVK GFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHE ALHNHYTQKSLSLSPGK
>8005_L|alemtuzumab|||L-KAPPA (V-KAPPA(1-107)+C-KAPPA(108-214))|||||||214||||MW 23571.3|MW 23571.3| DIQMTQSPSSLSASVGDRVTITCKASQNIDKYLNWYQQKPGKAPKLLIYNTNNLQTGVPS RFSGSGSGTDFTFTISSLQPEDIATYYCLQHISRPRTFGQGTKVEIKRTVAAPSVFIFPP SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT LSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC
>1ce1_H|CAMPATH-1H|Humanized||VH-CH1 (VH(1-121)+CH1(122-219))|||||||220||||MW 23526.4|MW 23526.4| QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTT EYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVS SASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVE
>1ce1_L|CAMPATH-1H|Humanized||L-KAPPA (V-KAPPA(1-107)+C-KAPPA(108-211))|||||||211||||MW 23282.0|MW 23282.0| DIQMTQSPSSLSASVGDRVTITCKASQNIDKYLNWYQQKPGKAPKLLIYNTNNLQTGVPS RFSGSGSGTDFTFTISSLQPEDIATYYCLQHISRPRTFGQGTKVEIKRTVAAPSVFIFPP SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT LSKADYEKHKVYACEVTHQGLSSPVTKSFNR
Download FASTA Format- Synonyms
- Alemtuzumab
Pharmacology
- Indication
LEMTRADA is indicated for the treatment of relapsing forms of multiple sclerosis (MS), including relapsing-remitting disease and active secondary progressive disease, in adults. Because of its safety profile, the use of LEMTRADA should generally be reserved for patients who have had an inadequate response to two or more drugs indicated for the treatment of MS.4 LEMTRADA contains the same active ingredient (alemtuzumab) found in CAMPATH, and CAMPATH is approved for the treatment of B-cell chronic lymphocytic leukemia (B-CLL), although generally administered at higher and more frequent doses (e.g., 30 mg) than recommended in the treatment of MS.4
Reduce drug development failure ratesBuild, train, & validate machine-learning modelswith evidence-based and structured datasets.Build, train, & validate predictive machine-learning models with structured datasets.- Associated Conditions
- B-Cell Chronic Lymphocytic Leukemia (B-CLL)
- Kidney Transplant Rejection
- Leukemia, Prolymphocytic, T-Cell
- Relapsing Remitting Multiple Sclerosis (RRMS)
- Secondary Progressive Multiple Sclerosis (SPMS)
- Steroid Refractory Acute Graft Versus Host Disease
- Refractory Autoimmune Hemolytic Anemia
- Refractory Idiopathic thrombocytopenic purpura
- Associated Therapies
- Contraindications & Blackbox Warnings
Avoid life-threatening adverse drug eventsImprove clinical decision support with information on contraindications & blackbox warnings, population restrictions, harmful risks, & more.Avoid life-threatening adverse drug events & improve clinical decision support.- Pharmacodynamics
Alemtuzumab depletes circulating T and B lymphocytes after each treatment course. In clinical trials, the lowest cell counts occurred 1 month after a course of treatment at the time of the first post-treatment blood count. Lymphocyte counts then increased over time: B cell counts usually recovered within 6 months; T cell counts increased more slowly and usually remained below baseline 12 months after treatment. Approximately 60% of patients had total lymphocyte counts below the lower limit of normal 6 months after each treatment course and 20% had counts below the lower limit of normal after 12 months.4
Reconstitution of the lymphocyte population varies for the different lymphocyte subtypes. At Month 1 in clinical trials, the mean CD4+ lymphocyte count was 40 cells per microliter, and, at Month 12, 270 cells per microliter. At 30 months, approximately half of patients had CD4+ lymphocyte counts that remained below the lower limit of normal.4
- Mechanism of action
The precise mechanism by which alemtuzumab exerts its therapeutic effects in multiple sclerosis is unknown but is presumed to involve binding to CD52, a cell surface antigen present on T and B lymphocytes, and on natural killer cells, monocytes, and macrophages. Following cell surface binding to T and B lymphocytes, alemtuzumab results in antibody-dependent cellular cytolysis and complement-mediated lysis.4 Research suggests that alemtuzumab can also exert immunomodulatory effects through the depletion and repopulation of lymphocytes, including alterations in the number, proportions, and properties of some lymphocyte subsets posttreatment, increasing representation of regulatory T cell subsets, and increasing representation of memory T- and B-lymphocytes.6 The reduction in the level of circulating B and T cells by alemtuzumab and subsequent repopulation may reduce the potential for relapse, which ultimately delays disease progression.6,5
Target Actions Organism ACAMPATH-1 antigen antibodyHumans ULow affinity immunoglobulin gamma Fc region receptor III-B binderHumans ULow affinity immunoglobulin gamma Fc region receptor III-A binderHumans UHigh affinity immunoglobulin gamma Fc receptor I binderHumans ULow affinity immunoglobulin gamma Fc region receptor II-a binderHumans ULow affinity immunoglobulin gamma Fc region receptor II-b binderHumans ULow affinity immunoglobulin gamma Fc region receptor II-c binderHumans - Absorption
Serum concentrations increased with each consecutive dose within a treatment course, with the highest observed concentrations occurring following the last infusion of a treatment course. The mean maximum concentration was 3014 ng/mL on Day 5 of the first treatment course, and 2276 ng/mL on Day 3 of the second treatment course.4
- Volume of distribution
Alemtuzumab is largely confined to the blood and interstitial space with a central volume of distribution of 14.1 L.4
- Protein binding
Not Available
- Metabolism
- Not Available
- Route of elimination
Alemtuzumab is a large-molecule monoclonal antibody and as such, it is cleared primarily through target-mediated clearance and through simple non-target specific IgG clearance mechanisms. Alemtuzumab is not excreted renally or eliminated via cytochrome P450 (CYP450) isoenzymes.6 Alemtuzumab is most likely removed by opsonization via the reticuloendothelial system when bound to B or T lymphocytes.1
- Half-life
The elimination half-life was approximately 2 weeks and was comparable between courses. The serum concentrations were generally undetectable (<60 ng/mL) within approximately 30 days following each treatment course.4
- Clearance
Clearance of alemtuzumab ranged from 0.012 – 0.096 l/h depending on the study, dose group, and anti-alemtuzumab antibody status. The inter-subject variability for clearance was large (58 %). Higher clearance values were observed in cycle 1 compared to cycle 2, with the decrease in clearance from cycle 1 to cycle 2 being less than 20%.6
- Adverse Effects
Improve decision support & research outcomesWith structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates.Improve decision support & research outcomes with our structured adverse effects data.- Toxicity
LEMTRADA induces persistent thyroid disorders [see Warnings and Precautions (5.8)]. Untreated hypothyroidism in pregnant women increases the risk of miscarriage and may have effects on the fetus including mental retardation and dwarfism. In mothers with Graves’ disease, maternal thyroid stimulating hormone receptor antibodies can be transferred to a developing fetus and can cause neonatal Graves’ disease. In a patient who developed Graves’ disease after treatment with alemtuzumab, placental transfer of anti-thyrotropin receptor antibodies resulted in neonatal Graves’ disease with thyroid storm in her infant who was born 1 year after alemtuzumab dosing.4
When LEMTRADA was administered to pregnant huCD52 transgenic mice during organogenesis (gestation days [GD] 6-10 or GD 11-15) at doses of 3 or 10 mg/kg IV, no teratogenic effects were observed. However, there was an increase in embryo lethality (increased postimplantation loss and the number of dams with all fetuses dead or resorbed) in pregnant animals dosed during GD 11-15. In a separate study in pregnant huCD52 transgenic mice, administration of LEMTRADA during organogenesis (GD 6-10 or GD 11-15) at doses of 3 or 10 mg/kg IV, decreases in B- and T-lymphocyte populations were observed in the offspring at both doses tested.4
In pregnant huCD52 transgenic mice administered LEMTRADA at doses of 3 or 10 mg/kg/day IV throughout gestation and lactation, there was an increase in pup deaths during the lactation period at 10 mg/kg. Decreases in T- and B-lymphocyte populations and in antibody response were observed in offspring at both doses tested.4
Before initiation of LEMTRADA treatment, women of childbearing potential should be counseled on the potential for serious risk to the fetus. To avoid in-utero exposure to LEMTRADA, women of childbearing potential should use effective contraceptive measures when receiving a course of treatment with LEMTRADA and for 4 months following that course of treatment.4
In huCD52 transgenic mice, administration of LEMTRADA prior to and during the mating period resulted in adverse effects on sperm parameters in males and a reduced number of corpora lutea and implantations in females.4
Two MS patients experienced serious reactions (headache, rash, and either hypotension or sinus tachycardia) after a single accidental infusion of up to 60 mg of LEMTRADA. Doses of LEMTRADA greater than those recommended may increase the intensity and/or duration of infusion reactions or their immune effects. There is no known antidote for alemtuzumab overdosage.4
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbatacept The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Abatacept. Abciximab The risk or severity of bleeding can be increased when Abciximab is combined with Alemtuzumab. Acenocoumarol The risk or severity of bleeding can be increased when Acenocoumarol is combined with Alemtuzumab. Acetylsalicylic acid The risk or severity of bleeding can be increased when Acetylsalicylic acid is combined with Alemtuzumab. Adalimumab The risk or severity of adverse effects can be increased when Adalimumab is combined with Alemtuzumab. Adenovirus type 7 vaccine live The risk or severity of infection can be increased when Adenovirus type 7 vaccine live is combined with Alemtuzumab. Aducanumab The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Aducanumab. Aldesleukin The risk or severity of adverse effects can be increased when Aldesleukin is combined with Alemtuzumab. Alefacept The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Alefacept. Alirocumab The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Alirocumab. 
Identify potential medication risksEasily compare up to 40 drugs with our drug interaction checker.Get severity rating, description, and management advice.Learn more - Food Interactions
- No interactions found.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Campath Injection 30 mg/1mL Intravenous Bayer 2009-04-20 2011-10-31 US 
Campath Injection 30 mg/1mL Intravenous Genzyme Corporation 2009-11-30 Not applicable US Lemtrada Injection, solution, concentrate 12 mg/1.2mL Intravenous Genzyme Corporation 2014-11-18 Not applicable US Lemtrada Solution 12 mg / 1.2 mL Intravenous Sanofi Genzyme, a Division of Sanofi Aventis Canada Inc 2014-01-29 Not applicable Canada 
Lemtrada Injection, solution, concentrate 12 mg Intravenous Sanofi Belgium 2020-12-22 Not applicable EU 
Mabcampath Solution 10 mg / mL Intravenous Genzyme Corporation 2006-05-01 2008-08-07 Canada Mabcampath Solution 30 mg / mL Intravenous Sanofi Genzyme, a Division of Sanofi Aventis Canada Inc 2007-09-07 Not applicable Canada
Categories
- ATC Codes
- L04AA34 — Alemtuzumab
- Drug Categories
- Amino Acids, Peptides, and Proteins
- Antibodies
- Antibodies, Monoclonal
- Antibodies, Monoclonal, Humanized
- Antineoplastic Agents
- Antineoplastic Agents, Immunological
- Antineoplastic and Immunomodulating Agents
- Blood Proteins
- Cancer immunotherapy
- CD52-directed Antibody Interactions
- CD52-directed Cytolytic Antibody
- Globulins
- Immunoglobulins
- Immunoproteins
- Immunosuppressive Agents
- Immunotherapy
- Myelosuppressive Agents
- Narrow Therapeutic Index Drugs
- Proteins
- Selective Immunosuppressants
- Serum Globulins
- Chemical TaxonomyProvided by Classyfire
- Description
- Not Available
- Kingdom
- Organic Compounds
- Super Class
- Organic Acids
- Class
- Carboxylic Acids and Derivatives
- Sub Class
- Amino Acids, Peptides, and Analogues
- Direct Parent
- Peptides
- Alternative Parents
- Not Available
- Substituents
- Not Available
- Molecular Framework
- Not Available
- External Descriptors
- Not Available
- Affected organisms
- Not Available
Chemical Identifiers
- UNII
- 3A189DH42V
- CAS number
- 216503-57-0
References
- General References
- Hale G, Bright S, Chumbley G, Hoang T, Metcalf D, Munro AJ, Waldmann H: Removal of T cells from bone marrow for transplantation: a monoclonal antilymphocyte antibody that fixes human complement. Blood. 1983 Oct;62(4):873-82. [Article]
- Riechmann L, Clark M, Waldmann H, Winter G: Reshaping human antibodies for therapy. Nature. 1988 Mar 24;332(6162):323-7. [Article]
- FDA Approved Drug Products: LEMTRADA (alemtuzumab) injection [Link]
- FDA Approved Drug Products: LEMTRADA (alemtuzumab) injection 2022 [Link]
- FDA Approved Products: CAMPATH (alemtuzumab) intravenous injection [Link]
- Assessment report: Lemtrada (International non-proprietary name ALEMTUZUMAB) [Link]
- External Links
- PubChem Substance
- 46507379
- 117055
- ChEMBL
- CHEMBL1201587
- Therapeutic Targets Database
- DAP000385
- PharmGKB
- PA164783958
- RxList
- RxList Drug Page
- Drugs.com
- Drugs.com Drug Page
- Wikipedia
- Alemtuzumab
- MSDS
- Download (39.4 KB)
Clinical Trials
- Clinical Trials
Phase Status Purpose Conditions Count 4 Completed Not Available End Stage Renal Disease (ESRD) / Living Donors 1 4 Completed Basic Science Relapsing Remitting Multiple Sclerosis (RRMS) 1 4 Completed Prevention Kidney Diseases / Kidney Failure / Kidney Transplantation 1 4 Completed Prevention Kidney Failure, Kidney Transplant 1 4 Completed Prevention Transplanted Organ Rejection 1 4 Completed Treatment Kidney Transplantation 3 4 Completed Treatment Living-Donor Kidney Transplants 1 4 Completed Treatment Multiple Sclerosis 2 4 Completed Treatment Relapsing Remitting Multiple Sclerosis (RRMS) 2 4 Recruiting Treatment Relapsing Remitting Multiple Sclerosis (RRMS) 1
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Bayer Healthcare
- Boehringer Ingelheim Ltd.
- Genzyme Inc.
- ILEX Pharmaceuticals LP
- Dosage Forms
Form Route Strength Injection Intravenous 30 mg/1mL Injection, solution, concentrate Intravenous 12 mg/1.2mL Injection, solution, concentrate Intravenous 12 mg Injection, solution, concentrate Intravenous; Parenteral 12 MG Solution Intravenous 12 mg / 1.2 mL Injection, solution, concentrate Solution Intravenous 12 mg/1.2ml Solution Intravenous 12 mg Injection, solution, concentrate Intravenous Solution Intravenous 10 mg / mL Solution Intravenous 30 mg / mL Solution, concentrate Intravenous Solution Intravenous 30 mg Solution Intravenous - Prices
Unit description Cost Unit Campath 30 mg/ml Solution (1 Box Contains Three 1ml Vials) 6179.24USD box Campath 30 mg/ml vial 2042.18USD ml DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region CA1339198 No 1997-08-05 2014-08-05 Canada
Properties
- State
- Liquid
- Experimental Properties
Property Value Source melting point (°C) 61 °C (FAB fragment), 71 °C (whole mAb) Vermeer, A.W.P. & Norde, W., Biophys. J. 78:394-404 (2000) hydrophobicity -0.431 Not Available isoelectric point 8.76 Not Available
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Antibody
- General Function
- Not Available
- Specific Function
- May play a role in carrying and orienting carbohydrate, as well as having a more specific role.
- Gene Name
- CD52
- Uniprot ID
- P31358
- Uniprot Name
- CAMPATH-1 antigen
- Molecular Weight
- 6613.67 Da
References
- Gilliland LK, Walsh LA, Frewin MR, Wise MP, Tone M, Hale G, Kioussis D, Waldmann H: Elimination of the immunogenicity of therapeutic antibodies. J Immunol. 1999 Mar 15;162(6):3663-71. [Article]
- James LC, Hale G, Waldmann H, Bloomer AC: 1.9 A structure of the therapeutic antibody CAMPATH-1H fab in complex with a synthetic peptide antigen. J Mol Biol. 1999 Jun 4;289(2):293-301. [Article]
- Rawstron AC, Rollinson SJ, Richards S, Short MA, English A, Morgan GJ, Hale G, Hillmen P: The PNH phenotype cells that emerge in most patients after CAMPATH-1H therapy are present prior to treatment. Br J Haematol. 1999 Oct;107(1):148-53. [Article]
- Rebello PR, Hale G, Friend PJ, Cobbold SP, Waldmann H: Anti-globulin responses to rat and humanized CAMPATH-1 monoclonal antibody used to treat transplant rejection. Transplantation. 1999 Nov 15;68(9):1417-20. [Article]
- Hederer RA, Guntermann C, Miller N, Nagy P, Szollosi J, Damjanovich S, Hale G, Alexander DR: The CD45 tyrosine phosphatase regulates Campath-1H (CD52)-induced TCR-dependent signal transduction in human T cells. Int Immunol. 2000 Apr;12(4):505-16. [Article]
- Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
- Geissinger E, Bonzheim I, Roth S, Rosenwald A, Muller-Hermelink HK, Rudiger T: CD52 expression in peripheral T-cell lymphomas determined by combined immunophenotyping using tumor cell specific T-cell receptor antibodies. Leuk Lymphoma. 2009 Jun;50(6):1010-6. doi: 10.1080/10428190902926981. [Article]
- Quintas-Cardama A, O'Brien S: Targeted therapy for chronic lymphocytic leukemia. Target Oncol. 2009 Jan;4(1):11-21. doi: 10.1007/s11523-008-0099-0. Epub 2009 Jan 27. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Not Available
- Specific Function
- Receptor for the Fc region of immunoglobulins gamma. Low affinity receptor. Binds complexed or aggregated IgG and also monomeric IgG. Contrary to III-A, is not capable to mediate antibody-dependent...
- Gene Name
- FCGR3B
- Uniprot ID
- O75015
- Uniprot Name
- Low affinity immunoglobulin gamma Fc region receptor III-B
- Molecular Weight
- 26215.64 Da
References
- Nagler A, Condiotti R, Lubina A, Deutsch VR: Enhancement of megakaryocytopoiesis by Campath-1G-treated natural killer cells. Bone Marrow Transplant. 1997 Oct;20(7):525-31. [Article]
- Brett S, Baxter G, Cooper H, Johnston JM, Tite J, Rapson N: Repopulation of blood lymphocyte sub-populations in rheumatoid arthritis patients treated with the depleting humanized monoclonal antibody, CAMPATH-1H. Immunology. 1996 May;88(1):13-9. [Article]
- Osterborg A, Werner A, Halapi E, Lundin J, Harmenberg U, Wigzell H, Mellstedt H: Clonal CD8+ and CD52- T cells are induced in responding B cell lymphoma patients treated with Campath-1H (anti-CD52). Eur J Haematol. 1997 Jan;58(1):5-13. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Not Available
- Specific Function
- Receptor for the Fc region of IgG. Binds complexed or aggregated IgG and also monomeric IgG. Mediates antibody-dependent cellular cytotoxicity (ADCC) and other antibody-dependent responses, such as...
- Gene Name
- FCGR3A
- Uniprot ID
- P08637
- Uniprot Name
- Low affinity immunoglobulin gamma Fc region receptor III-A
- Molecular Weight
- 29088.895 Da
References
- Lin TS, Flinn IW, Modali R, Lehman TA, Webb J, Waymer S, Moran ME, Lucas MS, Farag SS, Byrd JC: FCGR3A and FCGR2A polymorphisms may not correlate with response to alemtuzumab in chronic lymphocytic leukemia. Blood. 2005 Jan 1;105(1):289-91. Epub 2004 Jun 24. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Receptor signaling protein activity
- Specific Function
- High affinity receptor for the Fc region of immunoglobulins gamma. Functions in both innate and adaptive immune responses.
- Gene Name
- FCGR1A
- Uniprot ID
- P12314
- Uniprot Name
- High affinity immunoglobulin gamma Fc receptor I
- Molecular Weight
- 42631.525 Da
References
- White AL, Chan HT, French RR, Beers SA, Cragg MS, Johnson PW, Glennie MJ: FcgammaRIotaIotaB controls the potency of agonistic anti-TNFR mAbs. Cancer Immunol Immunother. 2013 May;62(5):941-8. doi: 10.1007/s00262-013-1398-6. Epub 2013 Mar 31. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Not Available
- Specific Function
- Binds to the Fc region of immunoglobulins gamma. Low affinity receptor. By binding to IgG it initiates cellular responses against pathogens and soluble antigens. Promotes phagocytosis of opsonized ...
- Gene Name
- FCGR2A
- Uniprot ID
- P12318
- Uniprot Name
- Low affinity immunoglobulin gamma Fc region receptor II-a
- Molecular Weight
- 35000.42 Da
References
- Lin TS, Flinn IW, Modali R, Lehman TA, Webb J, Waymer S, Moran ME, Lucas MS, Farag SS, Byrd JC: FCGR3A and FCGR2A polymorphisms may not correlate with response to alemtuzumab in chronic lymphocytic leukemia. Blood. 2005 Jan 1;105(1):289-91. Epub 2004 Jun 24. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Not Available
- Specific Function
- Receptor for the Fc region of complexed or aggregated immunoglobulins gamma. Low affinity receptor. Involved in a variety of effector and regulatory functions such as phagocytosis of immune complex...
- Gene Name
- FCGR2B
- Uniprot ID
- P31994
- Uniprot Name
- Low affinity immunoglobulin gamma Fc region receptor II-b
- Molecular Weight
- 34043.355 Da
References
- White AL, Chan HT, French RR, Beers SA, Cragg MS, Johnson PW, Glennie MJ: FcgammaRIotaIotaB controls the potency of agonistic anti-TNFR mAbs. Cancer Immunol Immunother. 2013 May;62(5):941-8. doi: 10.1007/s00262-013-1398-6. Epub 2013 Mar 31. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Transmembrane signaling receptor activity
- Specific Function
- Receptor for the Fc region of complexed immunoglobulins gamma. Low affinity receptor. Involved in a variety of effector and regulatory functions such as phagocytosis of immune complexes and modulat...
- Gene Name
- FCGR2C
- Uniprot ID
- P31995
- Uniprot Name
- Low affinity immunoglobulin gamma Fc region receptor II-c
- Molecular Weight
- 35577.96 Da
References
- White AL, Chan HT, French RR, Beers SA, Cragg MS, Johnson PW, Glennie MJ: FcgammaRIotaIotaB controls the potency of agonistic anti-TNFR mAbs. Cancer Immunol Immunother. 2013 May;62(5):941-8. doi: 10.1007/s00262-013-1398-6. Epub 2013 Mar 31. [Article]
Drug created at June 13, 2005 13:24 / Updated at December 04, 2022 18:48