Drug discovery firm AdAlta has partnered with biotech company GPCR Therapeutics to study the former’s CXCR4 inhibiting i-bodies as cancer therapeutics, using the latter’s proprietary combination inhibition approach.
As part of the collaboration, AdAlta will provide a panel of its CXCR4-inhibiting i-bodies. The i-bodies will be tested in along with a number of generic beta-blocking compounds from GPCR Therapeutics’ own platforms that block the B2AR GPCR.
The study is intended to examine how in vitro cell signalling, cell migration, and cell death is affected by the combination suppression of CXCR4 and B2AR.
GPCR Therapeutics will test the combined inhibition of these drugs in vivo in mice cancer models, if they are successful.
Under the deal, AdAlta will have the first option to licence and further commercialise products developed as a consequence of those trials if they are successful. If AdAlta does not exercise this option, GPCR Therapeutics will have the same choice.
Under these options, the parties have agreed that subject to development success, whichever is the licensee will pay the other pre-agreed up-front option exercise costs, development milestones, commercialization milestones, and low- to mid-single-digit royalties on sales.
GPCR Therapeutics CEO Dong Seung Seen said: “We are pleased to be working with AdAlta’s expert team to explore synergies between our approach for combination inhibition of GPCRs and AdAlta’s i-body technology.
“We believe combining AdAlta’s unique i-body technology with our innovative CXCR4 combination therapy-based approach could lead to best-in-class anticancer drugs.”
The i-body technology from AdAlta is made for interacting with a class of drug targets called G-protein coupled receptors (GPCRs) which include CXCR4.
AdAlta has a variety of i-bodies that block CXCR4 signalling in various ways. AdAlta’s flagship medication candidate AD-214, which has advanced to clinical development for fibrotic disorders, is on the panel.
According to research by GPCR Therapeutics, CXCR4 can be effectively inhibited more effectively when other GPCRs that are connected to CXCR4 in cancer are also blocked.
