{"id":30366,"date":"2024-11-19T17:40:48","date_gmt":"2024-11-19T12:10:48","guid":{"rendered":"https:\/\/www.delveinsight.com\/blog\/?p=30366"},"modified":"2024-11-19T17:40:49","modified_gmt":"2024-11-19T12:10:49","slug":"ctad-conference-2024","status":"publish","type":"post","link":"https:\/\/www.delveinsight.com\/blog\/ctad-conference-2024","title":{"rendered":"A Deep Dive into the 17th Clinical Trials on Alzheimer\u2019s Disease (CTAD) Conference"},"content":{"rendered":"\n

The 17th Clinical Trials on Alzheimer\u2019s Disease (CTAD)<\/strong> Conference, held in Madrid from October 29 to November 1, 2024,<\/strong> set the stage for groundbreaking updates in Alzheimer\u2019s research<\/strong>, as pharmaceutical leaders presented their latest findings on novel therapies and cutting-edge clinical trials. With an ever-growing urgency to tackle this devastating disease, the event attracted top industry players who shared pivotal insights into the future of Alzheimer\u2019s, a disease with a prevalence of approximately 6.9 million<\/strong> in the US alone with 97% of the patients aged 65 and above, as per Delveinsight\u2019s estimates in <\/strong>Alzheimer’s Disease Epidem Report<\/strong><\/a>. The conference illuminated significant advancements in Alzheimer\u2019s research, particularly in the realm of amyloid-targeting therapies<\/strong> and precision medicine<\/strong>.<\/p>\n\n\n\n

Eli Lilly<\/strong> dominated the stage with compelling updates on KISUNLA (donanemab)<\/strong>, its monoclonal antibody that has already received the US FDA<\/strong> approval for treating early symptomatic Alzheimer\u2019s in July 2024 <\/strong>followed by approval in Japan <\/strong>and Great Britain <\/strong>in September 2024 <\/strong>and October 2024 <\/strong>respectively. The TRAILBLAZER-ALZ 6<\/strong> Phase IIIb study revealed the potential for alternative dosing regimens<\/strong> to reduce amyloid-related imaging abnormalities (ARIA-E)<\/strong>, showcasing a 41% reduction<\/strong> in ARIA-E incidence with a modified titration approach. These results, along with the genetic insights showing a 67% reduction in ARIA-E<\/strong> risk in APOE4 carriers<\/strong>, underscore the growing significance of personalized treatments<\/strong> in improving safety and efficacy. Additionally, the TRAILBLAZER-ALZ 6<\/strong> study’s reaffirmation of amyloid plaque clearance<\/strong> as a key mechanism to slow cognitive decline solidified KISUNLA\u2019s role in the evolving landscape of Alzheimer\u2019s therapies.<\/p>\n\n\n\n

Alongside KISUNLA, Lilly also presented data on emerging assets such as Ceperognastat (LY3372689)<\/strong>, an O-GlcNAcase inhibitor<\/strong>, and remternetug (LY3372993)<\/strong>, which focus on tau pathology<\/strong> and microglial-mediated amyloid clearance<\/strong>, respectively. Although Ceperognastat<\/strong> failed to meet its primary endpoint in the PROSPECT-ALZ<\/strong> study, its biomarker data highlighted the ongoing relevance of tau-targeting approaches. Meanwhile, remternetug<\/strong> enters Phase III trials with a decentralized study design aimed at expanding participant accessibility and enhancing recruitment. The trial\u2019s focus on plasma P-tau levels<\/strong> as a biomarker for early-stage Alzheimer\u2019s reflects the growing shift toward blood-based diagnostics<\/strong> in clinical trials, offering a glimpse into the future of more efficient and inclusive Alzheimer\u2019s research. The conference underscored a collective drive toward multi-targeted therapies<\/strong> and personalized medicine<\/strong>, with both amyloid and tau remain central to future breakthroughs in Alzheimer’s treatment<\/a>.<\/p>\n\n\n\n

Next, Eisai<\/strong>, a longstanding leader in the Alzheimer\u2019s space showcased pivotal advancements in the Alzheimer’s treatment landscape, with key presentations focusing on LEQEMBI (lecanemab)<\/strong> and the company\u2019s broader pipeline. LEQEMBI<\/a>, an anti-amyloid beta (A\u03b2) protofibril antibody <\/strong>approved in July 2023<\/strong>, is designed to target the toxic protofibrils of amyloid beta that accumulate early in Alzheimer’s disease and drive neurodegeneration. The latest findings from the Phase III Clarity AD study<\/strong> further solidified LEQEMBI\u2019s position as a potential disease-modifying therapy<\/strong>. After three years of continuous treatment<\/strong>, the drug demonstrated significant long-term benefits, 59% of patients<\/strong> with low tau accumulation showed improvement or no decline<\/strong> in cognitive function, as measured by CDR-SB<\/strong>. Furthermore, LEQEMBI was associated with a 30% reduction in the risk of progression<\/strong> to more advanced stages of Alzheimer\u2019s, underscoring its potential as an early intervention<\/strong> treatment. Importantly, the long-term safety profile remained favorable, with minimal amyloid-related imaging abnormalities (ARIA)<\/strong> after the first six months, differentiating LEQEMBI from other amyloid-targeting agents that have faced greater safety concerns in extended use.<\/p>\n\n\n\n

\"Timeline<\/figure>\n\n\n\n

In addition to the LEQEMBI<\/strong> updates, Eisai also presented exciting data<\/strong> on E2814<\/strong>, an investigational anti-MTBR tau antibody<\/strong> developed in collaboration with University College London<\/strong>. E2814 targets the microtubule-binding region (MTBR)<\/strong> of tau, a protein implicated in the formation and spread of neurofibrillary tangles in Alzheimer\u2019s. Data from the Phase I\/II<\/strong> studies presented at CTAD showed substantial reductions in tau biomarkers<\/strong> like p-tau217<\/strong> and MTBR-tau243<\/strong> in cerebrospinal fluid, as well as stabilization or reduction in tau accumulation<\/strong> on tau PET scans. This evidence supports E2814\u2019s ability to halt tau propagation<\/strong>, a major driver of neurodegeneration in Alzheimer\u2019s. Notably, E2814 has been selected as the first investigational drug for the Dominantly Inherited Alzheimer\u2019s Network\u2019s (DIAN-TU)<\/strong> Tau NexGen<\/strong> study, a Phase II\/III<\/strong> trial designed to explore tau-targeting therapies in Dominantly Inherited Alzheimer\u2019s Disease (DIAD)<\/strong>. Additionally, Eisai launched Study 202<\/strong>, a Phase II trial investigating E2814 in sporadic early Alzheimer\u2019s<\/strong>, in combination with LEQEMBI. These findings underscore Eisai’s strategy to target both amyloid <\/strong>and tau<\/strong>, aiming for a comprehensive approach<\/strong> to disease modification. With ongoing trials and global submissions, Eisai is positioning itself at the forefront of Alzheimer\u2019s research, offering a multi-pronged approach that addresses the disease\u2019s hallmark pathologies.<\/p>\n\n\n\n

Alzheimer’s Severity Segmentation <\/strong><\/td>% Contribution in Approximation<\/strong><\/td><\/tr>
MCI<\/td>54%<\/td><\/tr>
Mild Dementia<\/td>19%<\/td><\/tr>
Moderate Dementia<\/td>16%<\/td><\/tr>
Severe Dementia<\/td>11%<\/td><\/tr>
Delveinsight\u2019s Estimates<\/em><\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n

Other significant presentations at CTAD 2024<\/strong> included Lexeo Therapeutics<\/strong>\u2019 transformative interim results from their Phase I\/II study<\/strong> of LX1001<\/strong>, a groundbreaking gene therapy<\/strong> targeting the APOE4 allele in individuals at 15 times higher risk<\/strong> for Alzheimer’s progression. LX1001 demonstrated dose-dependent increases in APOE2 protein expression<\/strong>, sustained for up to 12 months<\/strong>, effectively counteracting the toxic effects of the APOE4 allele. This was coupled with reliable reductions in tau biomarkers<\/strong>, including CSF T-tau<\/strong> and P-tau181<\/strong>, and tau PET<\/strong> scans, suggesting a potential breakthrough in reversing tau-driven neurodegeneration. Furthermore, amyloid pathology remained stable<\/strong> in most patients, signifying that LX1001<\/strong> has the potential to halt disease progression by addressing Alzheimer’s pathology at its very core. As FDA engagement<\/strong> intensifies, Lexeo<\/strong> is positioning LX1001<\/strong> for pivotal trials, paving the way for a new era of precision medicine<\/strong> in Alzheimer\u2019s treatment.<\/p>\n\n\n\n

In addition to Lexeo Therapeutics<\/strong>, Athira Pharma<\/strong> also presented intriguing insights from its Phase II\/III LIFT-AD trial<\/strong> of fosgonimeton<\/strong> in Alzheimer\u2019s disease. Despite failing to meet statistical significance for the primary endpoints, cognition,<\/strong> and function<\/strong> showed directional improvements, particularly among participants with moderate Alzheimer\u2019s<\/strong> and those carrying the APOE4 allele<\/strong>. The biomarker data<\/strong> revealed favorable trends in amyloid<\/strong>, tau<\/strong>, and neurodegeneration markers<\/strong>, highlighting fosgonimeton\u2019s<\/strong> potential to modulate hepatocyte growth factor (HGF)<\/strong> and offer neuroprotective benefits<\/strong> in Alzheimer\u2019s disease. This reinforces the growing interest in therapies that work by enhancing neuroprotection<\/strong> and slowing disease progression<\/strong> from the inside out<\/strong>.<\/p>\n\n\n\n

Moreover, Annovis Bio<\/strong> presented promising Phase II\/III buntanetap<\/strong> data, showing significant improvements in primary endpoints<\/strong>, including cognitive function<\/strong> (as measured by ADAS-Cog<\/strong>) and functional outcomes<\/strong> (via ADCS-ADL<\/strong>), in early Alzheimer’s patients<\/strong>. Buntanetap also demonstrated a reduction in tau and amyloid biomarkers<\/strong>, further positioning it as a disease-modifying therapy<\/strong> that targets both neurodegeneration<\/strong> and amyloid pathology<\/strong>\u2014key hallmarks of Alzheimer\u2019s disease. The company’s findings underscore the importance of multi-targeted approaches<\/strong> that can intervene at multiple stages of Alzheimer’s pathology, which is essential in slowing the relentless progression of this debilitating disease.<\/p>\n\n\n\n

The below-mentioned table provides a glimpse of upcoming competitors in Alzheimer\u2019s space<\/strong><\/a>:<\/p>\n\n\n\n

Emerging Competitive Landscape of Alzheimer\u2019s Disease<\/strong><\/td><\/tr>
Drug Name<\/strong><\/td>Company<\/strong><\/td>Indication<\/strong><\/td>Phase<\/strong><\/td>Molecule Type<\/strong><\/td>RoA<\/strong><\/td>MoA<\/strong><\/td><\/tr>
Masitinib<\/strong><\/td>AB Science<\/td>Mild-to-moderate Alzheimer’s disease<\/td>III<\/td>Small molecule<\/td>Oral<\/td>Inhibition of the c-Kit, Lyn, Fyn and CSF1R kinases<\/td><\/tr>
ACP-204<\/strong>a<\/sup><\/strong><\/td>ACADIA Pharmaceuticals Inc.<\/td>Adults with Alzheimer’s disease psychosis<\/td>III<\/td>Small molecule<\/td>Oral<\/td>5-HT2A serotonin receptor agonist<\/td><\/tr>
Valiltramiprosate\/ALZ-801<\/strong><\/td>Alzheon<\/td>Early Alzheimer’s disease and APOE4\/4 genotype<\/td>III<\/td>Small molecule<\/td>Oral<\/td>Amyloid beta-protein inhibitors; GABA A receptor agonists<\/td><\/tr>
Mirodenafil (AR1001)<\/strong><\/td>AriBio <\/td>Early Alzheimer’s disease<\/td>III<\/td>Small molecule<\/td>Oral<\/td>Type 5 cyclic nucleotide phosphodiesterase inhibitors<\/td><\/tr>
Bupropion\/dextromethorphan (AXS-05)<\/strong><\/td>Axsome Therapeutics<\/td>Alzheimer’s Disease Agitation<\/td>III<\/td>Small molecule<\/td>Oral<\/td>NMDA receptor antagonist<\/td><\/tr>
Bezisterim (NE3107)<\/strong><\/td>BioVie<\/td>Mild-to-moderate probable AD<\/td>III<\/td>Small Molecule<\/td>Oral<\/td>Anti-inflammatory<\/td><\/tr>
Simufilam (PTI-125)<\/strong><\/td>Cassava Sciences<\/td>Mild-to-moderate Alzheimer’s disease<\/td>III<\/td>Small Molecule<\/td>Oral<\/td>Microfilament protein modulators<\/td><\/tr>
Tricaprilin (CER0001)<\/strong><\/td>Cerecin<\/td>Mild-to-moderately severe probable Alzheimer disease<\/td>III<\/td>Medium-chain triglyceride (MCT)<\/td>Oral<\/td>Ketosis inducer<\/td><\/tr>
Lecanemab<\/strong>**<\/sup><\/strong><\/td>Eisai <\/td>Early Alzheimer’s disease<\/td>III<\/td>mAb<\/td>IV\/SC<\/td>Amyloid beta-protein inhibitors<\/td><\/tr>
Donanemab<\/strong>**<\/sup><\/strong><\/td>Eli Lilly and Company<\/td>Preclinical Alzheimer’s disease<\/td>III<\/td>mAb<\/td>IV<\/td>Pyroglutamyl(3)-amyloid beta-protein (3-42) inhibitors<\/td><\/tr>
Remternetug<\/strong>**<\/sup><\/strong><\/td>Eli Lilly and Company<\/td>Early symptomatic Alzheimer’s disease<\/td>III<\/td>mAb<\/td>IV\/SC<\/td>Pyroglutamyl(3)-amyloid beta-protein (3-42) inhibitors<\/td><\/tr>
KarXT (Trospium chloride\/xanomeline )<\/strong><\/td>Karuna Therapeutics (Bristol Myers Squibb)<\/td>Psychosis associated with Alzheimer’s disease<\/td>III<\/td>Small molecule<\/td>Oral<\/td>Muscarinic M1\/M4 receptor agonists<\/td><\/tr>
Semaglutide<\/strong><\/td>Novo Nordisk <\/td>Early Alzheimer\u00b4s disease<\/td>III<\/td>Peptides<\/td>Oral<\/td>GLP-1 analogue<\/td><\/tr>
Masupirdine (SUVN-502)<\/strong><\/td>Suven Life Sciences <\/td>Agitation in participants with dementia of the Alzheimer’s type<\/td>III<\/td>Small molecule<\/td>Oral<\/td>5-HT6 antagonist<\/td><\/tr>
E2814<\/strong>**<\/sup><\/strong><\/td>Eisai; University College London<\/td>Dominantly inherited Alzheimer’s disease<\/td>III<\/td>mAb<\/td>IV<\/td>Tau protein inhibitors<\/td><\/tr>
Sabirnetug (ACU193)<\/strong>b **<\/sup><\/strong><\/td>Acumen Pharmaceuticals<\/td>Early Alzheimer’s disease<\/td>II\/III<\/td>mAb<\/td>IV<\/td>Amyloid beta-protein inhibitors<\/td><\/tr>
AGB101<\/strong><\/td>AgeneBio<\/td>Mild cognitive Impairment due to Alzheimer’s disease<\/td>II\/III<\/td>Small molecule<\/td>Oral<\/td>SV2A protein modulators<\/td><\/tr>
ANAVEX2-73<\/strong>c<\/sup><\/strong> (Blarcamesine)<\/strong><\/td>Anavex Life Sciences <\/td>Early Alzheimer’s disease<\/td>II\/III<\/td>Small molecule<\/td>Oral<\/td>Muscarinic receptor modulators; Sigma-1 receptor agonists<\/td><\/tr>
Buntanetap (ANVS401 or posiphen)<\/strong><\/td>Annovis Bio<\/td>Mild-to-moderate Alzheimer’s disease<\/td>II\/III<\/td>Small molecule<\/td>Oral<\/td>Acetylcholinesterase inhibitors; Alpha-synuclein inhibitors; Amyloid beta-protein precursor inhibitors; HD protein inhibitors; Tau protein inhibitors<\/td><\/tr>
Fosgonimeton (ATH-1017)<\/strong> d<\/sup><\/strong><\/td>Athira Pharma<\/td>Mild-to-moderate Alzheimer’s disease<\/td>II\/III<\/td>Small molecule<\/td>SC<\/td>Hepatocyte growth factor stimulants; Proto-oncogene protein c-met stimulants<\/td><\/tr>
Piromelatine<\/strong><\/td>Neurim Pharmaceuticals <\/td>Mild dementia due to Alzheimer’s disease<\/td>II\/III<\/td>Small molecule<\/td>Oral<\/td>Melatonin MT1, 2, and 3 and serotonin 5-HT-1A and -1D receptors agonist<\/td><\/tr>
TRx0237<\/strong><\/td>TauRx Therapeutics <\/td>Alzheimer’s disease<\/td>III<\/td>Small molecule<\/td>Oral<\/td>Synuclein inhibitors; Tau protein inhibitors; TDP-43 protein inhibitors<\/td><\/tr>
ABBV-552<\/strong><\/td>AbbVie<\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>SV2A protein agonists<\/td><\/tr>
ABBV-916<\/strong>**<\/sup><\/strong><\/td>AbbVie<\/td>Alzheimer disease<\/td>II<\/td>mAb<\/td>IV<\/td>Amyloid beta-protein inhibitors<\/td><\/tr>
AL002<\/strong>**<\/sup><\/strong><\/td>AbbVie\/ Allector Pharma<\/td>Alzheimer disease<\/td>II<\/td>mAb<\/td>IV<\/td>TREM2 protein-stimulants<\/td><\/tr>
Trontinemab (RG6102)\/ RO 7126209<\/strong>**<\/sup><\/strong><\/td>Roche<\/td>Alzheimer disease<\/td>II<\/td>mAb<\/td>IV<\/td>Amyloid beta-protein inhibitors<\/td><\/tr>
bepranemab (RG6416)\/ UCB0107<\/strong>**<\/sup><\/strong><\/td>Roche\/ UCB Pharma \/ Genentech<\/td>Prodromal-to-mild Alzheimer\u2019s disease<\/td>II<\/td>mAb<\/td>IV infusion<\/td>Anti-tau antibody<\/td><\/tr>
Mevidalen<\/strong><\/td>Eli Lilly and Company<\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Dopamine D1 receptor modulators<\/td><\/tr>
LY3372689 ( O-GlcNAcase inhibitor)<\/strong><\/td>Eli Lilly and Company<\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Hexosaminidase C inhibitors<\/td><\/tr>
AL001<\/strong>e<\/sup><\/strong><\/td>Alzamend Neuro<\/td>Alzheimer disease<\/td>II<\/td>lithium-delivery system<\/td>Oral<\/td>Sortilin inhibitors<\/td><\/tr>
Human Mesenchymal Stem Cells<\/strong><\/td>Stemedica Cell Technologies<\/td>Alzheimer disease<\/td>IIa<\/td>Adult stem cll<\/td>IV<\/td>Reduction of amyloid-beta plaques and hyperphosphorylated tau<\/td><\/tr>
NEFLAMAPIMOD (VX-745)<\/strong><\/td>Cervomed<\/td>Early onset Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Inhibition of p38\u03b1<\/td><\/tr>
CT1812<\/strong><\/td>Cognition Therapeutics<\/td>Mild-to-moderate Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Prevent the binding of toxic oligomers<\/td><\/tr>
Varoglutamstat (PQ912)<\/strong>f<\/sup><\/strong><\/td>Vivoryon Therapeutics <\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Glutaminyl cyclase (QC) enzyme inhibitor<\/td><\/tr>
ACI-24.060<\/strong>g *<\/sup><\/strong><\/td>AC Immune SA<\/td>Alzheimer disease<\/td>II<\/td>Vaccine<\/td>IV<\/td>Immunostimulants<\/td><\/tr>
Seltorexant<\/strong><\/td>Janssen <\/td>Probable Alzheimer’s with clinically significant agitation\/aggression<\/td>II<\/td>Small Molecule<\/td>Oral<\/td>Selective antagonist of the human orexin-2 receptor<\/td><\/tr>
Posdinemab<\/strong>**<\/sup><\/strong><\/td>Janssen <\/td>Alzheimer’s disease (AUTONOMY)<\/td>II<\/td>mAb<\/td>IV<\/td>Immunomodulators<\/td><\/tr>
Pepinemab<\/strong>h **<\/sup><\/strong><\/td>Vaccinex <\/td>Alzheimer disease<\/td>II<\/td>mAb<\/td>IV<\/td>SEMA4D Inhibitor<\/td><\/tr>
T3D-959<\/strong><\/td>T3D Therapeutics<\/td>Alzheimer disease<\/td>II<\/td>Small Molecule<\/td>Oral<\/td>PPAR (Peroxisome Proliferator-Activated Receptor) delta agonist<\/td><\/tr>
GRF6019<\/strong><\/td>Alkahest\/ Grifols<\/td>Mild-to-moderate Alzheimer disease<\/td>II<\/td>plasma-derived product<\/td>IV<\/td>Neurogenesis stimulants<\/td><\/tr>
TB006<\/strong>i **<\/sup><\/strong><\/td>TrueBinding<\/td>Alzheimer disease<\/td>II<\/td>mAB<\/td>IV<\/td>Galectin-3 (Gal-3)<\/td><\/tr>
GSK4527226 (AL-101)<\/strong>**<\/sup><\/strong><\/td>GlaxoSmithKline\/Alector<\/td>Alzheimer disease<\/td>II<\/td>mAB<\/td>IV<\/td>Anti-sortilin monoclonal antibody<\/td><\/tr>
Hydroxypropyl Beta Cyclodextrin<\/strong><\/td>Cyclo Therapeutics<\/td>Early Alzheimer’s disease<\/td>IIb<\/td>Beta-Cyclodextrins<\/td>IV infusion<\/td>Cholesterol modulators<\/td><\/tr>
RG6289<\/strong><\/td>Roche<\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>\u03b3-secretase modulator (GSM)<\/td><\/tr>
Nanolithium (NP03)<\/strong><\/td>Medesis Pharma <\/td>Alzheimer disease<\/td>II<\/td>microdose lithium formulation<\/td>transmucosal<\/td>Inhibition of BACE1<\/td><\/tr>
AADvac1<\/strong>*<\/sup><\/strong><\/td>Axon Neuroscience <\/td>Alzheimer disease<\/td>II<\/td>Peptide vaccine<\/td>SC<\/td>Promotion of Tau Clearance<\/td><\/tr>
BPN14770<\/strong><\/td>Tetra Discovery Partners<\/td>Cognition Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>PDE4D Inhibitor<\/td><\/tr>
BMS-986446<\/strong>**<\/sup><\/strong><\/td>Bristol-Myers Squibb<\/td>Alzheimer disease<\/td>II<\/td>mAb<\/td>IV\/SC<\/td>Anti-MTBR Tau<\/td><\/tr>
IONIS MAPTRx\/ BIIB080<\/strong><\/td>Ionis Pharmaceutical\/ Biogen<\/td>Alzheimer disease<\/td>II<\/td>Antisense oligonucleotides<\/td>Intrathecal<\/td>Tau protein expression inhibitors<\/td><\/tr>
Allogeneic MSC<\/strong><\/td>Longeveron<\/td>Mild Alzheimer disease<\/td>II<\/td>Mesenchymal stem cell therapies<\/td>Infusion<\/td>Cell Replacement<\/td><\/tr>
AD-35<\/strong><\/td>Zhejiang Hisun Pharmaceutical<\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Amyloid beta-protein inhibitors; Astrocyte inhibitors<\/td><\/tr>
PRI-002<\/strong><\/td>PRInnovation GmbH\/ Priavoid<\/td>MCI-to-Mild dementia due to Alzheimer’s disease<\/td>II<\/td>Peptide<\/td>Oral<\/td>Amyloid Beta-protein inhibitor<\/td><\/tr>
Xanamem<\/strong><\/td>Actinogen Medical<\/td>Mild or moderate dementia due to AD<\/td>IIb<\/td>Small molecule<\/td>Oral<\/td>11\u03b2-HSD1 inhibitors<\/td><\/tr>
ABvac40<\/strong>*<\/sup><\/strong><\/td>Araclon Biotech <\/td>Alzheimer disease<\/td>II<\/td>Peptide vaccines<\/td>SC<\/td>Amyloid beta-protein inhibitors; Immunostimulants<\/td><\/tr>
BAC<\/strong><\/td>Charsire Biotechnology <\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Topical<\/td>–<\/td><\/tr>
Tertomotide (GV1001)<\/strong>*<\/sup><\/strong><\/td>GemVax & Kael<\/td>Alzheimer disease<\/td>II<\/td>Peptide Vaccine<\/td>SC<\/td>Immunostimulants<\/td><\/tr>
Dalzanemdor (SAGE-718)<\/strong><\/td>Sage Therapeutics<\/td>Alzheimer\u2019s disease mild cognitive impairment and mild dementia<\/td>II<\/td>Small molecule<\/td>Oral<\/td>NMDA receptor modulators<\/td><\/tr>
ITI-1284<\/strong><\/td>Intra-Cellular Therapies<\/td>Psychosis associated with Alzheimer’s disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Serotonin uptake inhibitors<\/td><\/tr>
APH-1105<\/strong><\/td>Aphios<\/td>Alzheimer disease<\/td>II<\/td>Amyloid precursor protein secretase modulators<\/td>Intranasal<\/td>Amyloid precursor protein secretase modulators<\/td><\/tr>
IGC-AD1<\/strong><\/td>IGC Pharma<\/td>Alzheimer disease<\/td>II<\/td>Small molecule<\/td>Oral<\/td>Neuroinflammation AB Plaque Neurofibrilaaru Tangles<\/td><\/tr>
ACI-35.030<\/strong>*<\/sup><\/strong><\/td>AC Immune<\/td>Alzheimer disease<\/td>II<\/td>Vaccine<\/td>IV<\/td>Immunostimulants<\/td><\/tr>
LX1001<\/strong><\/td>Lexeo Therapeutics<\/td>Alzheimer disease<\/td>I\/II<\/td>Gene therapy<\/td>Gene Transfer<\/td>Expression of APOE2 gene<\/td><\/tr>
ALZN002<\/strong><\/td>Alzamend Neuro<\/td>Alzheimer disease<\/td>I\/II<\/td>Biologics<\/td>IV<\/td>Dendritic Cell Activation<\/td><\/tr>
a<\/sup><\/strong>According to CT it is in Phase III but in the pipeline it is in Phase II<\/strong>b<\/sup><\/strong>Currently in recruting phase II\/III trial, results Phase Ib available<\/strong>c<\/sup><\/strong>Blarcamesine is an investigational drug that is not available for sale and has not been determined to be safe and effective by any regulatory authority.<\/strong>d<\/sup><\/strong>Negative clinical trial results<\/strong>e<\/sup><\/strong>Anticipate initiating a Phase II clinical studies in Alzheimer\u2019s patients in 2025<\/strong>f<\/sup><\/strong>latest trial is terminated Phase IIa<\/strong>g<\/sup><\/strong>Partnered with Takeda<\/strong>h<\/sup><\/strong>It is available only on pipeline. Do not have any details related to clinical trial<\/strong>i<\/sup><\/strong>TB006 received FDA renewal approval for expanded access program<\/strong>*<\/sup><\/strong>Vaccine candidates<\/strong>**<\/sup><\/strong>Monoclonal antibody<\/strong>
<\/strong>Updated as of September 2024<\/em><\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n

Several companies, including UCB, Hoffmann-La Roche, Janssen Research & Development, Anavex Life Sciences, Acumen Pharmaceuticals, Vaccinex, Cognition Therapeutics, <\/strong>and others<\/strong> also contributed to the conference with oral presentations<\/strong>, symposiums<\/strong>, and posters<\/strong> on their developing Alzheimer\u2019s treatments. These presentations demonstrated the broad scope of ongoing research and innovation in the Alzheimer’s space, signaling an exciting future with diverse strategies aimed at tackling the disease from every possible angle.<\/p>\n\n\n\n

Overall, <\/strong>the 17th CTAD<\/strong> conference highlighted a pivotal moment in Alzheimer\u2019s research, where the convergence of novel therapies<\/strong>, advanced biomarker technologies<\/strong>, and personalized medicine<\/strong> has laid the foundation for the next generation of treatments. From amyloid-targeting monoclonal antibodies<\/strong> like KISUNLA<\/strong> and LEQEMBI <\/strong>to gene therapies<\/strong> like LX1001<\/strong>, and tau-targeting agents<\/strong> like E2814<\/strong>, the therapeutic landscape is evolving rapidly. The data shared at CTAD demonstrate a clear shift towards multi-targeted approaches<\/strong> that address the root causes of Alzheimer\u2019s<\/strong>, offering more precise<\/strong>, personalized<\/strong> solutions for patients. The progress seen at CTAD 2024, coupled with promising early-phase results<\/strong> and pivotal clinical trial advancements<\/strong>, marks a crucial milestone on the path to disease-modifying therapies<\/strong>. This collective drive towards innovation<\/strong>, collaboration<\/strong>, and cutting-edge technology<\/strong> provides a hopeful outlook for the future, as the battle against Alzheimer\u2019s enters a new and more targeted<\/strong> phase.<\/p>\n\n\n\n

For more epidemiology, competitive landscape and market related insights on Alzheimer\u2019s Disease, refer to our reports:<\/p>\n\n\n\n