We have seen how results of bavi in trials depend on which combination drug is used. Is it possible that bavi could be combined with a different drug (say a downstream immuno drug) or other to fight HCV?
Shigekazu Nagata, Kyoto University, Japan Exposure of phosphatidylserine during apoptosis
In the previous post, Nagata went to Canada in 2013 and Brazil in 2014 (Keystone Symposia events..), talking exposure of Phosphatidylserine. Now, this Japanese based lab, is "ALL" about targeting phosphatidylserine. Shigekazu is the expert of "Interferon", just as Peregrine KOL Dmitry Gabrilovich is the expert of MDSC's.
I believe that Nagata knows very well that targeting flipped-PS, is far superior than interferon, or better yet, replace all combinations from Interferon to a PS Targeting based drug, such as Bavituximab.
Peregrine's Joe Shan already discussed that as well, from the prior post:
"We are pleased with the initial results we have seen from this clinical study evaluating the combination of bavituximab with an established antiviral drug in HCV patients. We see good evidence that the combination of bavituximab with ribavirin has a better safety profile than an interferon containing regimen which was one of the primary objectives of the study," said Joseph S. Shan, vice president of clinical and regulatory affairs at Peregrine Pharmaceuticals.
So whats new ?? Nothing... Nagata lab still fully concentrating on Phosphatidylserine, and who has all those patents for targeting flipped Phosphatidylserine ? Peregrine Pharmaceuticals
Exposure of phosphatidylserine by Xk-related protein family members during apoptosis
Sept 17, 2014
Abstract
Apoptotic cells expose phosphatidylserine (PtdSer) on their surface as an eat me signal. Mammalian Xk-related (Xkr) protein 8, which is predicted to contain 6 transmembrane regions, and its Caenorhabditis elegans homolog CED-8 promote apoptotic PtdSer exposure. The mouse and human Xkr families consist of 8 and 9 members, respectively. Here, we found that mouse Xkr-family members, with the exception of Xkr2, are localized to the plasma membrane. When Xkr8-deficient cells, which do not expose PtdSer during apoptosis, were transformed by mXkr family members, the transformants expressing Xkr4, Xkr8, or Xkr9 responded to apoptotic stimuli by exposing cell-surface PtdSer and were efficiently engulfed by macrophages. Like Xkr8, Xkr4 and Xkr9 were found to possess a caspase-recognition site in the C-terminal region and to require its direct cleavage by caspases for their function. Site-directed mutagenesis of the amino acid residues conserved among CED-8, Xkr4, Xkr8, and Xkr9 identified several essential residues in the second transmembrane and second cytoplasmic regions. Real-time PCR analysis indicated that unlike Xkr8, which is ubiquitously expressed, Xkr4 and Xkr9 expression is tissue-specific.
Douglas Green; Marie-Lise Gougeon; Michael Hengartner; H. Robert Horvitz; Marja Jäättelä; Adi Kimchi;Sharad Kumar; Sergio Lavandero; Richard A. Lockshin; Carlos Martínez; Shigekazu Nagata; Don Nicholson; Mauro Piacentini; Jun-Ying Yuan; Boris Zhivotovsky
..... so now we have Nagata, a big PS Targeting researcher with ties to ICDS, International Cell Death Society and maybe its just coincidence, but there seems to be much interest in various parts of the world and ICDS next meeting, in Iran Oct 14