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Genuv Inc.

Sungho HAN | Seoul, South Korea

Project Overview

  • Biotechnology/For Profit Organization Type
  • $600,000 Funding Amount
  • 2/1/24 — 2/1/25 Project Duration
  • Drug Discovery Program
  • Neuronal Regeneration and Repair Target
  • In Vivo Efficacy Therapeutic Stage
  • Active Status

Genuv Inc.

Sungho HAN | Seoul, South Korea

Preclinical study to explore the proof-of concept of trametinib at the lowest dose for the development of a disease-modifying treatment for Alzheimer’s disease

Alzheimer's disease (AD) is known to have accumulation of amyloid plaques or tau tangles before the patient recognizes symptoms. Most patients are diagnosed with AD after having suffered significant neuronal damage. In order to fundamentally treat AD, it is necessary to provide a strategy to restore the neural network with new neurons and protecting them from further damage in disease states. Genuv has taken the challenge to develop a drug that employs a new MOA that activates neurogenesis through differentiation of endogenous neural stem cells (NSCs) while exhibiting neuroprotective effects.

Genuv established ATRIVIEW®, a drug screening platform that identifies substances with both neurogenesis and neuroprotection properties using adult NSCs from the AD model mice, and discovered SNR1611. SNR1611 (trametinib; Mekinist®) is an anticancer drug approved by the USFDA for melanoma patients. Its molecular target is MEK1/2, which inhibits MEK-ERK signaling and can control cell proliferation, cell cycle, and cell death.

In vitro studies using amyloid beta, in vivo studies with 5XFAD mouse model of AD, and molecular biological analyses of AD patient brain samples suggested that MEK1/2 could be a new treatment target for AD. We also demonstrated that MEK1/2 inhibition by SNR1611 has therapeutic potential for AD treatment through neuroprotection by activating the autophagy-lysosomal pathway and through neurogenesis by activating cell cycle arrest. For the application of SNR1611 to AD patients, we developed a new formulation of SNR1611 (SNR1611NF), which can be administered in low doses and has improved stability and solubility than Mekinist®.

With the current proposal, we hope to secure the lowest effective concentration of SNR1611NF, determine the duration of administration, and identify biomarkers that can be applied to clinical trials based on the neurogenesis/neuroprotection mechanism. Our goal is to present a new therapeutic approach, activation of neurogenesis/neuroprotection, for the development of a fundamental treatment for AD.

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