Publication in ImmunoHorizons Highlights the Role of IL-27 in Upregulation of Multiple Checkpoint Proteins
16 Janeiro 2019 - 07:50PM
- Expression of IL-27 shown to contribute to upregulation of
PD-L1, LAG-3, CTLA-4, and TIGIT
Surface Oncology (Nasdaq:SURF), a clinical-stage
immuno-oncology company developing next-generation immunotherapies
that target the tumor microenvironment, today highlights the
publication of a paper describing the biological activity of IL-27,
an immunosuppressive cytokine. Previously, IL-27 has been referred
to as a key regulator for the expression of checkpoint proteins.1
The paper, “IL-27 and TCR Stimulation Promote T
Cell Expression of Multiple Inhibitory Receptors,” was published in
ImmunoHorizons, a peer-reviewed, open access, online-only journal
committed to advancing the knowledge of immunology. Among the
findings in the paper, results indicate that the local production
of IL-27 at sites of ongoing toxoplasmosis-induced inflammation
contributes to expression of PD-L1, LAG-3, CTLA-4, and TIGIT, all
key checkpoint proteins in the downregulation of immune
responses.
IL-27 is understood to play an important role in
turning off an immune response following viral and parasitic
infections. Beyond the role of IL-27 in restoring immunostasis,
Surface Oncology believes it has identified several cancers where
IL-27 may prevent the immune system from recognizing and killing
cancer cells.
“This paper is yet another validation of the
role of IL-27 as a regulatory cytokine for the upregulation of
checkpoint proteins. We are rapidly working toward filing an IND
for our IL-27 antibody, SRF388, which we believe will be the first
IL-27 antibody for the treatment of cancer. We applaud this
additional work in the field and are privileged to work alongside
thought leaders such as Dr. Chris Hunter, one of our SAB members
and senior author of this paper,” said Jeff Goater, chief executive
officer of Surface Oncology.
“We have now known for more than 15 years that
IL-27 can have remarkable suppressive activities,” said Christopher
Hunter, B.Sc., Ph.D., chairman, Department of Pathobiology,
University of Pennsylvania, and member of Surface Oncology’s
Scientific Advisory Board. “However, the ability of IL-27 to
promote inhibitory receptor expression in the context of infection,
autoimmune inflammation, and cancer may help to explain how it
tempers T cell responses.”
Surface Oncology is currently conducting
IND-enabling studies for its IL-27 antibody, SRF388. IND submission
for SRF388 is projected for Q4 2019. SRF388 is believed to be the
only IL-27 antibody in late-preclinical development.
1 Kuchroo, Et al. Nature 558, pages
454–459 (2018)
ABOUT SRF388SRF388 is a
fully human anti-IL-27 antibody. In preclinical studies, treatment
with SRF388 was observed to block IL-27 signaling and its
downstream immunosuppressive signaling effects. Preclinical
combination with a PD-1 inhibitor increased the production of key
inflammatory cytokines. SRF388 also demonstrates preclinical
anti-metastatic tumor activity.
Under Surface’s collaboration agreement with
Novartis, Novartis has the right to purchase an option to the
SRF388 program.
ABOUT SURFACE
ONCOLOGYSurface Oncology is an immuno-oncology
company developing next-generation antibody therapies focused on
the tumor microenvironment with lead programs targeting CD73, CD39,
IL-27 and CD47. Surface’s novel cancer immunotherapies are designed
to achieve a clinically meaningful and sustained anti-tumor
response and may be used alone or in combination with other
therapies. The company has a pipeline of seven novel
immunotherapies and a strategic collaboration
with Novartis focused on up to three next-generation
cancer immunotherapies.
For more information, please
visit www.surfaceoncology.com
Contacts: Seth Lewis slewis@surfaceoncology.com
617-655-5031
Ten Bridge Communications Krystle Gibbs
krystle@tenbridgecommunications.com 508-479-6358
Surface Oncology (NASDAQ:SURF)
Gráfico Histórico do Ativo
De Fev 2024 até Mar 2024
Surface Oncology (NASDAQ:SURF)
Gráfico Histórico do Ativo
De Mar 2023 até Mar 2024