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Fourth Midkine Symposium 

Budapest, Hungary | 28-30 April, 2016


The Fourth Midkine Symposium was held in Budapest, Hungary.

Following from the success of previous meetings, held in Sydney,  Istanbul, and Kyoto, the 4th symposium highlighted significant advances in midkine research, with presentations by twenty scientists from 9 countries.  Scientists presented new evidence  supporting midkines role in inter-organ signalling in a number of diseases including chronic kidney disease and vascular calcification.  Studies on MK biology, structure, mechanism of action and clinical utility were also presented, with much  of  the  work  recently submitted or nearing submission for peer reviewed publication.

Some of the key messages of the meeting included the following:      

  • Dr  Ulrich  Grabmaier  from  Ludwig Maximilians  University  in Munich presented data on Cellmid’s C and N terminal binding MK antibodies in a mouse model  of  myocarditis. N  terminal binding MK  antibodies  showed  marked  efficacy  in  the  model  not  only  pointing  to  a  novel  potential  clinical  application  but also demonstrating the difference in efficacy  between the two MK antibodies.  This  important  information  on MK  biology  is  instructive  for  future  studies

  • Two of Cellmid’s MK  antibodies have shown tumour supressing ability in glioblastoma cell  lines  resistant  to  cannabinoid  treatment . Professor  Guillermo  Velasco  of  Complutense  University  in  Madrid, is continuing this work with  Cellmid’s  C and N terminal binding antibodies to assess efficacy in animal models of the  disease

  • Cellmid’s  N  terminal  binding  MK  antibody  enhanced  bone  fracture  healing  in ovariectomised  mice  in  vivo  in  studies  conducted  by  Dr  Astrid  Liedert  from  the  University of Ulm in Germany. The model mimics the biology of osteoporosis in postmenopausal women and representative of the delayed bone healing that occurs in  this population.  Further in vivo work is expected to uncover the mechanism by which  MK contributes to delayed bone healing

  • New  insights  were  presented  into  the  structure  of  MK’s  binding  with  glycosaminoglycans  (GAGs)  and  how  it  may  effect  biological  function.  These  findings  were  presented by Professor  Xu Wang from Arizona State University (on the closeley relatred molecule Plieotrophin) and Dr Pedro Nieto of  the  University of  Seville, Spain.    Further collaboration is expected with  both groups to ascertain the binding characteristics of MK in biological systems

  • MK human diagnostic work by three separate groups included further understanding on urinary MK in prostate and bladder cancers, as well as in patients with acute and chronic  kidney  disease.   Cellmid’s  clinical  adviser,  Dr  Victoria  Campbell presented  early evidence that MK may be an important marker of chronic kidney disease.   This work is ongoing and involves several clinical centres in Australia

  • MK clinical development plans with two and five years’  time horizons were discussed with  key  outcomes  around  uncovering  mechanism  of  action  in  disease  states, additional  academic  and  commercial  collaborations,  engaging  with  key  opinion leaders overseas and surrogate markers of efficacy identified as key milestones in an adaptive  plan,  in  addition  to  the  traditional  drug  development  milestones  of manufacture, pharmacodynamics, pharmacokinetics, safety and efficacy