VSN Verseon (DI)

TIDMVSN

Verseon Corporation

06 December 2016

Press release December 6, 2016

Verseon Corporation

("Verseon" or the "Company")

ASH 2016: Explaining the lower bleeding risk of Verseon's anticoagulants

FREMONT, Calif.-Verseon presented preclinical results at the American Society of Hematology (ASH) Annual Meeting in San Diego yesterday that could explain the favorable bleeding profile of its novel class of oral direct thrombin inhibitors. The data indicate that Verseon's drug candidates do not disrupt platelet function while preventing thrombosis in preclinical efficacy models.

During the clotting process, thrombin cleaves fibrinogen as a basis for clot formation and also activates platelets, which play an important role in wound healing, hemostasis, and healthy tissue growth. By either directly or indirectly inhibiting thrombin, novel oral anticoagulants (NOACs) also reduce platelet activation, which may, in turn, increase a patient's bleeding risk.

Preclinical data presented at the conference show that while Verseon's direct thrombin inhibitors (VE--DTIs) prevent thrombosis in in vivo efficacy models such as the arteriovenous shunt and thrombin-induced thromboembolism models, the VE-DTIs leave platelet function unaffected. This finding has been confirmed by Verseon via tests that assess in vivo platelet activation in these models using flow cytometry with platelet-specific antibodies. These in vivo results support in vitro data that show that the VE-DTIs are highly selective thrombin inhibitors that effectively block fibrinogen cleavage, but are up to 900--fold less potent in the in vitro inhibition of platelet activation than currently available NOACs.

"This unique feature of our novel class of thrombin inhibitors provides a biological explanation for their low bleeding liability," said Dr. Mohan Sivaraja, Verseon's Associate Director of Discovery Biology, who presented these findings at ASH. "These encouraging results further establish the distinctive pharmacology of our compounds."

About Verseon's Anticoagulant Program

Verseon's potent, highly selective, oral direct thrombin inhibitors act through reversible covalent inhibition, a unique mode of action. Preclinical studies show that Verseon's inhibitors act as effective anticoagulants in multiple efficacy studies, but do not disrupt platelet function. This unique feature could explain their observed low bleeding risk. One of Verseon's lead candidates furthermore shows very low renal clearance, a highly desirable property for patients with impaired renal function.

About Verseon

Verseon Corporation (www.verseon.com, AIM: VSN) is a technology-based pharmaceutical company that employs its proprietary, computational drug discovery platform to develop novel therapeutics that are unlikely to be found using conventional methods. The Company is applying its platform to a growing drug pipeline and currently has three active drug programs in the areas of anticoagulation, diabetic macular edema, and oncology.

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Cautionary Note on Forward-Looking Statements

This press release contains forward-looking statements, which are generally statements that are not historical facts. Forward-looking statements can be identified by the words "expects," "anticipates," "believes," "intends, " "estimates," "plans," "will," "outlook," and similar expressions. Forward-looking statements are based on management's current plans, estimates, assumptions and projections, and speak only as of the date they are made. We undertake no obligation to update any forward-looking statement in light of new information or future events, except as otherwise required by law. Forward-looking statements involve inherent risks and uncertainties, most of which are difficult to predict and are generally beyond our control. Actual results or outcomes may differ materially from those implied by the forward-looking statements as a result of the impact of a number of factors.

This information is provided by RNS

The company news service from the London Stock Exchange

END

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December 06, 2016 02:01 ET (07:01 GMT)

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