“In 2016, I hope that there will be significant progress in the treatment of brain tumors with hopefully positive trials of the EGFRvIII vaccine rindopepimut for newly diagnosed glioblastomas and checkpoint inhibitors for recurrent glioblastomas. 2016 will hopefully also see the launch of major Bayesian biomarker-driven adaptive design trials such as INSIGHT and GBM AGILE that will hopefully accelerate the development of new therapies for our patients.” – Dr. Patrick Wen, Dana-Farber Cancer Institute
Aduro and Celldex have almost identical charts over the last month. Seems to be a common theme driving down stocks with antibody and vaccine platforms. Sorrento is in same boat.
23 trials now registered in EGFV111 for companies. Duke is doing Car-T EGFVv111 for glioblastoma. Seems Celldex started that trend. There appears to be too much literature any more around these mechanism of action around glio. Many of the other companies are trying to combine dual mechanism of action along with their EGFRV111. What appears to be the case is the market needs EGFRv111 mechanism of action and it will take years to find the right combo but anything is more than evident that Rindo needs to be approved to further development around glio and give confidence to others following steps. Rindo approval will only be the first step in cancer combination therapy for glioblastoma..
Celldex has checked in a lot of the current trials on going over the last 2 months. I expect a full 2016 report pretty soon. Noticed the Rindo study in newly diagnosed patients is probably ready for a glance around January. This below is one of the most important.
I encourage everyone to visit clinicaltrials.gov who invests in biotech to check whats going on.
A Study of Varlilumab (Anti-CD27) and Ipilimumab and CDX-1401 in Patients With Unresectable Stage III or IV Melanoma
This study is currently recruiting participants. (see Contacts and Locations)
Verified November 2015 by Celldex Therapeutics
Information provided by (Responsible Party):
First received: March 25, 2015
Last updated: November 16, 2015
Last verified: November 2015
History of Changes
All of cancers have combination therapy but the unique thing is that the mechanism are no longer break you down and hope the body can recover. Actually the data is suggesting that BET Inhibitors are going to be synergistic with EGFRV111. Rintega and GPNMB have not even scratched the surface on their possible combinations. That is why many other companies are also exploring the EGFRV111 not EGFR but specifically the site where Rintega works.
Epidermal growth factor receptor (EGFR) gene amplification and mutations are the most common oncogenic events in glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, genotyped clinical samples, and TCGA data, we show that EGFR mutations remodel the activated enhancer landscape of GBM, promoting tumorigenesis through a SOX9 and FOXG1-dependent transcriptional regulatory network in vitro and in vivo. The most common EGFR mutation, EGFRvIII, sensitizes GBM cells to the BET-bromodomain inhibitor JQ1 in a SOX9, FOXG1-dependent manner. These results identify the role of transcriptional/epigenetic remodeling in EGFR-dependent pathogenesis and suggest a mechanistic basis for epigenetic therapy.