AltPep Shows SOBIN-AD Peptide Improves Alzheimer’s Behavior in Preclinical Study at CTAD 2025

AltPep Corporation Presents New Preclinical Data Demonstrating SOBIN-AD Peptide Improves Cognition in Early and Symptomatic Alzheimer’s Disease Models at CTAD 2025

AltPep Corporation, a privately held biotechnology company dedicated to developing early disease-modifying therapies and innovative detection tools for amyloid-related diseases, announced today that it will present new preclinical data at the Clinical Trials on Alzheimer’s Disease Conference (CTAD 2025), held December 1–4 in San Diego, California. The findings further reinforce the potential of the company’s lead therapeutic candidate, SOBIN-AD (Soluble Oligomer Binding INhibitor), as a promising treatment for early-stage Alzheimer’s disease (AD).

Previously, at the Alzheimer’s Association International Conference (AAIC) in July 2025, AltPep showcased preclinical results demonstrating that SOBIN-AD selectively targets toxic α-sheet oligomers, enhances their clearance in vitro, inhibits amyloid plaque formation, and improves cognition in asymptomatic transgenic Alzheimer’s disease (Tg AD) mouse models. At CTAD 2025, AltPep will present additional data indicating that SOBIN-AD also enhances cognition in Tg AD mice after the onset of cognitive decline, highlighting its potential across multiple stages of disease progression.

Building on a Unique Mechanism of Action

“AltPep is thrilled to advance the development of SOBIN-AD as a disease-modifying therapeutic,” said Valerie Daggett, Ph.D., CEO and Founder of AltPep. “Our proprietary platform integrates both early detection and treatment strategies and is built upon the fundamental discovery that toxic oligomers—key early triggers of amyloid diseases such as AD—adopt a nonstandard protein structure known as the α-sheet. This mechanism differs substantially from that of existing Alzheimer’s therapeutics and may enable far more effective clinical outcomes by targeting the root cause of disease rather than downstream symptoms alone.”

SOBIN-AD is designed to selectively bind these α-sheet oligomers, preventing their aggregation into amyloid plaques and facilitating their clearance by microglial cells. By addressing the toxic oligomer species that drive neuronal damage, SOBIN-AD represents a fundamentally novel therapeutic approach that complements the growing emphasis on early intervention in Alzheimer’s disease.

Extending Preclinical Evidence Across Disease Stages

Carolyn Tallon, Ph.D., Principal Scientist at AltPep and presenter at CTAD 2025, noted, “Importantly, our latest results demonstrate that SOBIN-AD improves memory not only in asymptomatic Tg AD mice but also in mice that have already begun exhibiting cognitive deficits. In the asymptomatic group, SOBIN-AD treatment reduced amyloid plaque formation and mitigated age-related loss of synaptophysin, a protein crucial for neuronal signaling, at 15 months of age. The symptomatic group was studied at an earlier age, so age-related effects were not assessed in that cohort. These findings underscore the potential versatility of SOBIN-AD, supporting its development as a therapy suitable for both early and later stages of Alzheimer’s disease.”

The ability of SOBIN-AD to show efficacy both before and after the onset of cognitive decline is particularly noteworthy in the context of Alzheimer’s disease, where early intervention has been a focus but patients often present with symptoms at various stages. The preclinical evidence positions SOBIN-AD as a candidate capable of bridging this treatment gap, potentially benefiting a broad spectrum of patients.

Preclinical Findings Highlight Key Therapeutic Effects

Selected preclinical data to be presented at CTAD 2025 include the following:

  • Cognitive Improvement: SOBIN-AD administration improved cognition when started both prior to and after the onset of cognitive impairment. Tg2576 AD mice treated intranasally three times per week showed significant cognitive benefits after 24 weeks (pre-symptomatic) and 9 weeks (symptomatic), indicating both preventive and therapeutic potential.
  • Plaque Reduction and Synaptic Preservation: Treatment prior to cognitive impairment reduced amyloid-beta (Aβ) plaque formation and prevented synaptophysin loss in 15-month-old Tg AD mice. Synaptophysin is a key neuronal protein essential for signaling, and its preservation suggests maintained neuronal connectivity and function. These age-related effects were not evaluated in the symptomatic cohort, which was studied at a younger age.
  • Selective Targeting of Toxic α-Sheet Oligomers: SOBIN-AD exhibits high selectivity for α-sheet Aβ oligomers, which are widely recognized as the toxic species driving early neuronal damage, while sparing other forms of Aβ that are less pathogenic.
  • Enhanced Microglial Clearance: SOBIN-AD facilitates phagocytosis of toxic oligomers by microglial cells, a critical mechanism for removing pathogenic protein species from the brain and reducing downstream neuroinflammation.

These findings highlight SOBIN-AD’s unique multimodal mechanism, combining oligomer binding, plaque inhibition, synaptic preservation, and enhanced immune-mediated clearance to combat Alzheimer’s pathology from multiple angles.

CTAD 2025 Presentation Details

AltPep’s data will be presented as a poster at CTAD 2025:

  • Title: Targeting of Aβ Toxic Oligomers via a Designed Peptide Reduces Plaque Formation in an AD Mouse Model
  • Poster #: P269
  • Date/Time: Wednesday, December 3, 2025, 7:15 AM – 5:30 PM PT
  • Location: Hilton San Diego Bayfront – Poster Hall, Indigo Ballroom, Level 2

The poster will also be available for viewing in the Scientific Publications section of the AltPep website under “Presentations” at https://altpep.com/press/scientific-publications/.

Advancing Toward Clinical Development

Gil Block, M.D., Ph.D., Chief Medical Officer of AltPep, stated, “These data reinforce the promise of SOBIN-AD as a potential treatment for Alzheimer’s disease patients at various stages of progression. AltPep’s integrated platform for both early detection and treatment is especially timely, as the field urgently seeks new therapeutic options capable of modifying disease course rather than only alleviating symptoms. The demonstration of efficacy in both asymptomatic and symptomatic models supports our ongoing efforts to advance SOBIN-AD toward clinical testing.”

The AltPep platform, grounded in the discovery of α-sheet toxic oligomers, represents a departure from traditional approaches that target fibrillar amyloid plaques or downstream neurotransmitter dysfunction. By focusing on the early toxic species implicated in neuronal damage, SOBIN-AD has the potential to alter the trajectory of disease and preserve cognitive function more effectively than existing therapies.

About AltPep Corporation

AltPep Corporation is a biotechnology company pioneering early detection and disease-modifying therapies for amyloid diseases, including Alzheimer’s disease. The company’s proprietary technology platform is based on the identification and targeting of α-sheet toxic oligomers, a unique structural motif involved in the pathogenesis of multiple amyloid-related conditions. By integrating innovative therapeutic and diagnostic strategies, AltPep seeks to enable earlier interventions and improved outcomes for patients affected by these debilitating diseases.

The preclinical findings presented at CTAD 2025 strengthen the scientific rationale for SOBIN-AD as a versatile therapeutic candidate capable of improving cognitive function in both early and symptomatic stages of Alzheimer’s disease. With its selective targeting of α-sheet oligomers, ability to enhance microglial clearance, and preservation of synaptic integrity, SOBIN-AD represents a novel approach that could redefine disease-modifying strategies in AD.

AltPep’s continued research and forthcoming clinical development efforts aim to translate these preclinical successes into meaningful benefits for patients, addressing a critical unmet need in Alzheimer’s care. The company’s work underscores the importance of early intervention and the potential for targeted therapies to alter disease progression at its root.

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