Institut Curie

Centre National De La Recherche Scientifique

Institut National De La Sante Et De La Recherche Medicale

Muséum National D'histoire Naturelle

Onxeo

Dna Therapeutics

Museum National D'historie Naturelle

Muséum National D'histoire Naturelle (Mnhn)

Centre National De La Recherche Scientifique-Cnrs

Inserm

Jian-Sheng Sun

Marie Dutreix

Maria Quanz

Elodie Biet

Rosalie Maurisse

Jean-Paul Feugeas

Flavien Devun

Maria Quanz-Schoeffel

The present invention relates to an optimized in vivo delivery system with endosomolytic agents for nucleic acid of therapeutic interest conjugated to molecules facilitating endocytosis, in particular for use in the treatment of cancer.

Optimized in vivo delivery system with endosomolytic agents for nucleic acid conjugates

The present invention relates to a method for treating a cancer including a combination of a treatment by a nucleic acid molecule mimicking double strand breaks with hyperthermia.

Cancer treatment by combining DNA molecules mimicking double strand breaks with hyperthermia

The invention relates to compositions and methods for interfering with the DNA repair of double strand breaks (DSBs). The invention discloses double-stranded nucleic acid molecules that act as baits and hijack the holocomplex of enzymes responsible for DNA DSB sensing, signaling and/or repair pathways, in particular the non-homologous end joining (NHEJ) pathway of DSB repair. The invention discloses the use of these molecules as a standalone anticancer drug in an efficient amount to be introduced in the tumor cell nuclei in order to trigger their death.

Dbait and standalone uses thereof

The invention relates to compositions and methods for interfering with the DNA repair of double strand breaks (DSBs). The invention discloses novel double-stranded nucleic acid molecules. that act as baits and hijack the holocomplex of enzymes responsible of DNA DSB sensing, signaling and/or repair pathways, in particular the non homologous end joining (NHEJ) pathway of DSB repair. The invention discloses the use of these molecules as adjuvant compositions to be used in association with a DNA breaking treatment, particularly radiotherapy or chemotherapy, in combination with a pharmaceutically acceptable carrier, in an efficient amount to be introduced in the tumor cell nuclei in order to neutralize transiently their DNA repair capacity and trigger their death.

DBAIT and uses thereof

The invention relates to double-stranded nucleic acid fragments comprising a chemically modified backbone and at least 4-1000 bp, preferably 8-500 bp, and most preferably 16-200 bp. The disclosed molecules (DRIL molecules) may interfere with DNA damage signaling and repair pathways, in particular the non homologous NHEJ pathway of double-stranded break repair. The invention discloses the application of the DRIL molecules as adjuvant compositions to be used in association with a DNA breaking treatment, particularly radiotherapy or chemotherapy, in combination with a pharmaceutically acceptable carrier, in an efficient amount to be introduced in the tumoral cell nuclei in order to trigger DNA repair induced lethality (DRIL in short) of tumoral cells/tissues.

Nucleic acids useful for triggering tumor cell lethality

The invention relates to compositions and methods for interfering with the DNA repair of double strand breaks (DSBs). The invention discloses novel double-stranded nucleic acid molecules that act as baits and hijack the holocomplex of enzymes responsible of DNA DSB sensing, signaling and/or repair pathways, in particular the non homologous end joining (NHEJ) pathway of DSB repair. The invention discloses the use of these molecules as adjuvant compositions to be used in association with a DNA breaking treatment, particularly radiotherapy or chemotherapy, in combination with a pharmaceutically acceptable carrier, in an efficient amount to be introduced in the tumor cell nuclei in order to neutralize transiently their DNA repair capacity and trigger their death.

Dbait and uses thereof

This invention concerns a method for effecting directed mutagenesis based on a guided homologous recombination system that comprises (i) a triple helix forming oligonucleotide, (ii) a donor nucleic acid segment, and (iii) an adapter segment comprising an oligonucleotide sequence able to bind at least a portion of said donor nucleic acid through Watson-Crick base pairing.

Growing community of inventors

Saint Maur des Fosses, France

Jian-Sheng Sun