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933 Establishment of a new orthotopic in vivo examinable model of non-muscle invasive bladder cancer using RT112 reporter cells

European urology supplements : official journal of the European Association of Urology, 2016-03, Vol.15 (3), p.e933-e933

2016

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Structural basis for the inhibition of IAPP fibril formation by the co-chaperonin prefoldin

Nature communications, 2022-05, Vol.13 (1), p.2363-13, Article 2363

2022

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Aβ oligomer elimination decreases tau oligomer concentration in CSF and enhances cognition in cognitively impaired aged Beagle dogs ‐ a model of sporadic Alzheimer’s disease

Alzheimer's & dementia, 2022-12, Vol.18 (S10), p.n/a

2022

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In Vitro and In Vivo Efficacies of the Linear and the Cyclic Version of an All-d-Enantiomeric Peptide Developed for the Treatment of Alzheimer’s Disease

International journal of molecular sciences, 2021-06, Vol.22 (12), p.6553

2021

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Stabilization of Monomeric Tau Protein by All D-Enantiomeric Peptide Ligands as Therapeutic Strategy for Alzheimer's Disease and Other Tauopathies

International journal of molecular sciences, 2023-01, Vol.24 (3), p.2161

2023

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Deceleration of the neurodegenerative phenotype in pyroglutamate-Aβ accumulating transgenic mice by oral treatment with the Aβ oligomer eliminating compound RD2

Neurobiology of disease, 2019-04, Vol.124, p.36-45

2019

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Large-Scale Oral Treatment Study with the Four Most Promising D3-Derivatives for the Treatment of Alzheimer's Disease

Molecules (Basel, Switzerland), 2017-10, Vol.22 (10), p.1693

2017

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Ex vivo target engagement of the Abeta oligomer disassembling compound RD2 in patient derived brain homogenates

Alzheimer's & dementia, 2022-12, Vol.18 (S10), p.n/a

2022

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PEAβ Triggers Cognitive Decline and Amyloid Burden in a Novel Mouse Model of Alzheimer’s Disease

International journal of molecular sciences, 2021-07, Vol.22 (13), p.7062

2021

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Comparison of the Amyloid Load in the Brains of Two Transgenic Alzheimer’s Disease Mouse Models Quantified by Florbetaben Positron Emission Tomography

Frontiers in neuroscience, 2021-10, Vol.15, p.699926-699926

2021

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P2‐061: Aβ‐OLIGOMER ELIMINATING D‐PEPTIDES: A RATIONAL DRUG OPTIMIZATION STRATEGY LEADS TO A HIGHER IN VITRO EFFICACY

Alzheimer's & dementia, 2019-07, Vol.15 (7S_Part_11), p.P594-P594

2019

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EXPLORING A POTENTIALLY DIFFERENT OR ADDITIONAL MOA FOR THE CLINICAL STAGE COMPOUND PRI-002

Alzheimer's & dementia, 2019-07, Vol.15 (7), p.P1589-P1589

2019

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P4‐671: DO WE NEED ANTI‐PRIONIC COMPOUNDS TO TREAT ALZHEIMER'S DISEASE?

Alzheimer's & dementia, 2019-07, Vol.15 (7S_Part_30), p.P1588-P1589

2019

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DO WE NEED ANTI-PRIONIC COMPOUNDS TO TREAT ALZHEIMER’S DISEASE?

Alzheimer's & dementia, 2019-07, Vol.15 (7), p.P1588-P1589

2019

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P4‐672: EXPLORING A POTENTIALLY DIFFERENT OR ADDITIONAL MOA FOR THE CLINICAL STAGE COMPOUND PRI‐002

Alzheimer's & dementia, 2019-07, Vol.15 (7S_Part_30), p.P1589-P1589

2019

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Aβ-OLIGOMER ELIMINATING D-PEPTIDES: A RATIONAL DRUG OPTIMIZATION STRATEGY LEADS TO A HIGHER IN VITRO EFFICACY

Alzheimer's & dementia, 2019-07, Vol.15 (7), p.P594-P594

2019

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O4‐02‐06: ORAL TREATMENT WITH RD2 REDUCES Aβ OLIGOMER LOAD, ENHANCES COGNITION, DECELERATES NEURODEGENERATION, REVERSES DISEASE PHENOTYPE IN OLD‐AGED TG AD MICE, AND IS SAFE IN HUMANS

Alzheimer's & dementia, 2019-07, Vol.15 (7S_Part_23), p.P1233-P1234

2019

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ORAL TREATMENT WITH RD2 REDUCES Aβ OLIGOMER LOAD, ENHANCES COGNITION, DECELERATES NEURODEGENERATION, REVERSES DISEASE PHENOTYPE IN OLD-AGED TG AD MICE, AND IS SAFE IN HUMANS

Alzheimer's & dementia, 2019-07, Vol.15 (7), p.P1233-P1234

2019

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Cryo-EM of Aβ fibrils from mouse models find tg-APP ArcSwe fibrils resemble those found in patients with sporadic Alzheimer's disease

Nature neuroscience, 2023-12, Vol.26 (12), p.2073

2023

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Cryo-EM of Aβ fibrils from mouse models find tg-APPArcSwe fibrils resemble those found in patients with sporadic Alzheimer’s disease

Nature neuroscience, 2023-12, Vol.26 (12), p.2073-2080

2023

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Comparison of blood-brain barrier penetration efficiencies between linear and cyclic all-d-enantiomeric peptides developed for the treatment of Alzheimer's disease

European journal of pharmaceutical sciences, 2018-03, Vol.114, p.93-102

2018

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The Aβ oligomer eliminating D-enantiomeric peptide RD2 improves cognition without changing plaque pathology

Scientific reports, 2017-11, Vol.7 (1), p.16275-12, Article 16275

2017

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Aβ Oligomer Elimination Restores Cognition in Transgenic Alzheimer’s Mice with Full-blown Pathology

Molecular neurobiology, 2019-03, Vol.56 (3), p.2211-2223

2019

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Oral absorption enhancement of the amyloid-β oligomer eliminating compound RD2 by conjugation with folic acid

European journal of pharmaceutical sciences, 2021-01, Vol.156, p.105581, Article 105581

2021

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Behavioural characterization of a new Alzheimer′s disease mouse model

Alzheimer's & dementia, 2020-12, Vol.16, p.n/a

2020

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933 Establishment of a new orthotopic in vivo examinable model of non-muscle invasive bladder cancer using RT112 reporter cells

Structural basis for the inhibition of IAPP fibril formation by the co-chaperonin prefoldin

Aβ oligomer elimination decreases tau oligomer concentration in CSF and enhances cognition in cognitively impaired aged Beagle dogs ‐ a model of sporadic Alzheimer’s disease

In Vitro and In Vivo Efficacies of the Linear and the Cyclic Version of an All-d-Enantiomeric Peptide Developed for the Treatment of Alzheimer’s Disease

Stabilization of Monomeric Tau Protein by All D-Enantiomeric Peptide Ligands as Therapeutic Strategy for Alzheimer's Disease and Other Tauopathies

Deceleration of the neurodegenerative phenotype in pyroglutamate-Aβ accumulating transgenic mice by oral treatment with the Aβ oligomer eliminating compound RD2

Large-Scale Oral Treatment Study with the Four Most Promising D3-Derivatives for the Treatment of Alzheimer's Disease

Ex vivo target engagement of the Abeta oligomer disassembling compound RD2 in patient derived brain homogenates

PEAβ Triggers Cognitive Decline and Amyloid Burden in a Novel Mouse Model of Alzheimer’s Disease

Comparison of the Amyloid Load in the Brains of Two Transgenic Alzheimer’s Disease Mouse Models Quantified by Florbetaben Positron Emission Tomography

P2‐061: Aβ‐OLIGOMER ELIMINATING D‐PEPTIDES: A RATIONAL DRUG OPTIMIZATION STRATEGY LEADS TO A HIGHER IN VITRO EFFICACY

EXPLORING A POTENTIALLY DIFFERENT OR ADDITIONAL MOA FOR THE CLINICAL STAGE COMPOUND PRI-002

P4‐671: DO WE NEED ANTI‐PRIONIC COMPOUNDS TO TREAT ALZHEIMER'S DISEASE?

DO WE NEED ANTI-PRIONIC COMPOUNDS TO TREAT ALZHEIMER’S DISEASE?

P4‐672: EXPLORING A POTENTIALLY DIFFERENT OR ADDITIONAL MOA FOR THE CLINICAL STAGE COMPOUND PRI‐002

Aβ-OLIGOMER ELIMINATING D-PEPTIDES: A RATIONAL DRUG OPTIMIZATION STRATEGY LEADS TO A HIGHER IN VITRO EFFICACY

O4‐02‐06: ORAL TREATMENT WITH RD2 REDUCES Aβ OLIGOMER LOAD, ENHANCES COGNITION, DECELERATES NEURODEGENERATION, REVERSES DISEASE PHENOTYPE IN OLD‐AGED TG AD MICE, AND IS SAFE IN HUMANS

ORAL TREATMENT WITH RD2 REDUCES Aβ OLIGOMER LOAD, ENHANCES COGNITION, DECELERATES NEURODEGENERATION, REVERSES DISEASE PHENOTYPE IN OLD-AGED TG AD MICE, AND IS SAFE IN HUMANS

Cryo-EM of Aβ fibrils from mouse models find tg-APP ArcSwe fibrils resemble those found in patients with sporadic Alzheimer's disease

Cryo-EM of Aβ fibrils from mouse models find tg-APPArcSwe fibrils resemble those found in patients with sporadic Alzheimer’s disease

Comparison of blood-brain barrier penetration efficiencies between linear and cyclic all-d-enantiomeric peptides developed for the treatment of Alzheimer's disease

The Aβ oligomer eliminating D-enantiomeric peptide RD2 improves cognition without changing plaque pathology

Aβ Oligomer Elimination Restores Cognition in Transgenic Alzheimer’s Mice with Full-blown Pathology

Oral absorption enhancement of the amyloid-β oligomer eliminating compound RD2 by conjugation with folic acid

Behavioural characterization of a new Alzheimer′s disease mouse model

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