Preclinical Projects

Affimed has built a discovery engine which includes the
generation of TandAbs and Trispecific Abs for its own pipeline
or for the development in the context of partnerships.

 
 
     
 
 

AFM24 / AFM26

 
   
 
 
 
 
 
AFM24   About EGFRwt
 
   
 
The Epidermal Growth Factor Receptor wild type (EGFRwt) is ubiquitously expressed in healthy epithelial tissues, but, when constitutively activated through binding by growth factors or mutations, plays an important role in the pathophysiology of numerous solid cancers such as colorectal, lung or head and neck cancer. A number of EGFR-targeting drugs have been approved to treat solid tumors including tyrosine kinase inhibitors and monoclonal antibodies, but despite demonstrated clinical activity, intrinsic or acquired resistance is frequently observed. Displaying significant advances over IgG-based antibodies in recruiting NK-cells, AFM24 has the potential to overcome these limitations.   AFM24 specifically binds to Epidermal Growth Factor Receptor wild type (EGFRwt) on solid tumor cells. AFM24 is an NK-cell engaging TandAb targeting CD16A. Both targets are bound with high affinity, whereby NK-cells are redirected and activated to kill the cancer cells. AFM24 selectively binds to EGFRwt but not EGFRvIII. Importantly, AFM24 has demonstrated tumor cell killing independent of their mutational status (e.g. ras). AFM24 is in preclinical development for the treatment of solid tumors overexpressing EGFRwt.   
 
     
 
AFM26   About BCMA
 
   
 
AFM26 specifically binds to B-cell maturation antigen (BCMA) on myeloma cells. AFM26 is tetravalent bispecific NK-cell engager targeting CD16A. Both targets are bound with high affinity, whereby NK-cells are redirected and activated to kill the cancer cells. AFM26 interacts bivalently with NK-cells, resulting in high avidity, prolonged cell surface retention and potent induction of NK-cell-mediated in vitro lysis of target cells. Binding and cytotoxicity are not impaired at high levels of polyclonal IgG, suggesting that, AFM26, in contrast to classical mAbs, retains full ADCC activity at high serum IgG levels. This is particularly important as about half of multiple myeloma patients present with high levels of IgG-type M-protein.   While new treatments of multiple myeloma have been developed recently, an unmet need remains as most patients eventually relapse and/or become refractory to currently available treatments. B-cell maturation antigen (BCMA, CD269) has emerged as a particularly attractive target due to its limited expression on healthy tissues and almost universal expression on myeloma cells in the majority of patients.
 
 



Posters
AACR 2017 – AFM24  
   
AACR 2017 – AFM26  
   
 
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