Monoclonal antibodies have traditionally been produced in a mouse. Why a mouse? Because, as a host, it is cost effective, easy to manage, and truly a standard in many biotechnology applications.  But manufacturers and technicians alike have seen the limitations of mouse monoclonals, in that the resulting antibodies can have low affinities, which means that they have a weak attraction to bind to the protein targets. At times, the affinities are so low that extreme pretreatments, such as boiling the tissue sections, must be employed to modify the target, so that the low affinity antibody has a better chance to bind.  Others have used special diluents to obtain better antibody-to-target binding.  By modifying the pH and the salts in the buffers and/or diluents, the antibody can be modified such that it is in its optimal binding state.  Like pretreaments, this too will only optimize an already low affinity antibody.  So, instead of modifying the target, or the diluent, to give a weak antibody a better chance to bind, why not produce a higher affinity antibody?  Rabbit Monoclonal rabbit monoclonal rabbit monoclonal Rabbit monoclonal rabbit monoclonal 

That is EXACTLY what we have done!  The concept itself is simple.  Antibodies produced by rabbits are known to have a HIGHER AFFINITY than antibodies raised in mice.  Cloning techniques produce highly specific antibodies.  Additionally, the rabbit immuno-response recognizes antigens (epitopes) that are not immunogenic in mice.  Our technique combines these two production methods to produce… a RABBIT MONOCLONAL.  The resulting rabbit monoclonal antibody has ten times the affinity of the mouse antibody, thus resulting in a more SPECIFIC and much more SENSITIVE antibody.   Rabbit Monoclonal rabbit monoclonal rabbit monoclonal Rabbit monoclonal rabbit monoclonal 

Not surprisingly, our in-house studies with these RaMAb’s have shown that pretreaments may no longer be necessary to achieve optimal staining results, but may only be needed to standardize the tissue conditions.  This technique will continue to be employed to produce other important markers, for Ki67, Cyclin D1, and CD3, antibodies that historically are difficult in immunohistochemical applications.

References:

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   Diagn Cytopathol, 2003 Oct; 29(4): 207 -11. Click here to view this publication.
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   *Department of Pathology,Northwestern University, Chicago,+ Department of Pathology, University of Texas, Huston
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   Abstract presented at USCAP 2004. Modern Pathology 2004; 17 (suppl 1): 361A
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   Hartford Hospital, Hartford, CT.
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   Abstract presented at USCAP 2004. Modern Pathology 2004; 17 (suppl 1): 241A
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   Department of Pathology, Queen Elizabeth Hospital, Hong Kong
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   Cleveland Clinic Foundation, Cleveland, OH .
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    Department of Pathology and Laboratory Medicine. The Cleveland Clinic Foundation, Cleveland, Ohio. Lab Vision Corp., Fremont, Ca., Spring Bioscience Corp, Fremont ,CA
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    Abstract presented at Association for Molecular Pathology meeting, Los Angeles, 2004
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    Clinical Research Division , PhenoPath Laboratories and IMPRIS, Seattle, WA, USA
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    Abstract presented at USCAP 2005. Modern Pathology 2005; 18, suppl.1,pag 35A
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    Clinical Research Division , PhenoPath Laboratories and IMPRIS, Seattle, WA, USA
    Genetic Pathology Evaluation Centre, University of British Columbia, Vancouver, BC, Canada " "Significantly improved sensitivity for ER detection in breast cancer using a new rabbit monoclonal anti-ER antibody (SP1)"
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    1} Depart. Pathology, Hospital of Treviso, Italy, 2 Brescia University School of Medicine, Brescia, Italy
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