Background: Use of IL-2 (Proleukin) remains limited due to a short half-life, toxicity, and preferential
activation of Tregs driven by a high affinity for IL2Rα over IL2Rβ. To bypass these
limitations, we further engineered MDNA109, an IL-2 superkine, to generate MDNA11
by (1) addition of mutations to abrogate IL2Rα binding and (2) fusion with albumin
to extend half-life. We also leveraged the versatility of our superkine platforms
to engineer long-acting bispecific constructs to simultaneously activate IL-2 signaling
(i.e. pro-inflammatory) and suppress IL-4/IL-13 function (i.e. anti-inflammatory)
and/ or enable accumulation in tumors.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to European Journal of CancerAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
Article info
Identification
Copyright
© 2020 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
