Avid Bioservices Inc (CDMO)

[biopharm]

Kolltan and PS Targeting: Part III

This is about showing some background and ties to Carla Vanina Rothlin <> Greg Lemke, because Kolltan buys out the IP patent rights of Xertrios/Greg Lemke..etc and if you have been following these posts along you should know this but just for a refresher below and if you are just joining this gets interesting because Greg Lemke is welcomed into UTSWM next month with Dr. Rolf Brekken as host.

-------------------------------------------------------------

Sept 9, 2014

Kolltan Pharmaceuticals, Inc., a privately held biopharmaceutical company focused on the discovery and development of novel antibody-based drugs targeting receptor tyrosine kinases (RTKs), today announced the acquisition of privately held Xetrios Therapeutics, Inc., a company founded in 2009 by Greg Lemke, Ph.D., of the Salk Institute for Biological Studies in San Diego, California, Carla Rothlin, Ph.D., of Yale University, and biotech entrepreneur Lawrence C. Fritz, Ph.D. Through this acquisition, Kolltan has secured exclusive intellectual property (IP) rights focused on human therapeutics targeting the TAM RTK family.

http://www.businesswire.com/news/home/20140909006407/en/Kolltan-Pharmaceuticals-Acquires-Xetrios-Therapeutics-Exclusive-Rights#.Vgbq55f76So

-----------------------------------------------

Lawrence C. Fritz ?? funny how this name has not been brought up, yet he is big into PS Targeting...and Kolltan was very much aware how important PS Targeting would be..

https://www.linkedin.com/pub/larry-fritz/51/b/352

My question is Peregrine Pharmaceuticals has the full IP rights on targeting flipped PS and how the hell could a patent agent allow this one below to be approved ??? .... and the same Greg Lemke is welcomed into UTSWM next month...

REGULATING THE INTERACTION BETWEEN TAM LIGANDS AND LIPID MEMBRANES WITH EXPOSED PHOSPHATIDYL SERINE

Application number: 20150164800
Abstract: The present disclosure provides methods for modulating the interaction between a TAM ligand and a lipid membrane containing phosphatidylserine (PtdSer). In one example, such methods use a TAM receptor agonist having a PtdSer-containing lipid bilayer membrane with Gas6 and/or Protein S bound to the membrane to activate signaling from one or more TAM receptors and treat an autoimmune disease. In another example, methods are provided for treating a subject with a pathological condition characterized by overactivation of TAM signaling and/or reduction in Type I IFN response, such as infection by an enveloped virus, by use of agents that decrease the interaction between a TAM ligand and PtdSer. Also provided are methods for classifying a virus as susceptible to anti-TAM therapy. Methods of identifying an agent that blocks virus infectivity are also provided.

Type: Application
Filed: July 23, 2013
Issued: June 18, 2015
Assignees: Xetrios Therapeutics, Inc., Salk Institute For Biological Studies
Inventors: Greg E. Lemke, Lawrence C. Fritz, Benedikt Vollrath, Carla V. Rothlin

http://patents.justia.com/inventor/lawrence-c-fritz

---------------------------------------------------

Video - Published on Nov 14, 2013 (if you're still following along, you should watch the videos by Carla Rothlin because it follows exactly along what Greg Lemke has been saying...)

Carla V. Rothlin, PhD, assistant professor of immunobiology at Yale School of Medicine, and postdoctoral associate Eugenio A. Carrera Silva, Ph.D., discuss their findings regarding the role of protein S in tempering the immune response.

Our body's battlefield: The role of protein S in the immune response

------------------------------------------------

August 12, 2014

Researchers reveal weakness in defenses of deadly brain tumor

Glioblastoma is a complex, deadly, and hard-to-treat brain cancer, but Yale School of Medicine researchers may have found the tumor’s Achilles heel.

The researchers report in the Aug. 12 issue of the journal Science Signaling that targeting a protein crucial in the early development of the brain can block multiple signaling pathways implicated in glioblastoma growth. The approach also reduced human tumors in mouse models of the disease.

“In neurodevelopment, this protein (atyptical protein kinase or aPKC) helps regulate proliferation and migration of cells but when active in adults, can cause formation and spread of cancer,” said Sourav Ghosh, assistant professor of neurology and co-senior author of the paper.

About 13,000 people die of primary malignant brain tumors annually in the United States. Glioblastomas are particularly hard to treat because these tumors grow rapidly, spread quickly, and respond poorly to current anti-tumor therapies.

The new study shows that targeting this protein works in several ways. Inhibiting aPKC blocks a signal pathway that is the target of existing glioblastoma therapy. But it also blocks the action of some immune system cells called macrophages, which instead of attacking tumors, actively promote their growth.

Glioblastomas are hard to treat because they grow rapidly, spread quickly, and are resistant to current treatments.

“This is exciting because it ends up targeting multiple pathways involved in cancer,” said Carla Rothlin, Yale Cancer Center member and assistant professor of immunobiology and co-senior author of the paper.

The work was funded by the National Institutes of Health.

Yael Kusne of Arizona State University and Eugenio Carrera-Silva, of Yale are co-lead authors of the paper.

http://medicine.yale.edu/news/article.aspx?id=7824

----------------------------------------------------