ApTOLL molecule for the treatment of ischemic stroke and intracranial hemorrhage

ApTOLL, an aptamer targeting TLR-4, addresses the limitations of current stroke treatments by reducing hemorrhage and improving neurological recovery in acute ischemic stroke patients, achieving significant reductions in mortality and disability.

JP2026506313APending Publication Date: 2026-02-24MERCK PATENT GMBH
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Patent Information

Application Number
JP2025538558
Authority / Receiving Office
JP · JP
Patent Type
Applications
Current Assignee / Owner
Priority Date
2023-01-05
Filing Date
2024-01-04
Publication Date
2026-02-24

AI Technical Summary

Technical Problem

Current treatments for acute ischemic stroke, such as tissue plasminogen activator (tPA) and endovascular thrombectomy (EVT), are limited by a narrow therapeutic window and increased risk of hemorrhage, leading to poor neurological outcomes and high disability rates.

Method used

Administration of the ApTOLL molecule, an aptamer targeting TLR-4, in combination with EVT, reduces neurological damage and intracranial hemorrhage by inhibiting the inflammatory response, as demonstrated in a Phase Ib/IIa clinical study (APRIL study).

Benefits of technology

ApTOLL significantly reduces mortality, disability, and intracranial hemorrhage rates, improving neurological recovery and survival in acute ischemic stroke patients, with a 0.2 mg/kg dose showing a 73% reduction in deaths, 46.59% reduction in infarct volume, and 57.14% reduction in NIHSS score.

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Abstract

The APRIL study demonstrated that infusion of ApTOLL 0.2 mg / kg (SEQ ID NO: 1) in combination with endovascular treatment in selected stroke patients was safe and reduced mortality at 90 days. ApTOLL was demonstrated to limit the occurrence of intracranial hemorrhage and reperfusion injury that can occur after recanalization, and also improve early neurological dysfunction and long-term disability. The ApTOLL molecule is provided for use in reducing the risk of intracranial hemorrhage or secondary hemorrhage, reducing neurological damage, and improving neurological recovery after acute ischemic stroke in subjects.
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