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ImnovAth

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Targeting the Imidazoline I1 receptor as a novel treatment for Atherosclerosis

Atherosclerosis (AT) is one of the main causes of death worldwide. Current treatments (e.g. lipid-lowering therapies) are still insufficient to tackle future CV events and we urgently need new complementary treatments to improve t... see more

28/02/2026

CENTRO NACIONAL DE...

150K€

Project Budget: 150K€

Project leader

CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASC... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 28M€

PARTICIPATION DEPralty Sin fecha límite de participación.

Financing granted El organismo HORIZON EUROPE notifico la concesión del proyecto The day 2024-03-08

ERC-2023-POC: ERC PROOF OF CONCEPT GRANTS Objective:Objectives:The ERC Proof of Concept Grants aim at facilitating exploration of the commerci...

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characteristics of the participant

Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

Private Information

No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

CENTRO NACIONAL DE INVESTIGA...

150.00K€ | Leader

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Project duration: 23 months Date Start: 2024-03-08
End date: 2026-02-28

Project leader

CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASC... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 28M€

Project Budget 150K€

participation deadline Sin fecha límite de participación.

Project description Atherosclerosis (AT) is one of the main causes of death worldwide. Current treatments (e.g. lipid-lowering therapies) are still insufficient to tackle future CV events and we urgently need new complementary treatments to improve therapeutic efficacy. ImnovAth aims to develop the new idea of targeting a metabolite/metabolite receptor axis to complete our preclinical results with an existing pharmacological agent that blocks this pathway, with the long-term goal of moving towards clinical trials and to a marketable product. In the context of our ERC-funded project, we found a microbiota-derived metabolite that affects the development of innate and adaptive immunity. We have subsequently found that this metabolite is both associated with and causal for AT and that blockade of the sensing of this metabolite prevents AT progression. We propose: 1) Validation to demonstrate that blockade of the metabolite/metabolite receptor axis is effective in AT treatment. We will study toxicity/tolerability of the existing pharmacological agent and the effect/efficacy of the blockade of this axis with the pharmacological agent alone or in combination with other current gold-standard treatments for AT in a preclinical therapeutic setting. 2) We will reinforce our IPR position and strategy proceeding towards a marketable product based on our currently filed patent application, market analysis and industry sector contacts. 3) Dissemination and communication activities. In sum, we propose an alternative therapy for AT focused on the inhibition of a novel target that can generate an independent or a complementary therapy to existing gold-standard treatments for AT, thus increasing their effectiveness.

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