XBiotech Announces Presentation of Novel Findings for MABp1 in the Prevention of Coronary Thrombosis at the American Heart As...
November 14 2017 - 7:30AM
XBiotech Inc. (NASDAQ:XBIT) announced today a presentation of
findings on the role of IL-1 alpha (IL-1α) associated with
Neutrophil Extracellular Traps (NETs) in promoting endothelial
activation and thrombogenicity. The oral presentation, entitled,
“Neutrophil Extracellular Traps Increase Endothelial Activation and
Thrombogenicity via IL-1α and NF-κB: Implications for Superficial
Erosion”, was given by researcher Thomas L. Mawson, Icahn School of
Medicine at Mount Sinai, Sarnoff Fellow, Sarnoff Cardiovascular
Research Foundation, at the American Heart Association Scientific
Sessions on November 13 at 5:45 PM, PT. Dr. Eduardo Folco,
scientist at the Cardiovascular Division of Brigham and Women’s
Hospital and Harvard Medical School, contributed equally to this
study.
The findings resulted from an agreement between
XBiotech, Brigham and Women’s Hospital (BWH), and Massachusetts
General Hospital to provide XBiotech’s anti-IL-1α antibody, MABp1,
to Dr. Peter Libby. Dr. Libby, a cardiovascular medicine
specialist at BWH and the Mallinckrodt Professor of Medicine at
Harvard Medical School, was principal investigator of the
research.
“I believe these data represent an exciting step
forward in cardiovascular medicine,” stated Dr. Libby. He further
added, “They elucidate a novel mechanism that we believe can
contribute to coronary thrombosis, a major cause of sudden cardiac
death and acute myocardial infarction. We have demonstrated that
MABp1, an anti-IL-1⍺ antibody, can block induction of key molecules
in vascular endothelial cells that can promote erosion-associated
thrombosis.”
Coronary artery thrombosis can be caused by
either plaque rupture or plaque erosion1. Superficial plaque
erosion causes up to one-third of all acute coronary
syndromes2,[3]. Erosion-prone atheromatous plaques, rather
than lesions with stable or rupture-prone characteristics,
associate with neutrophil extracellular traps (NETs)4. The study
performed at Dr. Libby’s laboratory probed the influence of NETs on
the endothelial cell (EC) functions related to erosion-associated
thrombosis. These data show that exposure of human saphenous veins
ECs (HSVECs) to NETs increase expression of adhesion molecules on
the surface of endothelial cells such as VCAM-1 and ICAM-1, which
may participate in atherogenesis. In addition, pre-treatment
of NETs with MABp1, an anti-IL-1⍺-neutralizing antibody, or IL-1R
antagonist, but not with an anti-IL-1β-neutralizing antibody,
blocked the initiation of VCAM-1, ICAM-1, and TF expression, each
of which link to coronary thrombosis5. In conclusion, NETs increase
thrombogenicity in vitro through a response mediated by IL-1⍺.
These data point to an important role for MABp1 therapy in heart
disease. It also may expand treatment opportunities for other
inflammatory diseases in which NETs play a deleterious role, such
as cancer as well as pulmonary, autoimmune, and gastrointestinal
diseases.
About True Human™ Therapeutic
AntibodiesXBiotech’s True Human™ antibodies are derived
without modification from individuals who possess natural immunity
to certain diseases. With discovery and clinical programs across
multiple disease areas, XBiotech’s True Human antibodies have the
potential to harness the body’s natural immunity to fight disease
with increased safety, efficacy and tolerability.
About XBiotech XBiotech is
a fully integrated global biosciences company dedicated to
pioneering the discovery, development and commercialization of
therapeutic antibodies based on its True Human™ proprietary
technology. XBiotech currently is advancing a robust pipeline of
antibody therapies to redefine the standards of care in oncology,
inflammatory conditions and infectious diseases. Headquartered in
Austin, Texas, XBiotech also is leading the development of
innovative biotech manufacturing technologies designed to more
rapidly, cost-effectively and flexibly produce new therapies
urgently needed by patients worldwide. For more information, visit
www.xbiotech.com.
Cautionary Note on Forward-Looking
StatementsThis press release contains forward-looking
statements, including declarations regarding management's beliefs
and expectations that involve substantial risks and uncertainties.
In some cases, you can identify forward-looking statements by
terminology such as "may," "will," "should," "would," "could,"
"expects," "plans," "contemplate," "anticipates," "believes,"
"estimates," "predicts," "projects," "intend" or "continue" or the
negative of such terms or other comparable terminology, although
not all forward-looking statements contain these identifying words.
Forward-looking statements are subject to inherent risks and
uncertainties in predicting future results and conditions that
could cause the actual results to differ materially from those
projected in these forward-looking statements. These risks and
uncertainties are subject to the disclosures set forth in the "Risk
Factors" section of certain of our SEC filings. Forward-looking
statements are not guarantees of future performance, and our actual
results of operations, financial condition and liquidity, and the
development of the industry in which we operate, may differ
materially from the forward-looking statements contained in this
press release. Any forward-looking statements that we make in this
press release speak only as of the date of this press release. We
assume no obligation to update our forward-looking statements
whether as a result of new information, future events or otherwise,
after the date of this press release.
ContactAshley
Oteroaotero@xbiotech.com512-386-2930
1 Crea F, Libby P. Acute Coronary Syndromes: The Way Forward
From Mechanisms to Precision Treatment. Circulation
2017;136:1155–1166.
2 Franck G, et al. Flow Perturbation Mediates Neutrophil
Recruitment and Potentiates Endothelial Injury via TLR2 in Mice –
Implications for Superficial Erosion. Circ Res 2017;121:31-42.
3 Libby P. Superficial erosion and the precision
management of acute coronary syndromes: not one-size-fits-all. Eur
Heart J. 2017;38(11):801-803. doi:
10.1093/eurheartj/ehw599.
4 Quillard T et al. TLR2 and neutrophils potentiate endothelial
stress, apoptosis and detachment: implications for superficial
erosion. Eur Heart J. 2015 Jun 7;36(22):1394-404. doi:
10.1093/eurheartj/ehv044. Epub 2015 Mar 8.
5 Tousoulis D, et al. Inflammatory and thrombotic mechanisms in
coronary atherosclerosis. Heart. 2003;89(9):993-7.
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