Traitements10programmes
Essais4liés
Publications0liées
SourceDBlocale

Traitements

10
MoléculeIndication / populationPhaseObjectifPaysRésultat
Abatacept Injection [Orencia] and Proleukin (aldesleukin)Description non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 1 Ralentissement de la progression United States À vérifier
Autologous T-regulatory lymphocytesDescription non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 1 Immunomodulation United States À vérifier
IL-2 (Aldesleukin)Alzheimer's disease (AD) is the most common cause of dementia. Despite major research efforts, effective treatments that slow or stop disease progression remain limited. Growing evidence suggests that inflammation in the brain and the body plays a key role in the onset and progression of AD. In particular, immune cells called regulatory T cells (Tregs), which normally help control inflammation, are impaired in AD individuals. This leads to increased activity of harmful immune pathways that worsen brain injury. Interleukin-2 (IL-2) is a drug that can restore the function of Tregs. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), such as semaglutide, are a class of drugs currently used to treat diabetes and obesity. Beyond their metabolic effects, GLP-1RAs also reduce inflammation, protect brain cells, and improve cellular energy balance. Laboratory studies, including our own, show that combining IL-2 with semaglutide has stronger effects than either drug alone. Together, they enhance Treg function, dampen harmful inflammatory responses, and improve cell survival. These findings support testing IL-2 plus semaglutide as a novel combination therapy for AD. We now propose a clinical trial to evaluate the safety, feasibility, and biological effects of this strategy. The study will enroll 30 individuals with AD, ages 50 to 86, who have a confirmed diagnosis by amyloid PET brain imaging and a Mini-Mental State Exam score between 16 and 26. Participants will be randomly assigned to one of three groups: (1) placebo, (2) low-dose IL-2 alone, or (3) IL-2 combined with semaglutide. Throughout the trial, participants will undergo regular medical exams, blood tests, and safety monitoring. We will measure how the treatment affects Tregs and other immune cells, inflammatory markers in blood and CSF, and established Alzheimer's biomarkers such as amyloid beta, tau, and neurofilament light chain. Cognitive and functional assessments will also be conducted to explore potential benefits on memory and daily living skills. If successful, this study will provide the first evidence that a dual immunotherapeutic strategy can safely modify disease-related processes in AD. Such findings would lay the foundation for larger clinical trials and could open the door to a new, multimodal approach to slowing or preventing Alzheimer's progression. Alzheimer Phase 1/2 Immunomodulation United States À vérifier
Interleukin-2Description non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 1 Immunomodulation United States À vérifier
Monthly autologous Treg cells infusions + 3 times per week Interleukin-2 injectionsDescription non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 2 United States À vérifier
Semaglutide Plus IL-2Alzheimer's disease (AD) is the most common cause of dementia. Despite major research efforts, effective treatments that slow or stop disease progression remain limited. Growing evidence suggests that inflammation in the brain and the body plays a key role in the onset and progression of AD. In particular, immune cells called regulatory T cells (Tregs), which normally help control inflammation, are impaired in AD individuals. This leads to increased activity of harmful immune pathways that worsen brain injury. Interleukin-2 (IL-2) is a drug that can restore the function of Tregs. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), such as semaglutide, are a class of drugs currently used to treat diabetes and obesity. Beyond their metabolic effects, GLP-1RAs also reduce inflammation, protect brain cells, and improve cellular energy balance. Laboratory studies, including our own, show that combining IL-2 with semaglutide has stronger effects than either drug alone. Together, they enhance Treg function, dampen harmful inflammatory responses, and improve cell survival. These findings support testing IL-2 plus semaglutide as a novel combination therapy for AD. We now propose a clinical trial to evaluate the safety, feasibility, and biological effects of this strategy. The study will enroll 30 individuals with AD, ages 50 to 86, who have a confirmed diagnosis by amyloid PET brain imaging and a Mini-Mental State Exam score between 16 and 26. Participants will be randomly assigned to one of three groups: (1) placebo, (2) low-dose IL-2 alone, or (3) IL-2 combined with semaglutide. Throughout the trial, participants will undergo regular medical exams, blood tests, and safety monitoring. We will measure how the treatment affects Tregs and other immune cells, inflammatory markers in blood and CSF, and established Alzheimer's biomarkers such as amyloid beta, tau, and neurofilament light chain. Cognitive and functional assessments will also be conducted to explore potential benefits on memory and daily living skills. If successful, this study will provide the first evidence that a dual immunotherapeutic strategy can safely modify disease-related processes in AD. Such findings would lay the foundation for larger clinical trials and could open the door to a new, multimodal approach to slowing or preventing Alzheimer's progression. Alzheimer Phase 1/2 Immunomodulation United States À vérifier
Abatacept Injection [Orencia] and Proleukin (aldesleukin)Description non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 1 Ralentissement de la progression United States À vérifier
Autologous T-regulatory lymphocytesDescription non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 1 Immunomodulation United States À vérifier
IL-2 (Aldesleukin)Alzheimer's disease (AD) is the most common cause of dementia. Despite major research efforts, effective treatments that slow or stop disease progression remain limited. Growing evidence suggests that inflammation in the brain and the body plays a key role in the onset and progression of AD. In particular, immune cells called regulatory T cells (Tregs), which normally help control inflammation, are impaired in AD individuals. This leads to increased activity of harmful immune pathways that worsen brain injury. Interleukin-2 (IL-2) is a drug that can restore the function of Tregs. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), such as semaglutide, are a class of drugs currently used to treat diabetes and obesity. Beyond their metabolic effects, GLP-1RAs also reduce inflammation, protect brain cells, and improve cellular energy balance. Laboratory studies, including our own, show that combining IL-2 with semaglutide has stronger effects than either drug alone. Together, they enhance Treg function, dampen harmful inflammatory responses, and improve cell survival. These findings support testing IL-2 plus semaglutide as a novel combination therapy for AD. We now propose a clinical trial to evaluate the safety, feasibility, and biological effects of this strategy. The study will enroll 30 individuals with AD, ages 50 to 86, who have a confirmed diagnosis by amyloid PET brain imaging and a Mini-Mental State Exam score between 16 and 26. Participants will be randomly assigned to one of three groups: (1) placebo, (2) low-dose IL-2 alone, or (3) IL-2 combined with semaglutide. Throughout the trial, participants will undergo regular medical exams, blood tests, and safety monitoring. We will measure how the treatment affects Tregs and other immune cells, inflammatory markers in blood and CSF, and established Alzheimer's biomarkers such as amyloid beta, tau, and neurofilament light chain. Cognitive and functional assessments will also be conducted to explore potential benefits on memory and daily living skills. If successful, this study will provide the first evidence that a dual immunotherapeutic strategy can safely modify disease-related processes in AD. Such findings would lay the foundation for larger clinical trials and could open the door to a new, multimodal approach to slowing or preventing Alzheimer's progression. Alzheimer Phase 1/2 Immunomodulation United States À vérifier
Monthly autologous Treg cells infusions + 3 times per week Interleukin-2 injectionsDescription non affichée : incohérence de maladie détectée. Consultez l’essai clinique officiel associé. Sclérose latérale amyotrophique Phase 2 United States À vérifier

Essais cliniques

4
MoléculeIndication / populationPhaseNCTTitreStatut
Monthly autologous Treg cells infusions + 3 times per week Interleukin-2 injections Sclérose latérale amyotrophique Phase 2 NCT04055623 Tregs in ALS — T-regulatory Cells in ALS COMPLETED
IL-2 (Aldesleukin) Alzheimer Phase 1/2 NCT07651319 Interleukine-2 (IL-2) Plus Semaglutide in Alzheimer's Disease RECRUITING
Autologous T-regulatory lymphocytes Sclérose latérale amyotrophique Phase 1 NCT03241784 Ph1 T-Regulatory Cells in Amyotrophic Lateral Sclerosis COMPLETED
Abatacept Injection [Orencia] and Proleukin (aldesleukin) Sclérose latérale amyotrophique Phase 1 NCT06307301 Study in ALS With Abatacept & IL-2 COMPLETED

Publications

0
MoléculeIndication / populationTitreJournalDate
Aucune publication.