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

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Associated Conditions
Associated Therapies
Contraindications & Blackbox Warnings
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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

TargetActionsOrganism
ACAMPATH-1 antigen
antibody
Humans
ULow affinity immunoglobulin gamma Fc region receptor III-B
binder
Humans
ULow affinity immunoglobulin gamma Fc region receptor III-A
binder
Humans
UHigh affinity immunoglobulin gamma Fc receptor I
binder
Humans
ULow affinity immunoglobulin gamma Fc region receptor II-a
binder
Humans
ULow affinity immunoglobulin gamma Fc region receptor II-b
binder
Humans
ULow affinity immunoglobulin gamma Fc region receptor II-c
binder
Humans
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
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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.
DrugInteraction
AbataceptThe risk or severity of adverse effects can be increased when Alemtuzumab is combined with Abatacept.
AbciximabThe risk or severity of bleeding can be increased when Abciximab is combined with Alemtuzumab.
AcenocoumarolThe risk or severity of bleeding can be increased when Acenocoumarol is combined with Alemtuzumab.
Acetylsalicylic acidThe risk or severity of bleeding can be increased when Acetylsalicylic acid is combined with Alemtuzumab.
AdalimumabThe risk or severity of adverse effects can be increased when Adalimumab is combined with Alemtuzumab.
Adenovirus type 7 vaccine liveThe risk or severity of infection can be increased when Adenovirus type 7 vaccine live is combined with Alemtuzumab.
AducanumabThe risk or severity of adverse effects can be increased when Alemtuzumab is combined with Aducanumab.
AldesleukinThe risk or severity of adverse effects can be increased when Aldesleukin is combined with Alemtuzumab.
AlefaceptThe risk or severity of adverse effects can be increased when Alemtuzumab is combined with Alefacept.
AlirocumabThe risk or severity of adverse effects can be increased when Alemtuzumab is combined with Alirocumab.
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Food Interactions
No interactions found.

Products

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Brand Name Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
CampathInjection30 mg/1mLIntravenousGenzyme Corporation2009-11-30Not applicableUS flag
CampathInjection30 mg/1mLIntravenousBayer2009-04-202011-10-31US flag
LemtradaInjection, solution, concentrate12 mgIntravenousSanofi Belgium2020-12-22Not applicableEU flag
LemtradaInjection, solution, concentrate12 mg/1.2mLIntravenousGenzyme Corporation2014-11-18Not applicableUS flag
LemtradaSolution12 mg / 1.2 mLIntravenousSanofi Genzyme, a Division of Sanofi Aventis Canada Inc2014-01-29Not applicableCanada flag
MabcampathSolution30 mg / mLIntravenousSanofi Genzyme, a Division of Sanofi Aventis Canada Inc2007-09-07Not applicableCanada flag
MabcampathSolution10 mg / mLIntravenousGenzyme Corporation2006-05-012008-08-07Canada flag

Categories

ATC Codes
L04AA34 — Alemtuzumab
Drug Categories
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
  1. 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]
  2. Riechmann L, Clark M, Waldmann H, Winter G: Reshaping human antibodies for therapy. Nature. 1988 Mar 24;332(6162):323-7. [Article]
  3. FDA Approved Drug Products: LEMTRADA (alemtuzumab) injection [Link]
  4. FDA Approved Drug Products: LEMTRADA (alemtuzumab) injection 2022 [Link]
  5. FDA Approved Products: CAMPATH (alemtuzumab) intravenous injection [Link]
  6. Assessment report: Lemtrada (International non-proprietary name ALEMTUZUMAB) [Link]
PubChem Substance
46507379
RxNav
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
PhaseStatusPurposeConditionsCount
4CompletedNot AvailableEnd Stage Renal Disease (ESRD) / Living Donors1
4CompletedBasic ScienceRelapsing Remitting Multiple Sclerosis (RRMS)1
4CompletedPreventionKidney Diseases / Kidney Failure / Kidney Transplantation1
4CompletedPreventionKidney Failure, Kidney Transplant1
4CompletedPreventionTransplanted Organ Rejection1
4CompletedTreatmentKidney Transplantation3
4CompletedTreatmentLiving-Donor Kidney Transplants1
4CompletedTreatmentMultiple Sclerosis2
4CompletedTreatmentRelapsing Remitting Multiple Sclerosis (RRMS)2
4RecruitingTreatmentRelapsing Remitting Multiple Sclerosis (RRMS)1

Pharmacoeconomics

Manufacturers
Not Available
Packagers
  • Bayer Healthcare
  • Boehringer Ingelheim Ltd.
  • Genzyme Inc.
  • ILEX Pharmaceuticals LP
Dosage Forms
FormRouteStrength
InjectionIntravenous30 mg/1mL
Injection, solution, concentrateIntravenous12 mg
Injection, solution, concentrateIntravenous12 mg/1.2mL
Injection, solution, concentrateIntravenous; Parenteral12 MG
SolutionIntravenous12 mg / 1.2 mL
Injection, solution, concentrate
SolutionIntravenous12 mg/1.2ml
SolutionIntravenous12 mg
Injection, solution, concentrateIntravenous
SolutionIntravenous10 mg / mL
SolutionIntravenous30 mg / mL
Solution, concentrateIntravenous
SolutionIntravenous30 mg
SolutionIntravenous
Prices
Unit descriptionCostUnit
Campath 30 mg/ml Solution (1 Box Contains Three 1ml Vials)6179.24USD box
Campath 30 mg/ml vial2042.18USD ml
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)Region
CA1339198No1997-08-052014-08-05Canada flag

Properties

State
Liquid
Experimental Properties
PropertyValueSource
melting point (°C)61 °C (FAB fragment), 71 °C (whole mAb)Vermeer, A.W.P. & Norde, W., Biophys. J. 78:394-404 (2000)
hydrophobicity-0.431Not Available
isoelectric point8.76Not Available

Targets

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insights and accelerate drug research.
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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
  1. 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]
  2. 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]
  3. 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]
  4. 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]
  5. 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]
  6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
  7. 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]
  8. 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
  1. 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]
  2. 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]
  3. 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
  1. 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
  1. 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
  1. 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
  1. 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
  1. 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 08, 2022 17:54