argenx Announces Publication of Translational Data of Efgartigimod in Autoimmune Skin Blistering Diseases
19 Mai 2022 - 01:00PM
- Translational data from Phase 2 study of efgartigimod in
pemphigus further demonstrate argenx’s scientific leadership in
FcRn biology, providing new insights into pathophysiology of
autoimmune skin blistering diseases and potential role of FcRn
blockade
- Data to be included in symposium
presentation at Society for Investigative Dermatology (SID) Annual
Meeting being held today, May 19, 2022, 7:30am PT
May
19, 2022
Breda, the Netherlands – argenx
SE (Euronext & Nasdaq: ARGX), a global immunology company
committed to improving the lives of people suffering from severe
autoimmune diseases, today announced the publication of novel
translational data from the open-label Phase 2 study of
efgartigimod for the treatment of pemphigus that further support
the potential role of FcRn blockade and potential of efgartigimod
in autoimmune skin blistering disorders. The translational data,
“FcRn Antagonism Leads to a Decrease
of Desmoglein-Specific B Cells:
Secondary Analysis of a Phase 2 Study of Efgartigimod in Pemphigus
Vulgaris and Pemphigus Foliaceus” were published in the
journal Frontiers of Immunology.
The novel translational data, along with
previously published translational data in Cells, will also be
presented in a symposium today at the Society for Investigative
Dermatology (SID) Annual Meeting at 7:30am PT. The complete results
from the Phase 2 study of efgartigimod for the treatment of
pemphigus were published in the British Journal of Dermatology.
“The publication today highlights the value of
our collaborative research model with leading academic centers of
excellence, revealing an exciting set of new translational data on
the pathophysiology of autoimmune skin blistering diseases and the
therapeutic rationale of FcRn blockade in pemphigus and bullous
pemphigoid,” said Hans de Haard, Ph.D., Chief Scientific Officer of
argenx. “We believe the secondary analysis of our Phase 2 study
shows the potential role of FcRn blockade to extend beyond IgG
antibody reduction to include an immunomodulatory effect on
autoantigen-specific B-cells, which may account for the durable
responses observed in the study. We understand the serious unmet
need of people living with pemphigus and bullous pemphigoid and are
committed to continuing this research on their behalf to bring
forward an innovative new treatment option.”
Highlights from Published Translational
Data:
- Pemphigus and
BP are IgG-mediated autoimmune skin
blistering diseases
- In pemphigus, IgG autoantibodies
against Dsg-1 and Dsg-3 cause acantholysis or disruption of
keratinocyte adhesion; new data suggest role of additional
non-desmoglein IgG autoantibodies in pemphigus pathophysiology
- In BP, IgG autoantibodies against
hemidesmosomal proteins (BP180 and BP230) at the dermal-epidermal
junction drive pathophysiology of disease
- In a secondary analysis of
a subset of patients in the Phase 2
study of efgartigimod in
pemphigus:
- Efgartigimod treatment
resulted in sustained reduction of
antigen-specific
B-cells in participants
with pemphigus vulgaris (PV) and foliaceus, maintained following
treatment cessation, and which correlated with sustained clinical
improvement while total IgG returned to near baseline levels
- Median CD19+
B-cells remained within normal limits at
all timepoints measured, and no new safety signals were
detected
- No
observed effect on total leukocytes, neutrophils, monocytes, or
lymphocytes in patients treated with long-term
efgartigimod therapy, however frequency of CD19+ B-cells in
circulation was observed to decrease following efgartigimod
treatment
-
Efgartigimod was shown to efficiently
rescue the loss of keratinocyte adhesion upon anti-Dsg-3
antibodies (anti-Dsg3) and PV IgG treatment, indicating that
stabilization of keratinocyte adhesion may present a novel
treatment paradigm for pemphigus
About EfgartigimodEfgartigimod
is an antibody fragment designed to reduce pathogenic
immunoglobulin G (IgG) antibodies by binding to the neonatal Fc
receptor and blocking the IgG recycling process. Efgartigimod is
being investigated in several autoimmune diseases known to be
mediated by disease-causing IgG antibodies, including neuromuscular
disorders, blood disorders, and skin blistering diseases.
About PemphigusPemphigus is a
rare group of chronic blistering autoimmune diseases that affect
the skin and mucous membranes, and are characterized by painful
blisters, erosions and acantholysis, or disruption of keratinocyte
adhesion. Blisters often break open, causing serious pain and
increased risk of infection. Pemphigus vulgaris and pemphigus
foliaceous are the most common forms of pemphigus.
About Bullous Pemphigoid (BP)BP
is a severe, rare, chronic and recurrent autoimmune disorder
characterized by fluid-filled blisters, itching, and redness of the
skin. It is the most common subepidermal autoimmune blistering
disease. In severe cases with widespread blistering, risk of
infection can be life-threatening. Fear of infection and the
unpredictable nature of flare ups often has a significant impact on
quality of life and psychological well-being.
About argenxargenx is a global
immunology company committed to improving the lives of people
suffering from severe autoimmune diseases. Partnering with leading
academic researchers through its Immunology Innovation Program
(IIP), argenx aims to translate immunology breakthroughs into a
world-class portfolio of novel antibody-based medicines. argenx
developed and is commercializing the first-and-only approved
neonatal Fc receptor (FcRn) blocker in the U.S. and Japan. The
Company is evaluating efgartigimod in multiple serious autoimmune
diseases and advancing several earlier stage experimental medicines
within its therapeutic franchises. For more information, visit
www.argenx.com and follow us on LinkedIn, Twitter,
and Instagram.
For further information, please contact:
Media:Kelsey Kirkkkirk@argenx.com
Investors:Beth
DelGiaccobdelgiacco@argenx.com
Michelle Greenblattmgreenblatt@argenx.com
Forward-looking Statements The contents of
this announcement include statements that are, or may be deemed to
be, “forward-looking statements.” These forward-looking statements
can be identified by the use of forward-looking terminology,
including the terms “believes,” “hope,” “estimates,” “anticipates,”
“expects,” “intends,” “may,” “will,” or “should” and include
statements argenx makes concerning the potential for efgartigimod
in treatment of autoimmune skin blistering disorders, the potential
extension of the role of FcRn blockade and argenx’s ability to
complete the research and development of an innovative treatment
option for pemphigus and bullous pemphigoid. By their nature,
forward-looking statements involve risks and uncertainties and
readers are cautioned that any such forward-looking statements are
not guarantees of future performance. argenx’s actual results may
differ materially from those predicted by the forward-looking
statements as a result of various important factors. A further
list and description of these risks, uncertainties and other risks
can be found in argenx’s U.S. Securities and Exchange Commission
(SEC) filings and reports, including in argenx’s most recent annual
report on Form 20-F filed with the SEC as well as subsequent
filings and reports filed by argenx with the SEC. Given these
uncertainties, the reader is advised not to place any undue
reliance on such forward-looking statements. These forward-looking
statements speak only as of the date of publication of this
document. argenx undertakes no obligation to publicly update or
revise the information in this press release, including any
forward-looking statements, except as may be required by law.
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