JN Biosciences LLC

September 17, 2018

The therapeutic activity of HuABC2 in kidney transplantation was reported in a paper entitled "CD122 signaling in CD8+ memory T cells drivescostimulation-independent rejection" by Mathews et al. (J. Clin. Invest. online published on Sept. 17, 2018).  HuABC2 with belatacept (CTLA4-Ig) prolonged monkey survival much better than belatacept alone in a life-sustaining fully-MHC-mismatched renal allograft study.  While HuABC2 together with belatacept effectively suppressed immune reactions against renal allografts, suppression of Treg cells was not observed.  This study was conducted as a collaboration between JN Biosciences and Dr. Andrew Adams' lab at Emory University.  

August 21, 2018

A new U.S. patent (10053517) was issued for JN Bioscience' MultYmab™ antibody engineering platform, which strengthens the company's IP position for application of this technology to generate potent agonist antibodies against a wide range of membrane-bound proteins, including immune costimulatory molecules such as OX40, 4-1BB and ICOS, that trigger signal transduction upon multivalent cross-linking.  

July 18, 2018

The potent therapeutic activity of an anti-CD122 antibody for treatment of vitiligo in a mouse disease model was published in a paper entitled "Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo" (Richmond et al., Science Translational Medicine 2018 10:eaam7710).  Short-term administration of anti-CD122 either systemically or locally in the skin provided durable repigmentation in mice with established vitiligo.  This study was conducted as a collaboration between JN Biosciences and Dr. John Harris' lab at University of Massachusetts.

January 25, 2018

The positive therapeutic effect of an anti-CD122 antibody on type I diabetes in a NOD mouse model, which was carried out as a collaboration between JN Biosciences and Dr. Wenxian Fu's lab at University of California at San Diego, was published in a paper entitled "CD122 blockade restores immunological tolerance in autoimmune type 1 diabetes via multiple mechanisms" (Yuan et al. JCI insight 2018 3(2):e96600).  Anti-CD122 (ChMBC7) treatment selectively ablated NK and  CD8+  T cells, but not Treg cells, from pancreatic islets in NOD mice, and restored immune tolerance in type 1 diabetes.