Immutep Presents Positive IMP761 Preclinical Results at 14th Congress of European Crohn’s and Colitis Organisation
March 7th 2019
SYDNEY, Australia, March 07, 2019 (GLOBE NEWSWIRE) -- Immutep Limited (ASX: IMM; NASDAQ: IMMP) (Immutep or the Company), a biotechnology company developing novel immunotherapy treatments for cancer and autoimmune diseases, today announced positive results from its preclinical study of IMP761, a novel LAG-3 agonist antibody being developed for the treatment of autoimmune diseases. The results were presented at the 14th Congress of European Crohn’s and Colitis Organisation (ECCO) Conference in Denmark on 7 March 2019.
Consistent with earlier in vitro studies conducted by Immutep on the immunosuppressive activity of IMP761, this new study in a non-human primate animal model showed that IMP761 decreases inflammatory T cell infiltration induced by intra-dermal injection of an antigen. The key conclusions from this in vivo study are outlined below:
- Compared to control animals, CD3+ or CD8+ T cell infiltration was inhibited by IMP761 for both tested subcutaneous doses (0.03 mg/kg and 0.3 mg/kg) as observed via immunofluorescence staining of T cells in the skin tissue test site biopsy.
- Multivariate analysis of the test site parameters (erythema, CD3, CD4 and CD8 T cell infiltration) showed a significant decrease of this antigen-specific T cell induced intradermal reaction, compared to the control group.
At the site of chronic inflammation, auto-immune memory T cells are stimulated by the same self-peptides repeatedly, acquiring an “exhausted” phenotype. We used LAG-3, a marker for exhausted memory T cells, to target these self-reactive T cells in vivo. As LAG-3 is a T cell co-inhibitory receptor, we developed an agonist antibody, IMP761, to increase LAG-3 down-modulation of T cell receptor signaling in these autoimmune T cells.
Immutep CMO and CSO, Frédéric Triebel said, “Future directions in developing more targeted immunosuppressive antibodies should address the root cause of autoimmune diseases by specifically silencing the autoimmune memory T cells accumulating at the disease site. By increasing the physiological negative feedback loop of LAG-3 on T cell receptor signaling in response to self-peptides, IMP761 is preventing the activation of all downstream inflammatory pathways, such as the production of TNF-α, IL-6, IL-17 or IL-23.”
Based on the results of this in vivo study which confirms the immunosuppressive activity of IMP761 on the inflammation associated with an antigen-induced T cell response in non-human primate tissues, Immutep will advance IMP761 into clinical development. The Company has commenced CHO cell line development for Good Manufacturing Practice manufacturing.
Immutep CEO Marc Voigt said, “Our IMP761 preclinical study results are very encouraging. We believe that IMP761 represents a new, more targeted therapeutic approach working upstream from currently available immunosuppressive therapies. IMP761 will be an important part of our development efforts, in addition to our lead product candidate, eftilagimod alpha.”
The presentation materials from this event can be accessed via Immutep’s website.
Immutep CSO and CMO, Frédéric Triebel and CEO Marc Voigt will discuss the results and the Company’s plans to advance IMP761 into clinical development on a global webcast in the coming weeks. Details of the webcast will be announced separately.
Further information can be found on the Company’s website www.immutep.com or by contacting:
Jay Campbell, Chief Business Officer, Immutep Limited
+1 (917) 860-9404; firstname.lastname@example.org
Matthew Gregorowski, Citadel-MAGNUS
+61 2 8234 0105; email@example.com
Garth Russell, LifeSci Advisors
+1 (646) 876-3613; firstname.lastname@example.org