Publication in Nature Molecular Psychiatry Supports Genuv’s Alternate Theory for Treatment of Alzheimer’s Disease

The article presents findings from Genuvs preclinical experiments treating a mouse model of Alzheimers with SNR1611, a commercially available MEK 1/2 inhibitor.

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Thursday, August 18, 2022
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Summary
Key Points: 
  • The article presents findings from Genuvs preclinical experiments treating a mouse model of Alzheimers with SNR1611, a commercially available MEK 1/2 inhibitor.
  • All research relevant to the publication was conducted in Genuvs laboratories or under Genuvs supervision.
  • The new publication in Molecular Psychiatry comes just weeks after an investigation in the journal Science uncovered evidence of potential data fabrication in a paper on Alzheimers disease published in 2006.
  • The publication has intensified interest in alternative approaches to treating Alzheimers disease, including Genuvs novel neuroprotection/neurogenesis hypothesis.


Genuv Inc., a clinical-stage biotechnology company focused on innovative drug discovery for central nervous system disorders and advanced antibody therapies for immuno-oncology, announced the publication of a manuscript in Molecular Psychiatry, a peer-reviewed scientific journal published by Springer Nature Group. The new research provides important validation for the company’s six-year effort to develop new treatments for neurodegenerative diseases including Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS).

The article presents findings from Genuv’s preclinical experiments treating a mouse model of Alzheimer’s with SNR1611, a commercially available MEK 1/2 inhibitor. Treating the mice with SNR1611 was found to protect neurons by inducing autophagic lysosomal activity, which in turn led to reductions in the amyloid beta plaques that are the physiological hallmark of the disease.

In addition, the orally administered drug led to the recovery of impaired neuronal structures and synaptic function. The mice even regained cognitive functions that had been lost to the disease. SNR1611 is a drug approved by the U.S. Food and Drug Administration and marketed under the trade name Mekinist® for treatment of melanoma.

“We are excited to share these extremely encouraging preclinical results,” said Sungho Han, Ph.D., founder and CEO of Genuv. “We believe we have demonstrated early proof of a new approach to neurodegenerative disease, focused on neuroprotection and neurogenesis. We plan to continue our pre-clinical exploration of MEK 1/2 inhibitors.”

Dr. Han is a member of the team that conducted the research into SNR1611. All research relevant to the publication was conducted in Genuv’s laboratories or under Genuv’s supervision. SNR1611 is currently in a Phase 1/2a clinical trial in Korea for ALS.

In addition to clearing amyloid beta plaques by promoting autophagy and lysosomal activity, the study showed that the mice, which are bred to display a human form of Alzheimer’s disease, also regained brain functions they had lost: the mice treated with SNR1611 performed better in maze tests and also showed improved ability to recognize new objects placed in their environment.

“We conclude that MEK inhibition by activating autophagic and lysosomal clearance of [amyloid beta plaques] and restoring the neural network is an effective therapeutic approach for AD,” wrote the authors.

The new publication in Molecular Psychiatry comes just weeks after an investigation in the journal Science uncovered evidence of potential data fabrication in a paper on Alzheimer’s disease published in 2006. The publication has intensified interest in alternative approaches to treating Alzheimer’s disease, including Genuv’s novel neuroprotection/neurogenesis hypothesis.

SNR1611 was discovered using Genuv’s proprietary ATRIVIEW® platform, an innovative and proven method of screening substances for their effects preserving homeostasis in the brain and inducing adult neural stem cells to develop into neurons.

Along with clinical stage drug candidates for degenerative brain diseases, Genuv is rapidly advancing a suite of powerful, experimental immuno-oncology treatments GNUV201 and GNUV205 for a variety of solid tumors. Genuv is working to establish proof-of-concept for GNUV201, a super anti-PD-1 antibody as well as the fusion (GNUV205) of this antibody to engineered IL-2 designed to induce IL-2 activity only in PD-1+ T cells that are in the tumor microenvironment to minimize systemic toxicity while dramatically enhancing the anti-tumor activity.

ABOUT GENUV

Genuv Inc. is a leader in discovering drugs for central nervous system (CNS) disorders and advanced antibody therapies for immuno-oncology applications. The ATRIVIEW® screening platform uses cell phenotypic and biomarker analyses to discover substances for the development of neurodegenerative disease treatment. The company’s SHINE MOUSE®, NuvoFcTM and NuvoMabTM platforms aim to generate antibodies with more diverse and effective repertoires in a multi-specific way. Based in Seoul, South Korea, Genuv launched its first clinical trial in South Korea in 2020. Recently, Genuv established a U.S. subsidiary based in Cambridge, Massachusetts, to accelerate the ATRIVIEW®-based new business model and development of immuno-oncology therapeutics. Genuv uses scientific imagination and unique platform technologies to overcome the challenges of treating major debilitating diseases. Learn more at www.genuv.com.

ABOUT SNR1611

SNR1611 (trametinib) was the first drug candidate identified at Genuv with the ATRIVIEW® platform. It showed the most potent neurogenerative and neuroprotective effects in a library of FDA-approved drug compounds. It is an anti-cancer drug approved by the FDA and currently marketed as Mekinist®. Genuv has demonstrated that this drug shows efficacy in animal models of Alzheimer’s disease and amyotrophic lateral sclerosis (ALS), especially at doses lower than those required for anti-cancer activity. Specifically, SNR1611 recovers neuronal tissue and function in the AD model mice by inducing the differentiation of neurons and generation of functional neurons to promote neuronal homeostasis.

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