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XL-protein and DNX Biopharmaceuticals Announce Collaboration to Develop Novel Inflammasome-Directed Therapeutics using PASylation platform

02-26-2020 11:12 AM CET | Health & Medicine

Press release from: XL-protein GmbH

Freising, Germany and San Diego, CA, February 25, 2020 -- XL-protein has extended its existing partnership with DNX Biopharmaceuticals, a biopharmaceutical company developing nonimmunogenic, long-acting therapeutic proteins for the treatment of patients with life-long diseases, to develop novel inflammasome-directed therapeutics for the treatment of diseases linked to inflammation, autoinflammation and oncology. DNX has exercised an option for an exclusive license to research, develop and commercialize a novel antagonist from within the DNX portfolio, modified by XL-protein's PASylation technology. Financial terms of the collaboration were not disclosed.

The Inflammasome is involved in the initiation and regulation of innate and acquired immunity, sterile inflammation, tissue remodeling, cell death, hypoxia-ischemia and organ failure. Dysfunctional signaling related to the inflammasome complex leads to smoldering or chronic inflammation, which is implicated in a wide range of pathological conditions, including cancer, heart disease, several systemic autoinflammatory conditions such as cryopyrin-associated periodic syndromes (CAPS), type II diabetes, rheumatoid arthritis (RA) and gout.

"We are pleased that DNX has chosen PASylation technology for the design of biopharmaceuticals with extended plasma half-life and enhanced action," comments Claus Schalper, CEO of XL-protein, adding that "DNX's deal with Johnson & Johnson provides another validation of our proprietary platform."

"We are delighted to be collaborating with XL-protein and the use of their PASylation technology to progressing DNX's novel receptor antagonists into clinical development," said Rajiv Datar, Co-Founder and CEO of DNX.

XL-protein GmbH
Lise-Meitner-Str. 30
85354 Freising - Germany
E-mail: bd@xl-protein.com

About PASylation Technology
'PASylation' involves the genetic fusion or chemical conjugation of a therapeutic protein or pharmaceutically active compound with a conformationally disordered polypeptide of defined sequence comprising the small natural amino acids Pro, Ala, and/or Ser. Due to the biophysical size effect, the typically rapid clearance via renal filtration of the original drug can be retarded by a factor 10-100, depending on the length of the PAS chain. PAS sequences are highly soluble while lacking charges, they are biochemically inert, non-toxic and non-immunogenic, they offer efficient recombinant protein production in a variety of biotechnological host organisms, and they show high stability in blood plasma but are biodegradable by intracellular proteases.

About XL-protein GmbH
XL-protein is a German biotech company commercializing its ground-breaking PASylation? technology, which enables the design of biopharmaceuticals with extended plasma half-life and enhanced action. Based on a strong proprietary technology position, XL-protein focuses at the preclinical as well as clinical development of PASylated proteins in diverse disease areas. XLprotein is engaged in a growing number of partnerships with international pharmaceutical and biotech companies at various levels.

For more information, please visit: www.xl-protein.com

About DNX Biopharmaceuticals, Inc.
DNX is a biopharmaceutical company developing long-acting therapeutic proteins for the treatment of patients with life-long diseases. Founded in 2014 and headquartered in San Diego, CA, USA, DNX is pursuing the development of new therapeutic proteins designed to target pathways in the autoinflammation-inflammation spectrum aiming to block key mediators of immunity and inflammation for treating diseases and disorders. DNX is a resident of Johnson and Johnson Innovation - JLABS, Shanghai, a JLABS QuickFire Challenge (QFC) winner and has just closed a deal with the Lung Cancer Initiative at Johnson and Johnson.

For more information, please visit: www.dnxbio.com

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