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Therapeutic Drug for Alzheimer's Disease Targeted Beta-amyloid Aggregation/ Toxicity Blocker_Medifron_DBT
Korea Health Industry Development Institute (KHIDI) South Korea flag South Korea
Abstract ID:
Therapeutic drug for Alzheimer\'s disease targeted beta-amyloid aggregation/ toxicity blocker...
Contact Heajin Jung
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MECHANISM OF ACTION
• Small molecule direct bind to beta-amyloid • Small molecule inhibit aggregation of beta-amyloid and block toxic effect of beta-amyloid • Protect brain damage caused by beta-amyloid ch

1. Summary

• Alzheimer's disease (AD) is worldwide 4th causing death

• Number of AD patient increase rapidly coming after elderly society

• Most of dementia is AD (over 60%)

• The causing agent for AD is believed beta-amyloid peptide

• In the brain, beta-amyloid over produced and make plaque outside neuron

• Beta-amyloid in plaque is very resistance to protease attack

• Solubilized beta-amyloid can be transfer to BBB through LRP receptor and eventually degraded

• DWP09031 showed aggregation inhibitor as well as toxicity blocking activity

• Proof of concept done by transgenic animal model

2. Applications

• Neurodegenerative disease caused by protein aggregation

• Alzheimer's disease

3. Market Feasibility

• Global AD market reach to 10B US$

• In US, every year over 100B US$ spend AD care cost

• Disease modification drug can be developed and it will expend market size

4. Technical Advantages

• Drug candidate for aggregation/toxicity blocker

• DWP09031 is to bind beta-amyloid peptide and block aggregation of beta-amyloid, therefore toxic form of oligomers of beta-amyloid could not be formed and soluble beta-amyloid might be transported outside the brain via LRP, scavenger receptor of brain.

• Using hippocampus, DWP09031 can be restore LTP(long term potentiation) after beta-amyloid challenge

• In animal model, the concentrations of beta-amyloid are lowered by 50% in the brain and recover the memory deficit induced by toxic beta-amyloid in the brain.

• Human clinical trial study results showed that maximum dose (single dose 2,000mg) did not showed any sign of toxicity.

5. Technical Highlighted Summary

• The concentration of beta-amyloid is lowered by 50% in the brain after treatment of DWP09031

• Recover the memory deficit induced by toxic beta-amyloid in the brain.



• Relatively high bio-availability in rodent and non rodent species

• Good BBB penetration profile of DWP09031. Over 20% more compound detected in brain than plasma



• Less drug drug interaction prediction. Seven isoforms of CYP enzyme cannot inhibited by DWP09031



• GLP-compliant safety studies on rodent and non rodent including 4 weeks repeated dose toxicity, genotoxicity and safety pharmacology were done.

• More importantly, in vitro hERG channel study showed low binding potential.

• No moderate and significant safety issues occurred during safety and toxicity studies.

GO PREMIUM TO GET PATENT INFORMATION
Type of Business Relationship Sought
• We are actively seeking partner for global clinical trials.
• Out licensing deals for world exclusive sales right except Kore
FEATURED
Last Updated Jun 2016
Technology Type THERAPEUTIC
Phase of Development CLINICAL TRIALS
GOVERNMENT INSTITUTE