XBiotech, Inc: XBiotech Announces Presentation of Novel Findings for MABp1 in the Prevention of Coronary Thrombosis at the American Heart Association Scientific Sessions

IL-1a Neutralizing Antibody MABp1 Found to Block NETs' Ability to Increase
Endothelial Activation and Thrombogenicity 

AUSTIN, Texas, 2017-11-14 13:30 CET (GLOBE NEWSWIRE) --
XBiotech Inc. (NASDAQ:XBIT) announced today a presentation of findings on the
role of IL-1 alpha (IL-1a) 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-1a and NF-?B: 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-1a 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-1ß-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 Antibodies
XBiotech'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 Statements
This 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
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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. 

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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