Abrégé

The CRISPR-Cas9 system has revolutionized our ability to precisely modify the genome and has impelled gene editing into clinical applications. Comprehensive analysis of gene editing products at the targeted cut-site revealed a complex spectrum of outcomes. ON-target genotoxicity is underestimated with standard PCR-based methods and necessitates appropriate and sensitive detection methods. Here, the inventors developed two complementary Fluorescence-Assisted Megabase-scale Rearrangements Detection (FAMReD) systems that enable detection, quantification, and cell sorting of edited cells with megabase-scale loss of heterozygosity (LOH). They revealed rare complex chromosomal rearrangements caused by Cas9-nuclease and showed that LOH frequency depends on cell division rate during editing and p53 status. Cell cycle arrest during editing suppressed the appearance of LOH without compromising editing. These data were confirmed in human stem/progenitor cells, suggesting that clinical trials should consider p53 status and cell proliferation rate during editing to limit this risk and design safer protocols.

Classes IPC  ?

• C12N 15/10 - Procédés pour l'isolement, la préparation ou la purification d'ADN ou d'ARN
• C12N 15/90 - Introduction stable d'ADN étranger dans le chromosome

Abrégé

Cerebral small vessel disease (SVD) is a leading cause of stroke and a major contributor to cognitive decline and dementia in the population. Evidences indicate that blood brain barrier dysfunction may play a significant role in VD pathogenesis. Recently, an inverse association of TRIM47 expression in brain and vascular tissues with extensive-SVD severity was reported in a human genome wide association study combined with summary-based Mendelian randomization studies and profiling of human loss-of-function allele carriers. Now, the inventors demonstrate TRIM47 is a key regulator of actin cytoskeleton organization through KEAP1/NRF2 signalling pathway and might be protective from oxidative stress in brain EC. In particular, the in vitro TRIM47 knockdown decreases directed EC migration and delays EC adhesion process with loss of actin cortical reorganization and focal adhesion contacts. Furthermore, RNA sequencing and BioID results indicate that TRIM47 knockdown in brain EC, represses the expression of genes associated with cytoskeleton and NRF2 antioxidant pathway through a potential interaction with KEAP1. Accordingly, the present invention relates to the use of Nrf2 activators for the treatment of SVD.

Classes IPC  ?

• A61K 31/12 - Cétones
• A61K 31/05 - Phénols
• A61P 9/00 - Médicaments pour le traitement des troubles du système cardiovasculaire

Abrégé

The present invention concerns an ubiquitin ligase inhibitor for use for preventing and/or treating a disease linked with cerebral hypoperfusion, and an in vitro screening method for the identification of a candidate compound suitable for preventing and/or treating a disease linked with cerebral hypoperfusion.

Classes IPC  ?

• C12N 15/113 - Acides nucléiques non codants modulant l'expression des gènes, p. ex. oligonucléotides anti-sens
• A61P 25/28 - Médicaments pour le traitement des troubles du système nerveux des troubles dégénératifs du système nerveux central, p. ex. agents nootropes, activateurs de la cognition, médicaments pour traiter la maladie d'Alzheimer ou d'autres formes de démence
• C12N 15/115 - Aptamères, c.-à-d. acides nucléiques liant spécifiquement une molécule cible avec une haute affinité sans s'y hybrider

Abrégé

Heart failure with preserved ejection fraction (HFpEF) which results from diastolic dysfunction is a growing epidemiologic problem. However, the pathophysiology of this disease is poorly understood. Our goal is to investigate whether microvessel disease may promote HFpEF. To do so we have used Leptin receptor deficient (Leprdb/db) female mice as a model of HFpEF and performed a transcriptomic analysis via RNA sequencing of the cardiac vascular fraction of both these mice and their control Leprdb/+littermates. In Leprdb/db female mice, end diastolic pressure (EDP) signing diastolic dysfunction is significantly increased from 3 month of age. It is correlated with a cardiac and cardiomayocyte hypertrophy, vascular leakage, endothelial cell activation and leucocyte infiltration. As expected, the RNA sequencing analysis confirmed endothelial dysfunction. Besides, it also revealed a strong increase in several mast cell markers. We confirmed, via histology, an accumulation of mast cells in the heart of Leprdb/db mice. Importantly, it was associated with increased levels of circulating IgE. Leprdb/db mice were then treated or not with Cromolyn sodium, an inhibitor of mast cell degranulation. After a month treatment, EDP was significantly reduced in Leprdb/db mice demonstrating the critical role of mast cell in the development of diastolic dysfunction in diabetic obese mice.

Classes IPC  ?

• A61K 31/4422 - 1,4-Dihydropyridines, p. ex. nifédipine, nicardipine
• A61K 31/352 - Composés hétérocycliques ayant l'oxygène comme seul hétéro-atome d'un cycle, p. ex. fungichromine ayant des cycles à six chaînons avec un oxygène comme seul hétéro-atome d'un cycle condensés avec des carbocycles, p. ex. cannabinols, méthanthéline
• A61K 31/4545 - Pipéridines non condensées, p. ex. pipérocaïne contenant d'autres systèmes hétérocycliques contenant un cycle à six chaînons avec l'azote comme hétéro-atome du cycle, p. ex. pipampérone, anabasine
• A61K 31/495 - Composés hétérocycliques ayant l'azote comme hétéro-atome d'un cycle, p. ex. guanéthidine ou rifamycines ayant des cycles à six chaînons avec deux azote comme seuls hétéro-atomes d'un cycle, p. ex. pipérazine
• A61K 31/506 - PyrimidinesPyrimidines hydrogénées, p. ex. triméthoprime non condensées et contenant d'autres hétérocycles
• A61K 31/445 - Pipéridines non condensées, p. ex. pipérocaïne
• A61P 9/04 - Agents inotropes, c.-à-d. stimulants de la contraction cardiaqueMédicaments pour le traitement de l'insuffisance cardiaque

Abrégé

Deamidation is usually viewed as a post-translational modification that sets an expiration date on proteins. Among apoptosis regulators of the Bcl-2 family, Bcl-xL shows a unique eligibility to be either singly or doubly deamidated. The inventors therefore analysed Bcl-xL deamidation state in platelets from mice models where platelets lifespan was manipulated. In parallel, the inventors compared human platelets obtained at steady state from healthy controls, to platelets newly synthesized after recovery from acute thrombocytopenia: they found that while expression levels of Asn52 monodeamidated Bcl-xL remains unchanged, Asn52Asn66 doubly-deamidated Bcl-xL is virtually absent in young platelets and accumulates in old platelets. Therefor the Asn52Asn66 doubly-deamidated Bcl-xL could be used as a reliable biomarker for determining the age of platelets.

Classes IPC  ?

• G01N 33/569 - Tests immunologiquesTests faisant intervenir la formation de liaisons biospécifiquesMatériaux à cet effet pour micro-organismes, p. ex. protozoaires, bactéries, virus
• G01N 33/532 - Production de composés immunochimiques marqués

Abrégé

in vitroin vitro tissue/organ model applications.

Classes IPC  ?

• C12N 5/0793 - Neurones
• C12N 5/077 - Cellules mésenchymateuses, p. ex. cellules osseuses, cellules de cartilage, cellules stromales médulaires, cellules adipeuses ou cellules musculaires
• C12N 5/071 - Cellules ou tissus de vertébrés, p. ex. cellules humaines ou tissus humains
• B33Y 10/00 - Procédés de fabrication additive
• C12M 1/12 - Appareillage pour l'enzymologie ou la microbiologie avec des moyens de stérilisation, filtration ou dialyse

Abrégé

The present invention concerns an ubiquitin ligase inhibitor for use for preventing and/or treating a disease linked with cerebral hypoperfusion, and an in vitro screening method for the identification of a candidate compound suitable for preventing and/or treating a disease linked with cerebral hypoperfusion.

Classes IPC  ?

• C12N 15/113 - Acides nucléiques non codants modulant l'expression des gènes, p. ex. oligonucléotides anti-sens
• C07K 16/18 - Immunoglobulines, p. ex. anticorps monoclonaux ou polyclonaux contre du matériel provenant d'animaux ou d'humains
• A61K 31/7088 - Composés ayant au moins trois nucléosides ou nucléotides
• A61K 39/395 - AnticorpsImmunoglobulinesImmunsérum, p. ex. sérum antilymphocitaire
• A61P 9/10 - Médicaments pour le traitement des troubles du système cardiovasculaire des maladies ischémiques ou athéroscléreuses, p. ex. médicaments antiangineux, vasodilatateurs coronariens, médicaments pour le traitement de l'infarctus du myocarde, de la rétinopathie, de l'insuffisance cérébro-vasculaire, de l'artériosclérose rénale
• A61P 25/28 - Médicaments pour le traitement des troubles du système nerveux des troubles dégénératifs du système nerveux central, p. ex. agents nootropes, activateurs de la cognition, médicaments pour traiter la maladie d'Alzheimer ou d'autres formes de démence
• A61P 25/16 - Antiparkinsoniens

Abrégé

Heart failure with preserved ejection fraction (HFpEF) which results from diastolic dysfunction is a growing epidemiologic problem. However, the pathophysiology of this disease is poorly understood. Our goal is to investigate whether microvessel disease may promote HFpEF. To do so we have used Leptin receptor deficient (Leprdb/db) female mice as a model of HFpEF and performed a transcriptomic analysis via RNA sequencing of the cardiac vascular fraction of both these mice and their control Leprdb/+ littermates. In Leprdb/dbfemale mice, end diastolic pressure (EDP) signing diastolic dysfunction is significantly increased from 3 month of age. It is correlated with a cardiac and cardiomayocyte hypertrophy, vascular leakage, endothelial cell activation and leucocyte infiltration. As expected, the RNA sequencing analysis confirmed endothelial dysfunction. Besides, it also revealed a strong increase in several mast cell markers. We confirmed, via histology, an accumulation of mast cells in the heart of Leprdb/dbmice. Importantly, it was associated with increased levels of circulating IgE. Leprdb/dbmice were then treated or not with Cromolyn sodium, an inhibitor of mast cell degranulation. After a month treatment, EDP was significantly reduced in Leprdb/db mice demonstrating the critical role of mast cell in the development of diastolic dysfunction in diabetic obese mice.

Classes IPC  ?

• A61K 31/275 - NitrilesIsonitriles
• A61K 31/352 - Composés hétérocycliques ayant l'oxygène comme seul hétéro-atome d'un cycle, p. ex. fungichromine ayant des cycles à six chaînons avec un oxygène comme seul hétéro-atome d'un cycle condensés avec des carbocycles, p. ex. cannabinols, méthanthéline
• A61K 31/44 - Pyridines non condenséesLeurs dérivés hydrogénés
• A61K 31/4535 - Pipéridines non condensées, p. ex. pipérocaïne contenant d'autres systèmes hétérocycliques contenant un hétérocycle avec le soufre comme hétéro-atome du cycle, p. ex. pizotifène
• A61K 31/47 - QuinoléinesIsoquinoléines
• A61K 31/522 - Purines, p. ex. adénine ayant des groupes oxo liés directement à l'hétérocycle, p. ex. hypoxanthine, guanine, acyclovir
• A61P 9/04 - Agents inotropes, c.-à-d. stimulants de la contraction cardiaqueMédicaments pour le traitement de l'insuffisance cardiaque

Abrégé

The molecular damages leading to the deterioration of cellular and tissue functions occur at different rate in different people. Thus methods for screening anti-aging agents are highly desirable. The present fulfils this need by providing fusions proteins wherein the Bcl-xL protein is fused to a stability-affecting protein. By inducing the degradation of the fusion protein and then restoring said expression is thus possible to rejuvenate a marker of cell aging. The apparition of the mono-deamidated form will indeed correlate with the aging progression of the cells and thus will offer a reliable system of identifying agents that are capable of slowing down the aging process. The preferred fusion protein is a fusion of Bcl-XL with the mutant L106P of FKBP12.

Classes IPC  ?

• C12N 9/90 - Isomérases (5.)
• G01N 33/68 - Analyse chimique de matériau biologique, p. ex. de sang ou d'urineTest par des méthodes faisant intervenir la formation de liaisons biospécifiques par ligandsTest immunologique faisant intervenir des protéines, peptides ou amino-acides
• A61Q 19/08 - Préparations contre le vieillissement
• C07K 14/47 - Peptides ayant plus de 20 amino-acidesGastrinesSomatostatinesMélanotropinesLeurs dérivés provenant d'animauxPeptides ayant plus de 20 amino-acidesGastrinesSomatostatinesMélanotropinesLeurs dérivés provenant d'humains provenant de vertébrés provenant de mammifères

Abrégé

Deamidation is usually viewed as a post-translational modification that sets an expiration date on proteins. Among apoptosis regulators of the Bcl-2 family, Bcl-xL shows a unique eligibility to be either singly or doubly deamidated. The inventors therefore analysed Bcl-xL deamidation state in platelets from mice models where platelets lifespan was manipulated. In parallel, the inventors compared human platelets obtained at steady state from healthy controls, to platelets newly synthesized after recovery from acute thrombocytopenia: they found that while expression levels of Asn52 monodeamidated Bcl-xL remains unchanged, Asn52Asn66 doubly-deamidated Bcl-xL is virtually absent in young platelets and accumulates in old platelets. Therefor the Asn52Asn66 doubly-deamidated Bcl-xL could be used as a reliable biomarker for determining the age of platelets.

Classes IPC  ?

• G01N 33/569 - Tests immunologiquesTests faisant intervenir la formation de liaisons biospécifiquesMatériaux à cet effet pour micro-organismes, p. ex. protozoaires, bactéries, virus

Abrégé

Inflammation and oxidative stress play an important role in the pathogenesis of lower- extremity artery disease (LEAD). The inventors assessed the prognostic values of inflammatory and redox status biomarkers on the risk of LEAD in individuals with type 2 diabetes. In particular, plasma concentrations of TNF receptor-1 (TNFR1) and ischemia-modified albumin (IMA) were measured at baseline in the SURDIAGENE (SURvie, DIAbete de type 2 et GENEtique) cohort. High plasma concentrations of TNFR1 (HR [95%CI] for second versus first tertile and IMA (2.42 [1.38–4.23], p=0.002; 2.04 [1.17–3.57], p=0.01) were independently associated with increased risk of major LEAD. Plasma concentrations of TNFR1, but not IMA, yielded incremental information, over traditional risk factors, for the risk of major LEAD: c-statistic change (0.036 [0.013–0.059], p=0.002), IDI (0.012 [0.005–0.022], p<0.001), continuous NRI (0.583 [0.294–0.847], p<0.001), and categorical NRI (0.171 [0.027–0.317], p=0.02). In conclusion, this is the first report of independent associations between high plasma TNFR1 and/or IMA concentrations and increased 5.6-year risk of major LEAD in people with type 2 diabetes.

Classes IPC  ?

• G01N 33/68 - Analyse chimique de matériau biologique, p. ex. de sang ou d'urineTest par des méthodes faisant intervenir la formation de liaisons biospécifiques par ligandsTest immunologique faisant intervenir des protéines, peptides ou amino-acides

Abrégé

In vivoIn vivo intravitreal microinjection of mAbFzd7 or CRD receptor in mice after 5 days of exposure to 75% oxygen (P12) resulted in a significant decrease of pathological neovascularization in the treated eye compared to the control eye. Collectively, the results established that Fzd7 acts as an important regulator of retinal neovascularization and offers a promising anti-angiogenic strategy for the treatment of ischemic retinopathies. Accordingly, the present invention relates to use of Fzd7 inhibitors for the treatment of retinal neovascularization.

Classes IPC  ?

• C07K 16/28 - Immunoglobulines, p. ex. anticorps monoclonaux ou polyclonaux contre du matériel provenant d'animaux ou d'humains contre des récepteurs, des antigènes de surface cellulaire ou des déterminants de surface cellulaire
• A61P 27/02 - Agents ophtalmiques

Abrégé

Endothelial dysfunction is characterized by altered vasoactive properties especially through an impaired nitric oxide (NO) production, leading to a reduced lumen diameter consecutive to excessive vasoconstriction. In particular, endothelial dysfunction is a hallmark of peripheral arterial disease which is defined as vascular occlusion below the level of the inguinal ligament, and which is one of the most severe complications of diabetes. The inventors identify endothelial cell (EC)-derived Dhh as a critical regulator of vascular integrity downstream of Klf2 and as a new mediator of inflammation-induced endothelial dysfunction. Additionally, the inventors used the Hedgehog agonist SAG which is useful for preventing endothelial dysfunction and found that SAG administration decreased inflammation and edema in a model of critical limb ischemia. Accordingly, hedgehog agonists are suitable for the treatment of endothelial dysfunction and in particular for the treatment of peripheral arterial diseases.

Classes IPC  ?

• A61K 31/4436 - Pyridines non condenséesLeurs dérivés hydrogénés contenant d'autres systèmes hétérocycliques contenant un hétérocycle avec le soufre comme hétéro-atome du cycle
• A61K 31/00 - Préparations médicinales contenant des ingrédients actifs organiques
• A61P 9/08 - Vasodilatateurs pour des indications multiples
• A61P 9/10 - Médicaments pour le traitement des troubles du système cardiovasculaire des maladies ischémiques ou athéroscléreuses, p. ex. médicaments antiangineux, vasodilatateurs coronariens, médicaments pour le traitement de l'infarctus du myocarde, de la rétinopathie, de l'insuffisance cérébro-vasculaire, de l'artériosclérose rénale

Abrégé

Janus kinaseJAK2JAKJAK2V617F. Thrombosis reveals MPN in about 30% of patients and is a major cause of morbidity and mortality. The mechanisms underlying the MPN thrombotic diathesis are still largely elusive. In MPN patients, the inventors found: 1) increased neutrophils CD1 lb expression, 2) increased neutrophils TF expression in patients with history of thrombosis, 3) increased plasma levels of free DNA in all patients and increased plasma levels of MPO-DNA complex in patients with history of thrombosis. Accordingly, the present invention relates to a method of identifying whether a patient suffering from a myeloproliferative neoplasm is at risk of thrombosis comprising determining in a blood sample obtained from the patient whether neutrophils exhibit a hyperactivated state (e.g. by quantifying plasma levels of MPO-DNA by ELISA). The present invention also relates to a method of treating thrombosis in a patient suffering from a myeloproliferative neoplasm comprising administering to the patient a therapeutically effective amount of an anti-NET compound.

Classes IPC  ?

• C12Q 1/68 - Procédés de mesure ou de test faisant intervenir des enzymes, des acides nucléiques ou des micro-organismesCompositions à cet effetProcédés pour préparer ces compositions faisant intervenir des acides nucléiques
• A61K 45/06 - Mélanges d'ingrédients actifs sans caractérisation chimique, p. ex. composés antiphlogistiques et pour le cœur
• G01N 33/50 - Analyse chimique de matériau biologique, p. ex. de sang ou d'urineTest par des méthodes faisant intervenir la formation de liaisons biospécifiques par ligandsTest immunologique

Abrégé

The present invention relates to a method for reducing CD95-mediated cell motility. To identify chemicals disrupting CD95/PLCγ1 interaction, the inventors screened a chemical library of EMA/FDA-approved molecules against a protein-fragment complementation assay (PCA) monitoring the binding of CD95 to PLCγ1. From this screen, five chemical molecules showed the ability to disrupt CD95/PLCγ1 interaction and to neutralize the CD95-mediated calcium signaling pathway and cell migration in human peripheral blood lymphocytes (PBLs) and Th17 cells. Thus, the present invention relates to a method for reducing CD95-mediated cell motility, comprising administering the subject with at least one compound selected from the group consisting of HIV-protease inhibitors (e.g. ritonavir), diflunisal, anethole, rosiglitazone and daunorubicin. Particularly, the method of the invention find use in the treatment of cancer such as triple negative breast cancer, autoimmune inflammatory disease such as systemic lupus erythematosus, inflammatory condition and Th17-mediated disease.

Classes IPC  ?

• A61K 31/427 - Thiazoles non condensés et contenant d'autres hétérocycles
• A61K 31/125 - CamphreSes dérivés substitués sur le cycle
• A61K 31/4439 - Pyridines non condenséesLeurs dérivés hydrogénés contenant d'autres systèmes hétérocycliques contenant un cycle à cinq chaînons avec l'azote comme hétéro-atome du cycle, p. ex. oméprazole
• A61K 31/603 - Acide salicyliqueSes dérivés ayant d'autres cycles aromatiques, p. ex. diflunisal
• A61K 31/704 - Composés ayant des radicaux saccharide liés à des composés non-saccharide par des liaisons glycosidiques liés à un composé carbocyclique, p. ex. phloridzine liés à un système carbocyclique condensé, p. ex. sennosides, thiocolchicosides, escine, daunorubicine, digitoxine
• A61P 35/00 - Agents anticancéreux
• A61P 29/00 - Agents analgésiques, antipyrétiques ou anti-inflammatoires non centraux, p. ex. agents antirhumatismauxMédicaments anti-inflammatoires non stéroïdiens [AINS]
• A61P 37/00 - Médicaments pour le traitement des troubles immunologiques ou allergiques
• A61P 35/02 - Agents anticancéreux spécifiques pour le traitement de la leucémie

Abrégé

The present invention relates to methods for predicting acute severe colitis treatment response. Currently, there is no biomarker of drug response. The present invention provides the first prediction tool for responses to first- and second-line treatments in acute severe ulcerative colitis. Putative mRNA targets of dysregulated microRNAs were identified from patient biopsies. One classifier of fifteen colonic microRNAs plus five biological values at admission were identified with a prediction accuracy of 96.6% for discriminating responders from non-responders to steroids. Using a similar method, 6 and 4 mucosal microRNA-based algorithms were identified to classify responders from non-responders to infliximab and cyclosporine. In particular, the present invention relates to methods for predicting acute severe colitis treatment response by measuring the expression levels of several miRNAs selected from the group consisting of hp_hsa-mir-3934, hp_hsa-mir-100, hsa-miR-718, hp_hsa-mir-193b, hsa-miR-3150a-5p, hp_hsa-mir-1260b, hsa-miR-938, hsa-miR-518b and hsa-miR-1468.

Classes IPC  ?

• C12Q 1/68 - Procédés de mesure ou de test faisant intervenir des enzymes, des acides nucléiques ou des micro-organismesCompositions à cet effetProcédés pour préparer ces compositions faisant intervenir des acides nucléiques

Abrégé

The present invention relates to the use of an Internal Standard compound in a method for quantifying Bevacizumab in a sample by mass spectrometry, wherein the said Internal Standard compound is described in the specification.

Classes IPC  ?

• C12Q 1/68 - Procédés de mesure ou de test faisant intervenir des enzymes, des acides nucléiques ou des micro-organismesCompositions à cet effetProcédés pour préparer ces compositions faisant intervenir des acides nucléiques
• C12Q 1/34 - Procédés de mesure ou de test faisant intervenir des enzymes, des acides nucléiques ou des micro-organismesCompositions à cet effetProcédés pour préparer ces compositions faisant intervenir une hydrolase

Abrégé

The invention relates to methods and pharmaceutical compositions for the treatment of Ebola Virus Disease. In particular the present relates to a method of treating Ebola Virus Disease in a subject in need thereof comprising administering the subject with a therapeutically effective amount of Favipiravir.

Classes IPC  ?

• A61K 31/4965 - Pyrazines non condensées
• A61P 31/14 - Antiviraux pour le traitement des virus ARN

Abrégé

The present invention relates to methods and kits for predicting medically refractory acute severe colitis. In particular, the present invention relates to a method for predicting medically refractory acute severe colitis in a subject comprising the steps consisting of i) determining in a sample obtained from the subject the expression levels of miR-1825, miR- 938, miR-4699, miR-23c, miR-4659a-3p, miR-4477a, miR-320b-1, miR-3128, and miR- 4755, comparing the expression levels determined at step i) with their corresponding predetermined reference values and ii) concluding that the subject has a high risk of having medically refractory acute severe colitis when the expression level of miR-1825 and miR-938 are lower than their respective predetermined reference values and when the expression levels of miR-4699, miR-23c, miR-4659a-3p, miR-4477a, miR-320b-1, miR-3128, and miR- 4755 are higher than their respective predetermined reference values, or concluding that the subject has a low risk of having medically refractory acute severe colitis when the expression level of miR-1825 and miR-938 are higher than their respective predetermined reference values and when the expression levels of miR-4699, miR-23c, miR-4659a-3p, miR-4477a, miR-320b-1, miR-3128, and miR-4755 are lower than their respective predetermined reference values.

Classes IPC  ?

• C12Q 1/68 - Procédés de mesure ou de test faisant intervenir des enzymes, des acides nucléiques ou des micro-organismesCompositions à cet effetProcédés pour préparer ces compositions faisant intervenir des acides nucléiques

Abrégé

The present invention relates to a nucleic acid aptamer that binds specifically to human matrix metalloproteinase 9 (h MMP-9) and its use for imaging h MMP-9 in a subject in need thereof.

Classes IPC  ?

• C12N 15/115 - Aptamères, c.-à-d. acides nucléiques liant spécifiquement une molécule cible avec une haute affinité sans s'y hybrider