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ONCODESTROYER

Financiado

Targeting cancer vulnerabilities in acute leukemia

Background and rationale: Adult acute leukemias pose a great challenge to cancer therapy, with only few advances made in 50 years. As these malignancies are commonly associated with multiple epigenetic aberrations, epigenetic fact... ver más

30/09/2025

THE HEBREW UNIVERS...

3M€

Presupuesto del proyecto: 3M€

Líder del proyecto

THE HEBREW UNIVERSITY OF JERUSALEM No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 2 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2020-06-26

Línea de financiación objetivo El proyecto se financió a través de la siguiente ayuda:

ERC-2019-ADG: ERC Advanced Grant

I+D

Cerrada hace 5 años

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2 Participantes

THE HEBREW UNIVERSITY OF JER...

3.20M€ | Lider

EUROCIR

1.20M€ | Participante

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Últimas noticias

29-11-2024: IDAE En las últimas 48 horas el Organismo IDAE ha otorgado 4 concesiones

29-11-2024: ECE En las últimas 48 horas el Organismo ECE ha otorgado 2 concesiones

29-11-2024: CMVAMADRID En las últimas 48 horas el Organismo CMVAMADRID ha otorgado 37 concesiones

Duración del proyecto: 63 meses Fecha Inicio: 2020-06-26
Fecha Fin: 2025-09-30

Líder del proyecto

THE HEBREW UNIVERSITY OF JERUSALEM

TRL 4-5

Presupuesto del proyecto 3M€

Descripción del proyecto Background and rationale: Adult acute leukemias pose a great challenge to cancer therapy, with only few advances made in 50 years. As these malignancies are commonly associated with multiple epigenetic aberrations, epigenetic factors represent attractive leukemia drug targets. Nevertheless, most epigenetic-targeting drugs have displayed limited clinical benefit and key leukemia drivers like MYC, ERG and MYB remained mostly undruggable. We have developed a new class of small molecule kinase inhibitors, termed oncodestroyers (ODs), single molecules combining supreme p53 activation with selective disruption of multiple leukemia-specific super-enhancers (SEs) that drive oncogenes and dependency/vulnerability factors. These inhibitors demonstrate an unprecedented therapeutic potency in mouse models of human leukemia and are entering now leukemia clinical trials. With this project we wish to study the principles of oncodestruction, mechanisms of drug action, immune system interface, and preempt drug resistance. Relevant knowledge may be applied to other cancer diseases, sharing vulnerabilities with leukemia. Major Goal: To expand the therapeutic potential of ODs in leukemia and pre-leukemia by studying their vulnerability basis, mechanisms of drug action and indicators of therapeutic response in individual patients. Research plan: 1) Expand the collection of small molecule kinase inhibitor ODs and develop OD-based PROTACs to gain an optimal spectrum of kinase targets with good therapeutic window in AML; 2) Elucidate the mechanisms of action and what distinguishes an OD, with emphasis on SE disruption, p53 activation and OD-immune-cooperation; 3) Explore the translational aspects of OD treatment by: identifying OD resistance and relapse mechanisms; study clonal evolution in MDS and AML patients undergoing phase 1a/b clinical trial; predict a patient response to ODs and use ODs for ameliorating age-related clonal hematopoiesis, thus possibly averting leukemogenesis.

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